Research Radartracking 1,762 published studies · 471 human · 11 safety signals · 58 clinical trials · 44 cancer pages · updated Sep 2026Open the Research Map →

Lung Adenocarcinoma

The most common histologic subtype of lung cancer, driven by targetable oncogenic alterations (EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, HER2, KRAS G12C). Cure hinges on early surgical control; in advanced disease, matched targeted therapy and immunotherapy transform outcomes.

Educational only: This page is not medical advice. Coordinate decisions with your oncology team.

Reviewed Jun 2026 · thoracic oncology editor · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed· last updated Jun 2026

Evidence at a glanceHuman trial / meta-analysisMixed results⚠ Studies disagree
148 published studies that name Lung Adenocarcinoma23 human studies approved & graded (trial, observational, or meta-analysis)361 human clinical studies in the Lung Adenocarcinoma corpus4306 source documents in the Lung Adenocarcinoma corpus

last checked June 19, 2026

Why this grade?

Human trial / meta-analysis — Includes human trial or meta-analysis evidence.

Computed deterministically from the studies’ types and reported outcomes — not written by AI, and not a claim that anything works.

What the guidelines say

NCI PDQESMONCCNASCO

We link the authoritative guidelines rather than reproduce them. Below, the treatments on this page are split into standard care, guideline or regulatory options, supportive care, and studied but not standard so established care is not mixed with experimental or supportive items.

Standard care - guideline-backed
  • Anatomic resection (lobectomy/segmentectomy) with systematic nodal dissection when operable
  • Sublobar resection considered for small peripheral lesions or limited reserve
  • VATS/robotic approaches common
  • For oligometastatic disease responding to systemic therapy, consider metastasectomy case-by-case
  • SBRT for medically inoperable early-stage disease (curative intent)
  • Post-op or definitive chemoradiation for positive margins/unresectable disease
  • SRS for brain metastases
  • Palliative RT for symptomatic bone, chest wall, airway, or CNS lesions
  • Driver-positive: matched TKI first-line (EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, HER2)
  • Driver-negative: PD-L1 ≥50% → single-agent PD-1/PD-L1
  • Pemetrexed-based regimens favored in non-squamous NSCLC
  • Later lines guided by resistance profile (e
  • Platinum + Pemetrexed (± Pembrolizumab) (first-line driver-negative non-squamous)
  • Platinum + Taxane (± Pembrolizumab/Bevacizumab) (first-line non-squamous alternative)
  • Single-agent Pemetrexed Maintenance (post-induction)
  • Docetaxel (± Ramucirumab) (subsequent line)
  • Gemcitabine/Vinorelbine/Other Doublets (selected cases)
  • EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, HER2: prioritize matched TKIs with CNS-active options where possible
  • KRAS G12C: G12C inhibitors active
  • PD-L1 high driver-negative disease: consider IO monotherapy
  • Avoid initiating IO just before TKIs with high pneumonitis/hepatitis overlap
  • Re-biopsy/ctDNA at progression to reveal on-target mutations (e
  • Combinations to overcome resistance (TKI + MET/MEK/other) best pursued on trials
Guideline / FDA options - context-specific
  • etoposide
  • durvalumab
  • atezolizumab
  • crizotinib
  • paclitaxel
Supportive care - symptom / survivorship support
  • Smoking cessation with pharmacotherapy + behavioral support
  • Vaccinations (influenza, pneumococcal, COVID-19) and infection-prevention counseling
  • Pulmonary rehab/prehab to improve dyspnea and post-op outcomes
  • Nutrition optimization
  • Pain management (multimodal) and early palliative care integration
  • Psychosocial, sleep, and mood support
  • Bone health: consider DEXA/vitamin D/calcium
Studied, not standard - investigational
  • targeted therapy
  • targeted therapies
  • adjuvant immunotherapy
  • immunotherapies
  • chemotherapy
  • chemoradiotherapy
  • stereotactic body radiotherapy
  • definitive local therapy (radiation or surgery)
  • surgery
  • stereotactic radiosurgery
  • whole brain radiation therapy
  • Memantine
  • local therapy
  • lobectomy or greater (lobectomy + pneumonectomy)
  • sublobar resection (wedge resection + segmentectomy)
  • mediastinal lymph node dissection
  • radiotherapy
  • neoadjuvant or adjuvant radiation therapy
  • adjuvant chemoradiation (combination of chemotherapy + radiotherapy
  • carboplatin
  • cisplatin
  • nivolumab
  • Actinomycin D
  • Curcumin / Theracurmin
  • doxorubicin
  • Fuzuloparib
  • Genistein
  • ifosfamide
  • Indole-3-Acetic Acid
  • vincristine

Read the guidelines

Cancer-specific deep links aren’t curated yet — these search the authoritative sources for Lung Adenocarcinoma.

Treatment map: Lung Adenocarcinoma

Open as a full page →

Standard care plus every compound studied in the literature (each cited) and graded by evidence, organized by clinical readiness. A category, not a verdict that anything works — confirm anything here with your oncology team.

60
Interventions
23
Standard of care
7
Tested in people
10
Lab / animal
15
Named in lit.
7
Classes
Standard of care (23) Guideline option (5) Tested in people (7) Lab / animal only (10) Named in the literature (15)

Tested in people, by trial phase: phase not reported ×7

Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Surgery & procedures
4
—
2
—
4
Radiotherapy
4
—
2
—
4
Chemotherapy
7
2
1
5
3
Targeted therapy
6
1
1
1
1
Immunotherapy
2
2
—
1
2
Supplements & natural agents
—
—
1
3
—
Other
—
—
—
—
1

Columns group into clinical evidence (used in, or tested on, people) and preclinical evidence (lab/animal, or only named in the literature). Cell = number of interventions; a dashed cell means none recorded there.

Established care — detail (28)
Surgery & procedures
Anatomic resection (lobectomy/segmentectomy) with systematic nodal dissection when operable
Anatomic resection (lobectomy/segmentectomy) with systematic nodal dissection when operable.
CurativeStandardCurated
Sublobar resection considered for small peripheral lesions or limited reserve
Sublobar resection considered for small peripheral lesions or limited reserve.
CurativeStandardCurated
VATS/robotic approaches common
VATS/robotic approaches common; ERAS pathways for recovery.
CurativeStandardCurated
For oligometastatic disease responding to systemic therapy, consider metastasectomy case-by-case
For oligometastatic disease responding to systemic therapy, consider metastasectomy case-by-case.
CurativeStandardCurated
Radiotherapy
SBRT for medically inoperable early-stage disease (curative intent)
SBRT for medically inoperable early-stage disease (curative intent).
—StandardCurated
Post-op or definitive chemoradiation for positive margins/unresectable disease
Post-op or definitive chemoradiation for positive margins/unresectable disease.
—StandardCurated
SRS for brain metastases
SRS for brain metastases; WBRT for diffuse involvement.
—StandardCurated
Palliative RT for symptomatic bone, chest wall, airway, or CNS lesions
Palliative RT for symptomatic bone, chest wall, airway, or CNS lesions.
PalliativeStandardCurated
Chemotherapy
Pemetrexed-based regimens favored in non-squamous NSCLC
Pemetrexed-based regimens favored in non-squamous NSCLC; maintenance pemetrexed ± IO after induction.
MaintenanceStandardCurated
Later lines guided by resistance profile (e
Later lines guided by resistance profile (e.g., MET amp after EGFR) and clinical trial availability.
—StandardCurated
Platinum + Pemetrexed (± Pembrolizumab) (first-line driver-negative non-squamous)
Standard induction (4 cycles) followed by maintenance pemetrexed ± pembrolizumab; folate/B12 + steroid premed required.
—StandardCurated
Platinum + Taxane (± Pembrolizumab/Bevacizumab) (first-line non-squamous alternative)
Useful when pemetrexed contraindicated; consider bevacizumab if no bleeding/hemoptysis or recent surgery.
—StandardCurated
Single-agent Pemetrexed Maintenance (post-induction)
Non-squamous maintenance option; continue until progression/toxicity; add IO per initial plan.
MaintenanceStandardCurated
Docetaxel (± Ramucirumab) (subsequent line)
Post–IO/chemo progression; monitor for neutropenia, mucositis, edema; ramucirumab adds VEGF-related AEs.
—StandardCurated
Gemcitabine/Vinorelbine/Other Doublets (selected cases)
Alternatives when standard options exhausted/contraindicated; response rates modest.
—StandardCurated
etoposide
FDA-approved for this cancer.
—Guideline option
paclitaxel
FDA-approved for this cancer.
—Guideline option
Targeted therapy
Driver-positive: matched TKI first-line (EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, HER2)
Driver-positive: matched TKI first-line (EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, HER2).
—StandardCurated
EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, HER2: prioritize matched TKIs with CNS-active options where possible
EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, HER2: prioritize matched TKIs with CNS-active options where possible.
—StandardCurated
KRAS G12C: G12C inhibitors active
KRAS G12C: G12C inhibitors active; co-mutations (STK11/KEAP1) shape IO benefit.
—StandardCurated
Avoid initiating IO just before TKIs with high pneumonitis/hepatitis overlap
Avoid initiating IO just before TKIs with high pneumonitis/hepatitis overlap; sequence thoughtfully.
—StandardCurated
Re-biopsy/ctDNA at progression to reveal on-target mutations (e
Re-biopsy/ctDNA at progression to reveal on-target mutations (e.g., EGFR C797S) or bypass (MET/HER2 amp) for next-line strategy.
—StandardCurated
Combinations to overcome resistance (TKI + MET/MEK/other) best pursued on trials
Combinations to overcome resistance (TKI + MET/MEK/other) best pursued on trials.
—StandardCurated
crizotinib
FDA-approved for this cancer.
—Guideline option
Immunotherapy
Driver-negative: PD-L1 ≥50% → single-agent PD-1/PD-L1
Driver-negative: PD-L1 ≥50% → single-agent PD-1/PD-L1; otherwise IO + platinum doublet (commonly pembrolizumab + carboplatin/cisplatin + pemetrexed).
—StandardCurated
PD-L1 high driver-negative disease: consider IO monotherapy
PD-L1 high driver-negative disease: consider IO monotherapy; otherwise IO-chemotherapy.
—StandardCurated
durvalumab
FDA-approved for this cancer.
—Guideline option
atezolizumab
FDA-approved for this cancer.
—Guideline option

Established care shown from OncoForge editorial curation · reviewed September 25, 2025 — authoritative citations (NCI PDQ / FDA) are being added.

Supportive care (7)
  • Smoking cessation with pharmacotherapy + behavioral support.
  • Vaccinations (influenza, pneumococcal, COVID-19) and infection-prevention counseling.
  • Pulmonary rehab/prehab to improve dyspnea and post-op outcomes.
  • Nutrition optimization; address cachexia early; dietitian involvement.
  • Pain management (multimodal) and early palliative care integration.
  • Psychosocial, sleep, and mood support; caregiver resources.
  • Bone health: consider DEXA/vitamin D/calcium; antiresorptives for bone mets as indicated.
Investigational & adjunct compounds — detail (32)
Meta-analysis (6)
local therapyMemantineoff-labelstereotactic radiosurgerysurgerytargeted therapy· targetable driver alterationswhole brain radiation therapy
Tested in people (1)
carboplatinoff-label
Named in the literature
targeted therapiesadjuvant immunotherapy· Adjuvant (after surgery)immunotherapieschemotherapy· Adjuvant (after surgery)chemotherapy· Neoadjuvant (before surgery)chemoradiotherapystereotactic body radiotherapydefinitive local therapy (radiation or surgery)surgery· Adjuvant (after surgery)lobectomy or greater (lobectomy + pneumonectomy)sublobar resection (wedge resection + segmentectomy)mediastinal lymph node dissectionradiotherapyneoadjuvant or adjuvant radiation therapy· Neoadjuvant (before surgery)adjuvant chemoradiation (combination of chemotherapy + radiotherapy· Adjuvant (after surgery)

"Tested in people" rows show the highest trial phase found in that compound's cited human studies (Phase I–IV; "phase not reported" = a human study with no phase tag). "Studied" = named in the cited literature for this cancer. "FDA ✓" = FDA-approved for this cancer; "off-label" = an FDA-approved drug used outside its approved indications (per openFDA). Not a claim that anything works.

Reported figures

Get cited updates on Lung Adenocarcinoma
A monthly email when the research changes — $10/mo. Manage follows
Follow Lung Adenocarcinoma

Snapshot

The essentials in ~60 seconds — every line is drawn from the cited sources below.

What it is
A form of non–small cell lung cancer where accurate clinical staging and early molecular testing are critical to guide management. [1][2]
Standard treatment
Treatment is stage‑dependent and guided by guideline recommendations: surgery (preferably lobectomy) for medically fit patients with stage I, mediastinal nodal evaluation at surgery, adjuvant/neoadjuvant chemotherapy for selected patients, surgery ± (neo)adjuvant chemotherapy for single‑station N2, concurrent chemoradiotherapy followed by adjuvant immunotherapy for multi‑station N2, and radiation or surgery as definitive local therapy for oligometastatic disease; follow‑up uses chest CT every 6 months for 2 years then annually. [3][4][5][6][7][8]
Key test
Early molecular testing for actionable driver alterations (and PD‑L1) plus appropriate staging studies are key at diagnosis; testing methods include IHC, FISH, PCR, and next‑generation sequencing. [1][7][9][10]
Biggest challenge
Rapidly evolving evidence and limited data for some subgroups (for example within stage II and oligometastatic disease) make optimal, up‑to‑date management and staging decisions difficult. [11][4][6][12]

Ask about Lung Adenocarcinoma

Answers come only from the cited sources on this page — with the supporting evidence shown. If the sources here don't cover your question, it will say so. Educational information, not medical advice.

Key numbers & factors

Risk factors

  • ▲ increases riskTumor size — risk factor for occult mediastinal nodal disease [13]
  • ▲ increases riskRadiological nodal involvement — risk factor for occult mediastinal nodal disease [13]

Biomarkers

  • EGFR (including resistant EGFR mutations)ActionableIdentifies a targetable driver alteration in advanced NSCLC [9][7]
  • ALK rearrangementsActionableIdentifies a targetable driver alteration in advanced NSCLC [9][7]
  • ROS1 rearrangementsActionableIdentifies a targetable driver alteration in advanced NSCLC [9][7]
  • PD‑L1 overexpressionActionableBiomarker for immunotherapy decision‑making in advanced NSCLC [9][10]
  • Next‑generation sequencing (NGS), IHC, FISH, PCR · Methods for molecular screening to detect driver alterations [9]

9 sections — tap any heading to expand its cited detail. Key points are above.

OverviewLiving guidelines are developed for selected topic areas with rapidly evolving evidence and are not intended to substitute for independent professional judgment or account for individual patient variation. Accurate staging, early molecular testing, and knowledge of recent trials are critical to optimizing oncologic outcomes in surgically resectable lung cancer.6 points
  • Living guidelines are developed for selected topic areas with rapidly evolving evidence that drives frequent change in recommended clinical practice and are not intended to substitute for independent professional judgment of the treating clinician or to account for individual variation among patients. [2]
  • Accurate staging, early molecular testing, and knowledge of recent trials are critical to optimize oncologic outcomes in surgically resectable lung cancer. [1]
  • An ASCO guideline developed evidence-based recommendations addressing evaluation and staging workup, surgical management, neoadjuvant and adjuvant approaches, and management of unresectable stage III NSCLC. [14]
  • An ESMO expert consensus developed recommendations addressing topics including tissue and biomarkers analyses, early and locally advanced disease, and metastatic disease in EGFR-mutant non-small-cell lung cancer. [12]
  • The AJCC defines stage I NSCLC as a T1 or T2 primary tumor with no hilar or mediastinal nodal disease (N0) and no metastatic spread (M0). [3]
  • Stage II NSCLC is a heterogeneous group that includes patients with T1-2N1 or T3N0 tumors. [4]
Standard managementClinical practice guidelines provide recommendations for diagnosis, primary management, surveillance, and subsequent treatment of non‑small cell lung cancer. Management differs by stage and extent of disease (for example, stage I is primarily managed with surgery when patients are medically fit, N2 disease management differs for single‑station versus multi‑station disease), and surveillance after curative‑intent therapy uses chest CT at regular intervals while certain modalities are not recommended.12 points
  • The NCCN Clinical Practice Guidelines provide recommendations for the treatment of patients with non-small cell lung cancer, including diagnosis, primary disease management, surveillance, and subsequent treatment. [7]
  • For patients with single-station N2 disease, panelists agreed on the adoption as first-line treatment of surgery and (neo)adjuvant chemotherapy. [5]
  • For patients with multi-station N2 disease, panelists agreed on concurrent chemoradiotherapy followed by adjuvant immunotherapy. [5]
  • Radiation and surgery were the only primary definitive local therapy modalities recommended for use in the management of patients with oligometastatic disease. [6]
  • After definitive curative-intent therapy for stage I–III NSCLC, patients should undergo surveillance imaging every 6 months for 2 years and then annually for detection of new primary lung cancers. [8]
  • Chest computed tomography is identified as the optimal imaging modality for surveillance after curative-intent therapy in NSCLC. [8]
  • Fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) should not be used as a surveillance tool after curative-intent therapy in NSCLC; circulating biomarkers should not be used as a surveillance strategy for detection of recurrence; and brain magnetic resonance imaging should not be used for routine surveillance in stage I–III NSCLC. [8]
  • Surgical resection is the accepted treatment for medically fit patients with stage I NSCLC, with full lobar or greater resection (lobectomy, pneumonectomy) strongly suggested rather than sublobar resection (wedge resection, segmentectomy). [3]
  • Systematic sampling or full mediastinal lymph node dissection may improve pathologic staging but is unproven therapeutically. [3]
  • There are no data supporting the routine use of chemotherapy in an adjuvant or neoadjuvant setting for stage I NSCLC; recent phase II data suggest that neoadjuvant chemotherapy is feasible and safe and larger phase III trials are evaluating it. [3]
  • Primary radiation therapy should be considered for inoperable patients with stage I NSCLC; the use of neoadjuvant or adjuvant radiation therapy in patients with stage I NSCLC is of unproven benefit. [3]
  • For stage II NSCLC, studies of adjuvant therapy after complete resection are available from large, randomized studies of adjuvant radiation therapy, chemotherapy, or a combination of the two. [4]
Key biomarkersClinical practice guidelines from major organizations focus on treatment recommendations for advanced or metastatic non–small cell lung cancer (NSCLC) defined by actionable or driver biomarkers. Consensus guidance also identifies specific targetable alterations and describes a range of molecular diagnostic tests used for screening.3 points
  • Guidelines from the National Comprehensive Cancer Network (NCCN) and an ASCO living guideline provide treatment- and evidence-based recommendations for advanced, metastatic, or stage IV non–small cell lung cancer (NSCLC) that have actionable or driver alterations. [7][10]
  • Molecular screening tests discussed for NSCLC include immunohistochemistry, fluorescence in situ hybridization, polymerase chain reaction-based testing, and next-generation sequencing. [9]
Show 1 lab & early-research finding
  • Consensus guidance lists targetable alterations in NSCLC including epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK) rearrangements, ROS1 rearrangements, programmed cell death ligand-1 (PD-L1) overexpression, and resistant EGFR mutations. [9]
Staging & riskAccurate mediastinal nodal staging is essential in non-small cell lung cancer because it refines prognosis, guides multimodal treatment, and can affect survival; guidelines provide practical algorithms that stratify tumours by risk of occult mediastinal disease (for example by tumour size and radiological nodal involvement) and state that invasive mediastinal staging is not required for T1a and T1b tumours without radiological evidence of nodal disease. Endobronchial ultrasound/endoscopic ultrasound is the preferred initial method for staging paratracheal lymph nodes, surgical staging techniques demonstrate superior accuracy when there is intermediate suspicion of mediastinal disease, and an ASCO guideline gives recommendations on evaluation and staging workup for suspected stage III NSCLC; T3 tumours can include primary tumours invading the chest wall apex, mediastinum, diaphragm, or mainstem bronchus.7 points
  • Accurate mediastinal nodal staging is essential for the management of non-small cell lung cancer because it refines prognosis, guides multimodal treatment, and improves survival. [13]
  • The new recommendations state that invasive mediastinal staging is not required for T1a and T1b tumours without radiological evidence of nodal disease, regardless of their location. [13]
  • For cases with intermediate suspicion of mediastinal disease, surgical staging techniques demonstrate superior accuracy compared with endosonography alone. [13]
  • A practical staging algorithm stratifies tumours according to risk factors of occult mediastinal disease such as tumour size and radiological nodal involvement. [13]
  • Expert panellists reached agreement that endobronchial ultrasound/endoscopic ultrasound was the preferred method of initial mediastinal staging for paratracheal lymph nodes. [5]
  • An ASCO guideline provides recommendations on evaluation and staging workup for patients with suspected stage III NSCLC. [14]
  • T3 tumors can include primary tumors invading the chest wall apex, mediastinum, diaphragm, or mainstem bronchus. [4]
Treatments & compounds studied23 therapeutics and procedures across targeted therapies, immunotherapies, chemotherapy, radiotherapy, surgery/procedures, and other modalities are described in guideline and consensus documents for lung adenocarcinoma.21 treatments

Chemotherapy

  • (neo)adjuvant chemotherapy · chemotherapy · 2 findings
    • Adjuvant (after surgery)(Neo)adjuvant chemotherapy was part of the agreed first-line treatment approach in patients with single-station N2 disease alongside surgery. [5]
    • Neoadjuvant (before surgery)There are no data supporting the routine use of chemotherapy in an adjuvant or neoadjuvant setting for these patients. [3]

Targeted therapy

  • targeted therapy: targetable driver alterationsGuideline recommendations were updated to address first-, second-, and subsequent-line targeted treatment options for patients with targetable driver alterations. [10]
  • targeted therapies: The NCCN Guidelines Insights highlight recent updates to targeted therapies and their respective biomarkers in NSCLC. [15]

Immunotherapy

  • adjuvant immunotherapy: Adjuvant (after surgery)Adjuvant immunotherapy was recommended to follow concurrent chemoradiotherapy for patients with multi-station N2 disease. [5]
  • immunotherapies: The NCCN Guidelines Insights highlight recent updates to immunotherapies and their respective biomarkers in NSCLC. [15]

Radiotherapy

  • stereotactic body radiation therapy · stereotactic body radiotherapy: Recommendations were provided for the optimal technical use of hypofractionated radiation or stereotactic body radiation therapy, including dose and fractionation, as definitive local therapy for extracranial oligometastatic NSCLC. [6]
  • whole brain radiation therapy: SRS, whole brain radiation therapy, or their combination are described as reasonable options for other patients with brain metastases. [16]
  • radiation therapy · radiotherapy: Primary radiation therapy is recommended to be considered for inoperable patients. [3]
  • neoadjuvant or adjuvant radiation therapy: Neoadjuvant (before surgery)The use of neoadjuvant or adjuvant radiation therapy in patients with stage I NSCLC is of unproven benefit. [3]

Repurposed drugs

  • memantine: Memantine and hippocampal avoidance are recommended to be offered to patients who receive whole brain radiation therapy, have no hippocampal lesions, and have an expected survival of 4 months or more. [16]

Procedures & devices

  • surgery · 2 findings
    • Adjuvant (after surgery)Surgery was endorsed as part of first-line management together with (neo)adjuvant chemotherapy in patients with single-station N2 disease. [5]
    • Surgery is described as a reasonable option for patients with brain metastases. [16]
  • stereotactic radiosurgery (SRS) · stereotactic radiosurgery: Sources state that for patients with asymptomatic brain metastases and no systemic therapy options, SRS alone should be offered to those with one to four unresected brain metastases, excluding small-cell lung carcinoma. [16]
  • local therapy: Patients with symptomatic brain metastases should receive local therapy regardless of the systemic therapy used. [16]
  • lobectomy or greater (lobectomy, pneumonectomy): Surgical resection (full lobar or greater) is the accepted treatment for medically fit patients with stage I NSCLC. [3]
  • sublobar resection (wedge resection, segmentectomy): Sublobar resection (wedge resection, segmentectomy) is mentioned as an alternative but is less strongly suggested than full lobar resection for stage I NSCLC. [3]
  • mediastinal lymph node dissection: Systematic sampling or full mediastinal lymph node dissection may improve pathologic staging but is unproven therapeutically. [3]

Other

  • concurrent chemoradiotherapy · chemoradiotherapy: Concurrent chemoradiotherapy was recommended as part of the treatment approach for multi-station N2 disease. [5]
  • definitive local therapy (radiation or surgery): Conditional recommendations were given for definitive local therapies (radiation or surgery) in synchronous, metachronous, oligopersistent, and oligoprogressive extracranial disease when technically feasible and clinically safe to all disease sites. [6]
  • adjuvant chemoradiation (combination of chemotherapy and radiation): Adjuvant (after surgery)After complete resection of stage II NSCLC, data from large randomized studies are available for adjuvant radiation therapy, chemotherapy, or a combination of the two. [4]
Prognosis1 point
  • Presently, data regarding clinical benefits of local therapy on overall and other survival outcomes is still sparse for oligometastatic NSCLC. [6]
What we don't know yetEvidence about lung adenocarcinoma treatment is rapidly evolving; ASCO maintains living guidelines that are updated on a regular schedule, and ESMO produced an expert consensus to develop recommendations on topics not covered in detail by existing guidelines and where available evidence is limited or conflicting.3 points
  • Evidence is rapidly evolving; ASCO maintains living guidelines that are updated on a regular schedule, and the ESMO expert consensus aimed to develop recommendations on topics not covered in detail by existing guidelines and where available evidence is limited or conflicting. [11][12]
  • The extent of the data available regarding treatment of the different subgroups within stage II NSCLC is limited, and the quality of the data is limited because information often comes from small series of patients. [4]
  • Larger phase III trials are evaluating the role of neoadjuvant chemotherapy. [3]
Safety & interactions1 point
  • Patients with asymptomatic brain metastases who have either Karnofsky Performance Status ≤50 or Karnofsky Performance Status <70 with no systemic therapy options do not derive benefit from radiation therapy according to guideline findings. [16]
Epidemiology1 point
  • Based on clinical assessment alone, patients with stage II NSCLC comprise only 5% of all patients with NSCLC. [4]

Common questions

What is Lung Adenocarcinoma?

Living guidelines are developed for selected topic areas with rapidly evolving evidence and are not intended to substitute for independent professional judgment or account for individual patient variation. Accurate staging, early molecular testing, and knowledge of recent trials are critical to optimizing oncologic outcomes in surgically resectable lung cancer.

Which biomarkers are important in Lung Adenocarcinoma?

Clinical practice guidelines from major organizations focus on treatment recommendations for advanced or metastatic non–small cell lung cancer (NSCLC) defined by actionable or driver biomarkers. Consensus guidance also identifies specific targetable alterations and describes a range of molecular diagnostic tests used for screening.

How is Lung Adenocarcinoma treated?

Clinical practice guidelines provide recommendations for diagnosis, primary management, surveillance, and subsequent treatment of non‑small cell lung cancer. Management differs by stage and extent of disease (for example, stage I is primarily managed with surgery when patients are medically fit, N2 disease management differs for single‑station versus multi‑station disease), and surveillance after curative‑intent therapy uses chest CT at regular intervals while certain modalities are not recommended.

What treatments are studied for Lung Adenocarcinoma?

23 therapeutics and procedures across targeted therapies, immunotherapies, chemotherapy, radiotherapy, surgery/procedures, and other modalities are described in guideline and consensus documents for lung adenocarcinoma.

What is still being researched in Lung Adenocarcinoma?

Evidence about lung adenocarcinoma treatment is rapidly evolving; ASCO maintains living guidelines that are updated on a regular schedule, and ESMO produced an expert consensus to develop recommendations on topics not covered in detail by existing guidelines and where available evidence is limited or conflicting.

What do studies report about staging & risk in Lung Adenocarcinoma?

Accurate mediastinal nodal staging is essential in non-small cell lung cancer because it refines prognosis, guides multimodal treatment, and can affect survival; guidelines provide practical algorithms that stratify tumours by risk of occult mediastinal disease (for example by tumour size and radiological nodal involvement) and state that invasive mediastinal staging is not required for T1a and T1b tumours without radiological evidence of nodal disease. Endobronchial ultrasound/endoscopic ultrasound is the preferred initial method for staging paratracheal lymph nodes, surgical staging techniques demonstrate superior accuracy when there is intermediate suspicion of mediastinal disease, and an ASCO guideline gives recommendations on evaluation and staging workup for suspected stage III NSCLC; T3 tumours can include primary tumours invading the chest wall apex, mediastinum, diaphragm, or mainstem bronchus.

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked June 19, 2026.

  1. GuidelineThe American Association for Thoracic Surgery (AATS) 2023 Expert Consensus Document: Staging and multidisciplinary management of patients with early-stage non-small cell lung cancer · 2023
  2. GuidelineTherapy for Stage IV Non-Small Cell Lung Cancer With Driver Alterations: ASCO Living Guideline, 2026.3.1 · 2026
  3. GuidelineTreatment of stage I non-small cell lung carcinoma · 2003
  4. GuidelineTreatment of stage II non-small cell lung cancer · 2003
  5. GuidelineReaching multidisciplinary consensus on the management of non-bulky/non-infiltrative stage IIIA N2 non-small cell lung cancer · 2023
  6. GuidelineTreatment of Oligometastatic Non-Small Cell Lung Cancer: An ASTRO/ESTRO Clinical Practice Guideline · 2023
  7. GuidelineNon-Small Cell Lung Cancer, Version 4.2026, NCCN Clinical Practice Guidelines In Oncology · 2026
  8. GuidelineLung Cancer Surveillance After Definitive Curative-Intent Therapy: ASCO Guideline · 2020
  9. GuidelineBiomarkers in Non-Small Cell Lung Cancers: Indian Consensus Guidelines for Molecular Testing · 2019
  10. GuidelineTherapy for Stage IV Non-Small Cell Lung Cancer With Driver Alterations: ASCO Living Guideline, Version 2023.3 · 2024
  11. GuidelineTherapy for Stage IV Non-Small-Cell Lung Cancer With Driver Alterations: ASCO Living Guideline, Version 2023.1 · 2023
  12. GuidelineESMO expert consensus statements on the management of EGFR mutant non-small-cell lung cancer · 2022
  13. GuidelineSEPAR-SECT Recommendations for Perioperative Invasive Mediastinal Staging of Non-small Cell Lung Cancer · 2026
  14. GuidelineManagement of Stage III Non-Small-Cell Lung Cancer: ASCO Guideline · 2022
  15. GuidelineNCCN Guidelines Insights: Non-Small Cell Lung Cancer, Version 2.2021 · 2021
  16. GuidelineTreatment for Brain Metastases: ASCO-SNO-ASTRO Guideline · 2022

What supports this page

The kinds of sources behind this page, strongest at the top. Faint rungs show what is not here yet.

Guideline
67
Meta-analysis
213
Systematic review
90
Randomized trial
9
Clinical trial
44
Observational
12
Case report
232
Review
3613
Preclinical
0
Other
26

Living document — last change June 19, 2026: Cancer page updated.

Pooled evidence across studies

PubMed
  • Cancer-specific survival: HR 1.623 (0.452–7.065 across studies) · (regimen unspecified)
    10 studies · 40% agree · heterogeneous · 3 flagged36125491
  • ORR (subgroup): 21% (19–27 across studies) · cofetuzumab pelidotin
    3 studies · 67% agree · moderate34083232
  • 5-year RFS: 85% (69–93 across studies) · (regimen unspecified)
    3 studies · 67% agree · moderate32537765
  • ASCVD incidence: HR 1.56 (0.91–2.8 across studies) · (regimen unspecified)
    3 studies · 33% agree · heterogeneous40445187
  • ORR: 32.099999999999994% (29.4–34.8 across studies) · (regimen unspecified)
    2 studies · 100% agree · consistent40319778
  • DCR: 42.35% (41.2–43.5 across studies) · (regimen unspecified)
    2 studies · 100% agree · consistent40319778
  • Brain metastasis at diagnosis: OR 1.6695 (1.564–1.775 across studies) · (regimen unspecified)
    2 studies · 100% agree · consistent36125491
  • Colorectal cancer incidence: RR 1.135 (1.1–1.17 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Colon cancer incidence: RR 1.19 (1.17–1.21 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Rectal cancer incidence: RR 1.24 (1.22–1.26 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Lung cancer incidence: RR 1.23 (1.2–1.26 across studies) · red meat
    2 studies · 100% agree · consistent34455534
  • Histology distribution: 50% (26–74 across studies) · etoposide + adenocarcinoma + squamous cell carcinoma
    2 studies · 0% agree · heterogeneous35147672

Numbers pooled deterministically across 108 published studies that passed our figure-accuracy checks — a quick synthesis, not a formal meta-analysis. Updated 8/31/2026.

Compounds compared by evidence

PubMed

How to read this: Ranked by the strength and volume of the evidence — NOT by how well a treatment works. A higher rank means a compound has been studied more, or in stronger study designs (e.g. randomized trials over lab studies), not that it produces better outcomes. The effect column shows the largest pooled figure reported, not a head-to-head comparison.

#CompoundEvidence strengthStudiesLargest pooled effect
1Etoposide OtherHuman · observational1Histology distribution: 50%
2Doxorubicin ChemotherapyAnimal only1—
3Indole-3-Acetic Acid OtherAnimal only1—
4Actinomycin D OtherInsufficient evidence1—
5Cisplatin ChemotherapyInsufficient evidence1—
6Crizotinib Targeted therapyInsufficient evidence1—
7Curcumin / Theracurmin OtherInsufficient evidence1—
8Fuzuloparib OtherInsufficient evidence1—
9Genistein OtherInsufficient evidence1—
10Ifosfamide OtherInsufficient evidence1—
11Nivolumab †Rx ImmunotherapyInsufficient evidence1—
12Pembrolizumab OtherInsufficient evidence1—
13Vincristine OtherInsufficient evidence1—

Ranked across 13 compounds with published studies for this cancer. Updated 8/31/2026.

Medicines & supplements studied for Lung Adenocarcinoma

PubMedFDAClinicalTrials.gov

Every drug, supplement, and other agent the published studies cover for Lung Adenocarcinoma, ranked by how strong the evidence is — what studies report, not a recommendation. Tap any to see its full profile.

Medicines · 17

EtoposideHuman trial / meta-analysisReported positive2 human

Includes human trial or meta-analysis evidence.

Largest credible effect: LCNEC/AD proportion 74%, n=96 PMID 35147672 · response rates 7–74 across 4 studies

Most authoritative study: Study protocol of an open-label prospective phase II study of Durvalumab plus Carboplatin and Etoposide in advanced large cell neuroendocrine carcinoma of the lung (LOGIK2401: NECTAR study)

ChemotherapyFDA approved2 studiesFull profile →
CarboplatinHuman trial / meta-analysisInconclusive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: enrolled patients 30, n=30 PMID 41037966

Most authoritative study: Study protocol of an open-label prospective phase II study of Durvalumab plus Carboplatin and Etoposide in advanced large cell neuroendocrine carcinoma of the lung (LOGIK2401: NECTAR study)

Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
DurvalumabHuman trial / meta-analysisInconclusive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: enrolled patients 30, n=30 PMID 41037966

Most authoritative study: Study protocol of an open-label prospective phase II study of Durvalumab plus Carboplatin and Etoposide in advanced large cell neuroendocrine carcinoma of the lung (LOGIK2401: NECTAR study)

Based on a single study.
ImmunotherapyFDA approved1 studyFull profile →
DoxorubicinAnimal onlyReported positive1 animal

Animal studies only — no human data.

Largest credible effect: doxorubicin loading rate 73.24% PMID 38445013

Most authoritative study: Oxygen-producing and pH-responsive targeted DNA nanoflowers for enhanced chemo-sonodynamic therapy of lung cancer

No human studies yet · Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
PembrolizumabInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Recent Advances in Adjuvant Therapy for Non-Small-Cell Lung Cancer

No human studies yet · Findings conflict across studies · No numeric effect sizes reported.
Other3 studiesFull profile →
CisplatinInsufficient evidenceMixed results

No primary experimental studies yet.

Largest credible effect: number_of_cycles 4 PMID 24102012

Most authoritative study: Platinum-based targeted chemotherapies and reversal of cisplatin resistance in non-small cell lung cancer (NSCLC)

No human studies yet · Findings conflict across studies · Effect sizes reported in only 1 of 2 studies.
ChemotherapyFDA off-label2 studiesFull profile →
Nivolumab †RxInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Targeting PD-L1 for non-small-cell lung cancer

No human studies yet · Findings conflict across studies · No numeric effect sizes reported.
Immunotherapy2 studiesFull profile →
Actinomycin DInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: chemotherapy duration 10 months 10 mo, n=1 PMID 11558020 · effect sizes 2–10 across 2 studies

Most authoritative study: Pleuropulmonary blastoma

No human studies yet · Based on a single study.
Chemotherapy1 studyFull profile →
AtezolizumabInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Recent Advances in Adjuvant Therapy for Non-Small-Cell Lung Cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
ImmunotherapyFDA approved1 studyFull profile →
BevacizumabInsufficient evidenceReported negative

No primary experimental studies yet.

Most authoritative study: Large cell neuroendocrine carcinoma of the lungs: case report and literature review

No human studies yet · No numeric effect sizes reported · Based on a single study.
Other1 studyFull profile →
CrizotinibInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: ALK-rearrangement in non-small-cell lung cancer (NSCLC)

No human studies yet · No numeric effect sizes reported · Based on a single study.
Targeted therapyFDA approved1 studyFull profile →
DocetaxelInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: time_to_brain_metastasis 44 mo, n=1 PMID 37158392 · effect sizes 8–44 across 2 studies

Most authoritative study: Brain and lung metastasis of uterine leiomyosarcoma: illustrative case

No human studies yet · Based on a single study.
Chemotherapy1 studyFull profile →
FuzuloparibInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Fuzuloparib: First Approval

No human studies yet · No numeric effect sizes reported · Based on a single study.
Targeted therapy1 studyFull profile →
GemcitabineInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: time_to_brain_metastasis 44 mo, n=1 PMID 37158392 · effect sizes 8–44 across 2 studies

Most authoritative study: Brain and lung metastasis of uterine leiomyosarcoma: illustrative case

No human studies yet · Based on a single study.
Chemotherapy1 studyFull profile →
IfosfamideInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: chemotherapy duration 10 months 10 mo, n=1 PMID 11558020 · effect sizes 2–10 across 2 studies

Most authoritative study: Pleuropulmonary blastoma

No human studies yet · Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →
PaclitaxelInsufficient evidenceReported negative

No primary experimental studies yet.

Most authoritative study: Large cell neuroendocrine carcinoma of the lungs: case report and literature review

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA approved1 studyFull profile →
VincristineInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: chemotherapy duration 10 months 10 mo, n=1 PMID 11558020 · effect sizes 2–10 across 2 studies

Most authoritative study: Pleuropulmonary blastoma

No human studies yet · Based on a single study.
ChemotherapyFDA off-label1 studyFull profile →

Supplements & natural agents · 3

Indole-3-Acetic AcidAnimal onlyReported positive1 animal

Animal studies only — no human data.

Most authoritative study: Bifidobacterium animalis suppresses non-small cell lung cancer progression and modulates tumor immunity through indole-3-acetic acid

No human studies yet · No numeric effect sizes reported · Based on a single study.
Supplements & natural agents1 studyFull profile →
Curcumin / TheracurminInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Curcumin and Its Analogs in Non-Small Cell Lung Cancer Treatment: Challenges and Expectations

No human studies yet · No numeric effect sizes reported · Based on a single study.
Supplements & natural agents1 studyFull profile →
GenisteinInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Biological activities and therapeutic potential of soy isoflavones: a focus on anticancer activity

No human studies yet · No numeric effect sizes reported · Based on a single study.
Supplements & natural agents1 studyFull profile →

What recent studies report in Lung Adenocarcinoma

These are reviewed studies whose abstracts concern Lung Adenocarcinoma. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Lung Adenocarcinoma. Most are early lab, animal, or small human studies, and findings often conflict.

60 studies10 human4 animal⚠ Conflicting evidenceMechanism (22)Trial (5)Supportive care (2)Formulation (1)

Tracking 60 published studies of Lung Adenocarcinoma: 10 in humans, 4 in animals, 46 reviews/other.

Reported direction across studies: 23 positive, 15 mixed, 1 negative, 21 inconclusive.

Findings conflict — both supportive and negative/mixed results exist (see below). Human evidence is limited.

These counts summarize what the studies reported; they are not a measure of whether anything works for Lung Adenocarcinoma.

Compounds with studies mentioning Lung Adenocarcinoma

Genistein (1)Indole 3 acetic acid (1)Durvalumab (1)Carboplatin (1)Etoposide (1)Doxorubicin (1)Atezolizumab (1)Pembrolizumab (1)Cisplatin (1)Docetaxel (1)Gemcitabine (1)
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 107

Proteogenomic characterization of pulmonary large-cell neuroendocrine carcinoma identifies molecular features and therapeutic strategy

Science advances · Aug 2026 · Proteogenomic analysis of tumors and paired normal adjacent tissues from 107 patients; preclinical optimization and testing of recombinant IL-33 in mouse models and pharmacokinetics in cynomolgus monkeys

pulmonary large-cell neuroendocrine carcinomanon-small cell lung carcinoma

Researchers performed proteogenomic analysis on tumors and matched normal tissues from 107 patients with pulmonary large-cell neuroendocrine carcinoma and identified molecular features, mutational signatures, and three LCNEC subtypes. Interleukin-33 (IL-33) was identified as a biomarker associated with increased T cell infiltration and antitumor activity; the authors optimized recombinant IL-33 and developed a PEGylated form that showed prolonged circulation in cynomolgus monkeys and stronger immune agonist activity in mouse models.

Key findings
  • Proteogenomic analysis was performed on tumors and paired normal adjacent tissues from 107 LCNEC patients (81 pure LCNEC and 26 combined LCNEC).
  • APOBEC mutational signatures strongly correlate with processes of tumor initiation and immune suppression in LCNEC.
  • KEAP1 mutations correlate with metabolic reprogramming in LCNEC combined with NSCLC.
  • A conflicting relationship was observed between neuroendocrine and immune phenotypes.
  • Three LCNEC subtypes were identified, each with distinct prognosis features, microenvironment dysregulation, genetic alterations, and potential therapeutic targets.
  • Interleukin-33 (IL-33) emerged as a critical therapeutic biomarker associated with enhanced T cell infiltration and antitumor activity.
  • Recombinant IL-33 was optimized via site-directed mutagenesis and PEGylation.
  • PEGylated recombinant IL-33 demonstrated prolonged circulation time in cynomolgus monkeys and superior immune agonist activity in mouse models.
Limitations: Therapeutic optimization and activity of recombinant/PEGylated IL-33 were tested only in animal models (mice) and assessed for circulation in cynomolgus monkeys; no clinical (human interventional) data are reported.; Proteogenomic analyses are observational and associative; causality of identified correlations (e.g., APOBEC signatures, KEAP1 mutations) is not established in patients.; The human cohort, while sizable for a rare tumor, is limited to 107 patients and subgroup sizes (81 vs 26) may limit power for some subtype analyses.; The abstract does not report dosing, safety, or efficacy endpoints in humans, nor detailed statistical measures for the reported associations.; Translatability of mouse and nonhuman primate findings to human clinical benefit is not demonstrated in this study..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewReported positivePreclinical onlyTier 1 · lab

Biological activities and therapeutic potential of soy isoflavones: a focus on anticancer activity

Molecular biology reports · May 2026 · narrative review

Genisteinbreast cancerovarian cancerprostate cancergliomaneuroblastomahepatocellular carcinomalung cancerbladder cancerosteosarcomarhabdomyosarcoma

This is a narrative review of the biological activities and potential therapeutic roles of soy isoflavones (including genistein and daidzein). The authors summarize proposed anticancer mechanisms (estrogen receptor modulation, apoptosis, anti-angiogenesis, epigenetic effects, etc.) and report that in vitro and in vivo studies have shown promising results across a range of tumor types. They conclude that further research—especially studies combining isoflavones with established chemotherapeutics—is needed.

Studied with: chemotherapeutic agents.

Key findings
  • Soy isoflavones (genistein, daidzein) have estrogenic and non-estrogenic activities including anti-inflammatory, antioxidant, and immunomodulatory effects.
  • Proposed anticancer mechanisms include modulation of estrogen receptors, copper ion-dependent induction of cell death, promotion of apoptosis, inhibition of angiogenesis and metastasis, regulation of epigenetic processes, and effects on platelet function.
  • Because of estrogen receptor interactions, isoflavones have been studied particularly in hormone-dependent cancers such as breast, ovarian, and prostate cancer.
  • In vitro and in vivo studies have reported promising results in multiple malignancies (gliomas, neuroblastoma, hepatocellular carcinoma, lung and bladder cancers, osteosarcoma, rhabdomyosarcoma).
  • Authors recommend further investigation, particularly combining isoflavones with established chemotherapeutics, to evaluate potential synergy.
Limitations: This article is a narrative review and does not present new clinical trial data.; The evidence summarized is primarily preclinical (in vitro and in vivo) with no clinical trial data provided in the abstract.; Mechanistic proposals are not proven clinical effects and require further experimental and clinical validation.; Safety and efficacy in patients, optimal dosing, and interactions with standard therapies are not established in this review..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismMixed resultsModerate evidenceTier 4 · clinical

Non-Small Cell Lung Cancer, Version 4.2026, NCCN Clinical Practice Guidelines In Oncology

Journal of the National Comprehensive Cancer Network : JNCCN · Apr 2026

non-small cell lung cancer

These NCCN guidelines summarize recommendations for diagnosis, primary management, surveillance, and subsequent treatment of patients with non-small cell lung cancer. The panel updated the list of recommended targeted therapies based on recent FDA approvals and clinical data. This selection focuses on treatment recommendations for advanced or metastatic NSCLC with actionable biomarkers.

Key findings
  • The guideline provides recommendations for diagnosis, primary disease management, surveillance, and subsequent treatment of NSCLC.
  • The panel updated the list of recommended targeted therapies based on recent FDA approvals and clinical data.
  • This selection focuses on treatment recommendations for advanced or metastatic NSCLC with actionable biomarkers.
Limitations: This is a clinical practice guideline summary, not primary research reporting new experimental data.; The abstract provides no quantitative outcomes, study methods, or details of evidence grading.; No single compound or specific treatment regimen is described in the abstract.; Details on how recommendations were derived (e.g., evidence review methods) are not provided in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewTrialInconclusiveLimited evidenceTier 4 · clinical

KRAS G12C inhibitors versus chemotherapy in second line and beyond in adults with advanced or metastatic non-small cell lung cancer (NSCLC) harbouring the KRAS G12C mutation

The Cochrane database of systematic reviews · Feb 2026 · protocol for a Cochrane Review (intervention)

non-small cell lung cancer (NSCLC)

This publication is a protocol for a Cochrane systematic review. The planned review will assess the benefits and harms of KRAS G12C inhibitors compared with chemotherapy in adults with advanced or metastatic NSCLC harboring the KRAS G12C mutation who are receiving second-line or later therapy; no results are reported in this protocol.

Key findings
  • This is a protocol to assess the benefits and harms of G12C-inhibitors compared to chemotherapy in second line and beyond in adults with advanced/metastatic NSCLC with a KRAS G12C mutation.
Limitations: This document is a review protocol and reports no study results or pooled data.; No sample size, outcomes, or trial data are presented in the abstract..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismReported positiveLimited evidenceTier 3 · early human

Microflora: a promising potential in the diagnosis and treatment of non-small cell lung cancer

International journal of clinical oncology · Feb 2026 · review

non-small cell lung cancer

This narrative review summarizes studies linking the human microbiome (microflora) with non-small cell lung cancer (NSCLC). It reports that patients with NSCLC have distinct microbial communities in tumors, airways, and intestines and that characteristic microbes and circulating microbial DNA may assist diagnosis. The review states that microbiome alterations can influence the efficacy and adverse effects of immunotherapy, and that interventions such as antibiotics, inhaled or oral probiotics, prebiotics, and dietary changes are proposed to rebalance microflora and may enhance immunotherapy. It also discusses possible molecular mechanisms and the potential for microbe-specific testing and targeted microbial therapies in NSCLC.

Studied with: immunotherapy.

Key findings
  • Patients with NSCLC have distinct microflora within the tumor, airways, and intestines compared with healthy or benign lung disease patients.
  • Characteristic microflora and circulating microbial DNA may assist in the diagnosis of NSCLC.
  • Microflora changes can affect the efficacy of immunotherapy and treatment-related adverse effects during lung cancer therapy.
  • Modulating microflora imbalance through antibiotics/probiotics nebulization, oral probiotic, prebiotics, and dietary modifications is proposed to rebalance microflora and enhance the effectiveness of immunotherapy.
  • Microbe-specific testing and targeted microbial therapy are presented as potential new approaches for diagnosis and treatment of NSCLC.
Limitations: This article is a review (narrative) and does not present primary experimental or clinical trial data.; The abstract does not report quantitative results, randomized trial evidence, or systematic review/meta-analysis methodology.; Clinical effectiveness and safety of the proposed microbiome interventions are not demonstrated in this abstract and appear to be proposed rather than proven..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed

Human trialTrialReported positiveModerate evidenceTier 4 · clinicaln = 298

Tumor Treating Fields Therapy After Stereotactic Radiosurgery for Brain Metastases From Non-Small Cell Lung Cancer: Final Results of the Phase 3 METIS Study

International journal of radiation oncology, biology, physics · Feb 2026 · Phase 3 randomized controlled multicenter trial

non-small-cell lung cancer brain metastases (NSCLC BM)

This phase 3 randomized trial compared stereotactic radiosurgery (SRS) followed by Tumor Treating Fields (TTFields, 150 kHz) versus SRS alone in 298 adults with 1–10 newly diagnosed brain metastases from NSCLC. TTFields significantly delayed time to intracranial progression (HR 0.72) and reduced intracranial progression rates at multiple time points; device-related adverse events were mainly grade ≤2 skin events and there was no deterioration in quality of life or cognitive function. Subgroup analyses in patients receiving immune checkpoint inhibitors (n = 118) showed more pronounced delays in intracranial progression. Some analyses were reported post hoc and median follow-up was 8.6 months.

Reported effects: TTIP HR 0.72 [0.53–0.98], p P = .044, n=298 · Intracranial progression rate at month 2 13.6%, p P = .034, n=298 · +6 more

Studied with: stereotactic radiosurgery (SRS), immune checkpoint inhibitors.

Key findings
  • TTFields significantly delayed time to intracranial progression (TTIP) compared with SRS alone (HR 0.72, 95% CI 0.53-0.98; Fine-Gray P = .044).
  • Intracranial progression rates for TTFields versus SRS alone were 13.6% versus 22.1% at month 2 (P = .034), 33.7% versus 46.4% at month 6 (P = .018), 46.9% versus 59.4% at month 12 (P = .023), and 53.6% versus 65.2% at month 24 (P = .031; post hoc).
  • Time to distant intracranial progression favored TTFields but was not statistically significant (HR 0.76, 95% CI 0.51-1.12; log-rank P = .165; post hoc).
  • In the subgroup receiving immune checkpoint inhibitors (n = 118), TTIP delay had HR 0.63 (95% CI 0.39-1.0; Cox P = .049; Fine-Gray P = .055) and time to distant intracranial progression HR 0.41 (95% CI 0.21-0.81; log-rank P = .0087; post hoc).
  • Device-related adverse events were mainly grade ≤2 skin events.
  • TTFields did not cause quality-of-life deterioration, and post hoc analyses showed improvements in deterioration-free survival and time to deterioration for global health status, physical functioning, and fatigue domains.
Limitations: Median follow-up was relatively short (median 8.6 months, range 0.07–85.2).; Several analyses reported were post hoc (intracranial progression at 24 months, distant progression analyses, QoL domain analyses).; Subgroup analyses (patients receiving immune checkpoint inhibitors, n = 118) are smaller and may be underpowered or exploratory.; Abstract does not report long-term neurotoxicity beyond the follow-up range stated..

AI summary of the abstract, published automatically under the strong-evidence tier · Jul 2026; an editor has not yet reviewed it. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveModerate evidenceTier 4 · clinical

Processed Meat Health Risks: Pathways and Dietary Solutions

The Journal of nutrition · Nov 2025 · review

colorectal cancerbreast cancerendometrial cancerlung cancer

This review summarizes epidemiologic evidence linking red and processed meat consumption with higher risks of multiple chronic diseases, including colorectal, breast, endometrial, and lung cancers, type 2 diabetes, cardiovascular disease, and all-cause mortality. It reports that processed meats show stronger associations than unprocessed red meat, with dose-response relationships indicating elevated risks even at moderate intakes. The authors describe plausible biological mechanisms (carcinogen formation, inflammation, gut microbiome changes, heme iron, TMAO, and metabolic effects) and note inconsistencies such as short-term randomized trial biomarker findings and modification of risk by overall diet, lifestyle, and genetics. The review concludes that minimizing processed meat and replacing red/processed meats with plant proteins, poultry, or fish is expected to reduce disease risk, and it calls for further research on causality, mechanisms, and population diversity.

Studied with: plant proteins, poultry, fish.

Key findings
  • Observational studies and meta-analyses show positive associations between red/processed meat consumption and multiple chronic diseases, including colorectal, breast, endometrial, and lung cancers, type 2 diabetes, cardiovascular disease, and all-cause mortality.
  • Dose-response relationships indicate elevated risks even at moderate intakes.
  • Processed meats consistently show stronger detrimental associations than unprocessed red meats.
  • Mechanistic pathways discussed include carcinogen formation, proinflammatory effects, gut microbiome dysbiosis, heme iron, trimethylamine N-oxide (TMAO), saturated fats, and effects on lipid metabolism and insulin resistance.
  • Replacing red/processed meats with plant proteins, poultry, or fish is associated with reduced disease risk according to the review.
  • Evidence complexities include inconsistent randomized controlled trial findings on short-term biomarkers and substantial modification of risk by processing, cooking methods, overall diet, lifestyle, and genetic factors.
Limitations: Predominantly observational epidemiologic evidence, which is susceptible to confounding and cannot establish causality.; Inconsistent randomized controlled trial findings limited to short-term biomarkers rather than clinical endpoints.; Heterogeneity introduced by differences in processing methods, cooking techniques, and definitions of processed versus unprocessed meat.; Potential modification of associations by overall diet, lifestyle, and genetic factors, complicating interpretation.; Identified gaps include need for greater mechanistic specificity, more diverse populations, and integrated health-environment assessments..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Emerging Targets in Non-Small Cell Lung Cancer

Lung Cancer (Auckland, N.Z.) · Sep 2025

non-small cell lung cancer

This is a review article summarizing how the identification of molecular driver mutations has altered treatment approaches for non-small cell lung cancer (NSCLC). The authors note that many driver mutations and associated targeted therapies have been discovered over the past 20 years, improving survival for some patients, and they highlight ongoing research and emerging molecular targets and strategies for NSCLC.

Key findings
  • Identification of molecular driver mutations has changed the therapeutic landscape for NSCLC.
  • Over the last 20 years an increasing number of driver mutations and new targeted therapies have been identified, resulting in improved survival for a subset of patients.
  • There is ongoing research to identify additional molecular targets and therapeutic strategies to improve outcomes for more patients with lung cancer.
  • This review highlights new therapeutic strategies targeting known driver mutations and data regarding emerging molecular targets for NSCLC.
Limitations: Review article with no original experimental or clinical trial data presented in this abstract.; Abstract contains no methodological details (e.g., search strategy), so it is unclear whether this is a systematic review.; No quantitative results, specific agents, or detailed outcomes are reported in the abstract..

AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

DICER1 Syndrome: What Do We Know of the Pathogenetic Mechanisms?

Cancers · Sep 2025 · review

pleuropulmonary blastomaSertoli-Leydig cell tumorcystic nephromacervical embryonal rhabdomyosarcomacystic lung lesionsthyroid follicular nodular disease

This is a narrative review of DICER1 syndrome, a hereditary cancer predisposition caused by germline loss-of-function variants in DICER1 and characteristic second somatic hotspot mutations in the RNase IIIb domain. The review summarizes the range of associated benign and malignant tumors, describes DICER1's role as an endoribonuclease in RNA interference and microRNA processing, and concludes that the exact molecular mechanisms linking altered DICER1 function to tumorigenesis remain incompletely understood and require further research.

Key findings
  • DICER1 syndrome is a hereditary cancer predisposition syndrome with a broad phenotype including pleuropulmonary blastoma, Sertoli-Leydig cell tumor, cystic nephroma, cervical embryonal rhabdomyosarcoma, cystic lung lesions, and thyroid follicular nodular disease.
  • The syndrome is caused by loss-of-function germline variants in the DICER1 gene and DICER1-related tumors commonly have second somatic hotspot variants in the RNase IIIb domain.
  • DICER1 encodes an endoribonuclease important for RNA interference and microRNA biogenesis.
  • The review highlights gaps in knowledge about the precise molecular mechanisms by which altered DICER1 function contributes to tumorigenesis and calls for more research.
Limitations: Narrative review without original experimental or patient-level data.; Conclusions limited by existing incomplete knowledge of molecular mechanisms as noted by the authors.; Review methodology is not described in the abstract (e.g., not specified as a systematic review), so selection bias in covered literature is possible..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Modeling large cell neuroendocrine carcinoma of the lung for molecular, therapeutic and microenvironmental inferences: current knowledge and future perspectives

Expert review of anticancer therapy · Sep 2025 · narrative review

large cell neuroendocrine carcinoma of the lung

This narrative review summarizes current knowledge about large cell neuroendocrine carcinoma (LCNEC) of the lung, focusing on diagnostic criteria, molecular alterations, the tumor microenvironment including immune components, and ongoing clinical trials including immuno-oncology. The authors emphasize that LCNEC is a heterogeneous disease with distinct developmental trajectories that complicate diagnosis and clinical decision-making. They suggest this heterogeneity may provide a rationale for personalized targeted approaches or immunotherapy in patient subsets, but conclude that further studies using a holistic framework are needed.

Key findings
  • LCNEC of the lung is described as a high-grade non-small cell carcinoma with neuroendocrine morphology and neuroendocrine markers.
  • Diagnosis and therapeutic decision-making are challenging, likely because LCNEC comprises a heterogeneous mix of genetic and epigenetic alterations intertwined with the host microenvironment.
  • The review structures LCNEC knowledge across three outlooks: (i) diagnostic criteria and molecular alterations; (ii) microenvironmental changes, including the immune system; and (iii) available clinical trials, including immune-oncology studies.
  • Different developmental trajectories of LCNEC may explain diagnostic and treatment difficulties and may offer a rationale for personalized targeted therapies or immunotherapy in subsets of patients.
  • The authors call for future studies to frame LCNEC within a broader, holistic context among lung cancers rather than viewing it as a single, isolated tumor type.
Limitations: Narrative review that does not present original experimental or clinical data.; Abstract emphasizes heterogeneity and diagnostic challenges, which limit definitive clinical recommendations.; No quantitative synthesis or meta-analysis is reported in the abstract.; Authors state that readiness for a major change in understanding LCNEC is unresolved and further studies are needed..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

OtherMixed resultsModerate evidenceTier 4 · clinical

NCCN Guidelines® Insights: Non-Small Cell Lung Cancer, Version 7.2025

Journal of the National Comprehensive Cancer Network : JNCCN · Sep 2025 · Practice Guideline

non-small-cell lung cancer (NSCLC)

This document summarizes recent updates to the NCCN Guidelines for non-small cell lung cancer (NSCLC). The updates focus on systemic therapy options for patients with nonmetastatic NSCLC and on corresponding molecular testing considerations.

Key findings
  • The NCCN Guidelines Insights present recent updates for NSCLC management.
  • The discussion emphasizes systemic therapy options for nonmetastatic NSCLC.
  • The guidance highlights molecular testing considerations that correspond to systemic therapy choices.
Limitations: Abstract provides no details on specific therapies, recommended regimens, or testing algorithms.; No primary data, numerical results, or methods are reported in the abstract.; As a guideline summary, it synthesizes evidence rather than presenting new experimental or clinical trial data..

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Animal studyReported positivePreclinical onlyTier 2 · animal

Bifidobacterium animalis suppresses non-small cell lung cancer progression and modulates tumor immunity through indole-3-acetic acid

Cell reports · Aug 2025 · mouse models and NSCLC cell lines; gut microbiota comparison in patients with NSCLC and healthy controls

Indole-3-acetic-acidnon-small cell lung cancer

This study looked at gut bacteria and a bacterial metabolite in non-small cell lung cancer. The authors found that Bifidobacterium animalis was lower in patients with NSCLC, and in mouse models and cell lines it was associated with less tumor progression. They identified indole-3-acetic acid as a key metabolite and reported that it affected AHR/METTL3/STAT3 signaling and immune cells in ways linked to reduced tumor growth.

Key findings
  • Bifidobacterium animalis was markedly decreased in patients with NSCLC compared with healthy controls.
  • B. animalis suppressed tumor progression in two NSCLC mouse models and NSCLC cell lines.
  • Indole-3-acetic acid was identified as the pivotal metabolite of B. animalis with anti-NSCLC properties.
  • B. animalis and IAA activated AHR and suppressed METTL3 and STAT3 m6A methylation.
  • B. animalis and IAA reduced M2 macrophage polarization and enhanced CD8+ T cell functions by suppressing IL-6.
Limitations: Preclinical findings dominate the study; the anticancer effects were shown in mouse models and cell lines, not in a human trial.; Human data were observational/comparative microbiome profiling only, so causality cannot be established.; The abstract does not provide sample sizes, doses, or follow-up duration.; The abstract does not report clinical outcomes in patients..

The study links a gut bacterium and its metabolite to NSCLC progression and antitumor immunity in preclinical models.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

Browse all studies mentioning Lung Adenocarcinoma →

Where the evidence is

What has been studied, and how strong it is, by topic. A dashed cell means no studies were found for that combination — a gap, not evidence of no effect. Open a row to see its studies.

CompoundHuman evidenceMechanismSafetyTrial
Etoposide22—1
Carboplatin11—1
Durvalumab11—1
Pembrolizumab—2—1
Cisplatin—2——
Nivolumab †Rx—2——
Actinomycin D————
Atezolizumab—1—1
Bevacizumab—1——
Crizotinib—1——
Curcumin / Theracurmin————
Docetaxel————
Doxorubicin—1——
Fuzuloparib—1—1
Gemcitabine————
Genistein—1——

Study mix

148 published studies by what they were done in. Lab and animal findings often do not carry over to people.

23 Human4 Animal121 Review/other
Reported directionReported positive50Mixed results35Reported negative3Inconclusive60

Compounds with reported-positive results in Lung Adenocarcinoma

Where at least one study reported a positive result, shown with the full picture, not just the wins. Positive results are more likely to be published, and most of these are early lab or animal studies that may not translate to people. This reports what studies found, not what works.

Human evidence

Etoposide1 positive2 human
Limitations: Retrospective observational design; Relatively small sample size (n = 96); Non-randomized comparison of adjuvant therapy regimens; Potential for residual confounding despite propensity score matching; Abstract does not report follow-up duration or details of centers (possible limited generalizability).
Cited positive studies (1)
Preclinical only: lab / animal (12)
Pembrolizumab2 positive1 negative/mixed
Limitations: Single-patient case report (n=1), no control group.; No detailed dosing schedule or exact follow-up duration provided in the abstract.; Durability of response is stated but follow-up duration and objective duration data are not given in the abstract.; Potential publication/selection bias inherent to case reports.; Review article — does not present original patient-level data or new primary results.; Abstract provides no quantitative efficacy or safety outcomes, trial details, or comparative results..
Cited positive studies (2)
Genistein1 positive
Limitations: This article is a narrative review and does not present new clinical trial data.; The evidence summarized is primarily preclinical (in vitro and in vivo) with no clinical trial data provided in the abstract.; Mechanistic proposals are not proven clinical effects and require further experimental and clinical validation.; Safety and efficacy in patients, optimal dosing, and interactions with standard therapies are not established in this review..
Cited positive studies (1)
Indole-3-Acetic Acid1 positive1 animal
Limitations: Preclinical findings dominate the study; the anticancer effects were shown in mouse models and cell lines, not in a human trial.; Human data were observational/comparative microbiome profiling only, so causality cannot be established.; The abstract does not provide sample sizes, doses, or follow-up duration.; The abstract does not report clinical outcomes in patients..
Cited positive studies (1)
Doxorubicin1 positive1 animal
Limitations: Preclinical work only: evidence is limited to in vitro and in vivo experiments, no human data reported in the abstract.; Abstract does not report species, sample sizes, dosing regimens, or detailed safety/toxicity data.; No information on long-term outcomes, pharmacokinetics, or translational feasibility in humans in the abstract..
Cited positive studies (1)
Cisplatin1 positive1 negative/mixed
Limitations: Narrative review article; no original patient-level data reported in the abstract.; Abstract provides recommendations but no methods, selection criteria, or systematic review process are described.; No quantitative outcomes (survival, response rates, or comparative statistics) are provided.; No dosing details, toxicity data, or follow-up duration reported..
Cited positive studies (1)
Docetaxel1 positive
Limitations: Single-patient case report (n=1), so findings are not generalizable.; Short reported follow-up (8 months) limits assessment of long-term outcomes.; Literature review methods are not described in the abstract (potentially non-systematic and subject to bias).; No control group or randomized comparison to establish causality for the observed outcomes.; No chemotherapy dosing or detailed regimen schedule reported in the abstract..
Cited positive studies (1)
Gemcitabine1 positive
Limitations: Single-patient case report (n=1), so findings are not generalizable.; Short reported follow-up (8 months) limits assessment of long-term outcomes.; Literature review methods are not described in the abstract (potentially non-systematic and subject to bias).; No control group or randomized comparison to establish causality for the observed outcomes.; No chemotherapy dosing or detailed regimen schedule reported in the abstract..
Cited positive studies (1)
Fuzuloparib1 positive
Limitations: Review article; no original study data in the abstract.; No efficacy or safety results are reported in the abstract.; No comparator, sample size, or quantitative outcomes are provided..
Cited positive studies (1)
Nivolumab †Rx1 positive1 negative/mixed
Limitations: Review article — does not present original patient-level data or new primary results.; Abstract provides no quantitative efficacy or safety outcomes, trial details, or comparative results.; No specific clinical trial data, dosing, or follow-up durations are reported in the abstract..
Cited positive studies (1)
Ifosfamide1 positive
Limitations: Single-patient case report (n=1) limits generalizability.; No control or comparison group, so causality between interventions and outcome cannot be established.; No specific chemotherapy dose amounts provided in the abstract.; Short-to-moderate follow-up (two years) for long-term outcomes is limited..
Cited positive studies (1)
Vincristine1 positive
Limitations: Single-patient case report (n=1) limits generalizability.; No control or comparison group, so causality between interventions and outcome cannot be established.; No specific chemotherapy dose amounts provided in the abstract.; Short-to-moderate follow-up (two years) for long-term outcomes is limited..
Cited positive studies (1)
Actinomycin D1 positive
Limitations: Single-patient case report (n=1) limits generalizability.; No control or comparison group, so causality between interventions and outcome cannot be established.; No specific chemotherapy dose amounts provided in the abstract.; Short-to-moderate follow-up (two years) for long-term outcomes is limited..
Cited positive studies (1)

Evidence at a glance: compounds studied in Lung Adenocarcinoma

A deterministic grade of what published studies report for each: strength of evidence, the reported direction, and the largest credible effect, strongest-evidence first. This summarizes findings; it is not a claim that anything works.

EtoposideHuman trial / meta-analysisReported positive2 human

Includes human trial or meta-analysis evidence.

Largest credible effect: LCNEC/AD proportion 74%, n=96 PMID 35147672 · response rates 7–74 across 4 studies

Most authoritative study: Study protocol of an open-label prospective phase II study of Durvalumab plus Carboplatin and Etoposide in advanced large cell neuroendocrine carcinoma of the lung (LOGIK2401: NECTAR study)

CarboplatinHuman trial / meta-analysisInconclusive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: enrolled patients 30, n=30 PMID 41037966

Most authoritative study: Study protocol of an open-label prospective phase II study of Durvalumab plus Carboplatin and Etoposide in advanced large cell neuroendocrine carcinoma of the lung (LOGIK2401: NECTAR study)

Based on a single study.
DurvalumabHuman trial / meta-analysisInconclusive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: enrolled patients 30, n=30 PMID 41037966

Most authoritative study: Study protocol of an open-label prospective phase II study of Durvalumab plus Carboplatin and Etoposide in advanced large cell neuroendocrine carcinoma of the lung (LOGIK2401: NECTAR study)

Based on a single study.
DoxorubicinAnimal onlyReported positive1 animal

Animal studies only — no human data.

Largest credible effect: doxorubicin loading rate 73.24% PMID 38445013

Most authoritative study: Oxygen-producing and pH-responsive targeted DNA nanoflowers for enhanced chemo-sonodynamic therapy of lung cancer

No human studies yet · Based on a single study.
Indole-3-Acetic AcidAnimal onlyReported positive1 animal

Animal studies only — no human data.

Most authoritative study: Bifidobacterium animalis suppresses non-small cell lung cancer progression and modulates tumor immunity through indole-3-acetic acid

No human studies yet · No numeric effect sizes reported · Based on a single study.
PembrolizumabInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Recent Advances in Adjuvant Therapy for Non-Small-Cell Lung Cancer

No human studies yet · Findings conflict across studies · No numeric effect sizes reported.
CisplatinInsufficient evidenceMixed results

No primary experimental studies yet.

Largest credible effect: number_of_cycles 4 PMID 24102012

Most authoritative study: Platinum-based targeted chemotherapies and reversal of cisplatin resistance in non-small cell lung cancer (NSCLC)

No human studies yet · Findings conflict across studies · Effect sizes reported in only 1 of 2 studies.
Nivolumab †RxInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Targeting PD-L1 for non-small-cell lung cancer

No human studies yet · Findings conflict across studies · No numeric effect sizes reported.
Actinomycin DInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: chemotherapy duration 10 months 10 mo, n=1 PMID 11558020 · effect sizes 2–10 across 2 studies

Most authoritative study: Pleuropulmonary blastoma

No human studies yet · Based on a single study.
AtezolizumabInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Recent Advances in Adjuvant Therapy for Non-Small-Cell Lung Cancer

No human studies yet · No numeric effect sizes reported · Based on a single study.
BevacizumabInsufficient evidenceReported negative

No primary experimental studies yet.

Most authoritative study: Large cell neuroendocrine carcinoma of the lungs: case report and literature review

No human studies yet · No numeric effect sizes reported · Based on a single study.
CrizotinibInsufficient evidenceInconclusive

No primary experimental studies yet.

Most authoritative study: ALK-rearrangement in non-small-cell lung cancer (NSCLC)

No human studies yet · No numeric effect sizes reported · Based on a single study.
Curcumin / TheracurminInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Curcumin and Its Analogs in Non-Small Cell Lung Cancer Treatment: Challenges and Expectations

No human studies yet · No numeric effect sizes reported · Based on a single study.
DocetaxelInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: time_to_brain_metastasis 44 mo, n=1 PMID 37158392 · effect sizes 8–44 across 2 studies

Most authoritative study: Brain and lung metastasis of uterine leiomyosarcoma: illustrative case

No human studies yet · Based on a single study.
FuzuloparibInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Fuzuloparib: First Approval

No human studies yet · No numeric effect sizes reported · Based on a single study.
GemcitabineInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: time_to_brain_metastasis 44 mo, n=1 PMID 37158392 · effect sizes 8–44 across 2 studies

Most authoritative study: Brain and lung metastasis of uterine leiomyosarcoma: illustrative case

No human studies yet · Based on a single study.
GenisteinInsufficient evidenceReported positive

No primary experimental studies yet.

Most authoritative study: Biological activities and therapeutic potential of soy isoflavones: a focus on anticancer activity

No human studies yet · No numeric effect sizes reported · Based on a single study.
IfosfamideInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: chemotherapy duration 10 months 10 mo, n=1 PMID 11558020 · effect sizes 2–10 across 2 studies

Most authoritative study: Pleuropulmonary blastoma

No human studies yet · Based on a single study.
PaclitaxelInsufficient evidenceReported negative

No primary experimental studies yet.

Most authoritative study: Large cell neuroendocrine carcinoma of the lungs: case report and literature review

No human studies yet · No numeric effect sizes reported · Based on a single study.
VincristineInsufficient evidenceReported positive

No primary experimental studies yet.

Largest credible effect: chemotherapy duration 10 months 10 mo, n=1 PMID 11558020 · effect sizes 2–10 across 2 studies

Most authoritative study: Pleuropulmonary blastoma

No human studies yet · Based on a single study.

Clinical trials in Lung Adenocarcinoma

72 ongoing · 90 completed · tracked from ClinicalTrials.gov. Recruiting is not the same as proven, and completed is not the same as positive — read the results. Not a recommendation.

Completed
39 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Lung Adenocarcinoma — advocacy, paying for treatment, second opinions, and caregivers.

If you’re struggling emotionally, you don’t have to wait.

Advocacy & community

No dedicated organization for this specific cancer is curated yet — these general organizations can help in the meantime.

Financial help

  • PAN Foundation ↗ — Copay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell Foundation ↗ — Copay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistance ↗ — Limited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family Reach ↗ — Help with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMeds ↗ — Searchable directory of drug patient-assistance and discount programs. · status changes often — check the fund’s site
What you’ll typically need to apply
  • Your diagnosis and, if you have it, the specific drug/treatment name (from your care team).
  • Insurance details — your member ID card, or a note that you're uninsured (some funds require active insurance, some don't).
  • Proof of income and household size (recent pay stubs, a tax return, or a benefits letter) — most funds are income-based.
  • Your prescriber's contact information; some programs need the clinic to submit part of the application.
  • Apply early and re-check: funds open and close as money is available, so a closed fund may reopen.

General guidance — each program sets its own eligibility. Confirm requirements on the program’s site.

Help paying for the medicines on this page

Second opinions

Caregiver support

We list only non-profit and government resources — never product sellers — and take no affiliate fees. If a link is broken or a resource doesn't meet that bar, tell us.

Interactions & safety to check: Lung Adenocarcinoma

This is not a complete interaction check. It only covers the compounds we track and the signals reported in studies. A drug or supplement not listed here is not therefore safe. Bring your full medication and supplement list to your pharmacist and oncologist before changing anything.

Potential interactions: highest-stakes first

  • Curcumin / Theracurmin×CYP3A4/P-gp substrates (e.g., TKIs, chemo)high-stakesmoderate
    Monitor: May alter levels; pharmacist review.
  • Curcumin / Theracurmin×Anticoagulantshigh-stakesminor
    Monitor: Possible bleeding risk.
  • Curcumin / Theracurmin×Platinum chemotherapyhigh-stakesbeneficial
    Consider: Resensitization; enhanced efficacy.
  • Nivolumab †Rx×immunosuppressantshigh-stakeshigh
    Avoid: Blunts efficacy (e.g., chronic steroids).
  • Nivolumab †Rx×Ipilimumabmoderate
    Synergize: Higher irAE but OS gains in melanoma.
  • Nivolumab †Rx×corticosteroidslow
    Use For IrAE: High-dose for toxicity; low-dose physiologic OK.

Safety considerations

Heading to an appointment? Get a printable one-page summary — studied compounds, open trials, interactions, and questions to ask.
Bring this to your appointment →

Biomarkers — what to test for, and what it could unlock

PubMedFDA

A positive result may make you eligible for the linked options — it doesn’t mean a treatment will work, and not every test is standard everywhere. Confirm testing and results with your care team.

Many of these can be checked at once from a single tumor (or blood) sample — ask your team whether a comprehensive multi-gene (NGS) panel is right for you, rather than one test at a time.

ALK fusions (e.g., EML4-ALK)oncogenic driver (TKI sensitive) · occasionalPrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for ALK fusions (e.g., EML4-ALK) →

ALK/ROS1/RET false-positive pitfalls (IHC only)preanalytic/analytic caveat · variablePrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for ALK/ROS1/RET false-positive pitfalls (IHC only) →

Hereditary cancer gene — a germline (inherited) result can affect blood relatives. Consider genetic counseling ↗; your team can advise whether germline testing is right for you.

BRAF V600Eoncogenic driver · rarePrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for BRAF V600E →

EGFR activating mutations (ex19 del, L858R; uncommon: G719X, L861Q, S768I)oncogenic driver (TKI sensitive) · commonPrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for EGFR activating mutations (ex19 del, L858R; uncommon: G719X, L861Q, S768I) →

ERBB2 (HER2) mutations (exon 20 ins and others)oncogenic driver · occasionalPrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for ERBB2 (HER2) mutations (exon 20 ins and others) →

KRAS (esp. G12C; others G12D/V/R)oncogenic driver (historically ‘undruggable’) · commonPrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for KRAS (esp. G12C; others G12D/V/R) →

MET exon 14 skipping / MET amplificationoncogenic driver · occasionalPrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for MET exon 14 skipping / MET amplification →

MSI/MMRDNA repair biomarker · rarePrognostic / other

How it’s tested: MSI/MMR

Pre-screen recruiting trials for MSI/MMR →

NTRK1/2/3 fusionstumor-agnostic kinase driver · rarePrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for NTRK1/2/3 fusions →

PD-L1 (TPS)immune checkpoint biomarker · variablePrognostic / other

How it’s tested: PD-L1 IHC (TPS)

Pre-screen recruiting trials for PD-L1 (TPS) →

RET fusionsoncogenic driver · rarePrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for RET fusions →

Hereditary cancer gene — a germline (inherited) result can affect blood relatives. Consider genetic counseling ↗; your team can advise whether germline testing is right for you.

ROS1 fusionsoncogenic driver · rarePrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for ROS1 fusions →

STK11/LKB1, KEAP1, TP53 (co-mutations)prognostic/biologic context · commonPrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for STK11/LKB1, KEAP1, TP53 (co-mutations) →

Hereditary cancer gene — a germline (inherited) result can affect blood relatives. Consider genetic counseling ↗; your team can advise whether germline testing is right for you.

TMB (tumor mutational burden)immunotherapy biomarker · variablePrognostic / other

How it’s tested: Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA

Pre-screen recruiting trials for TMB (tumor mutational burden) →

Marker → medicine links are derived from this page’s published claims for Lung Adenocarcinoma; resistance and companion-diagnostic notes appear only where an established, sourced entry exists.

Go deeper

Questions to ask your oncologist

  • Do I have a targetable driver (EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, HER2, KRAS G12C)?
  • If no driver, what is my PD-L1 and best IO±chemo plan?
  • Is surgery or SBRT an option for my stage? Could oligomet sites be consolidated after response?
  • What is our plan if first-line therapy stops working—when and how will we test for resistance?
  • Do my co-mutations (STK11/KEAP1/TP53) affect treatment choice?
  • How will we monitor and manage IO irAEs and TKI toxicities?
  • Would I benefit from pulmonary rehab, nutrition support, or prehab before treatment?
  • Am I eligible for clinical trials now or at progression?
  • What is the plan for brain surveillance and treatment if needed?
  • How will we coordinate supplements/OTC meds to avoid interactions?

Find a trial

Search active and completed trials at these registries:

Citations

  1. NCCN Guidelines: NSCLC (Professional/Patient)

    NCCN

  2. ESMO Clinical Practice Guidelines: Metastatic and Early-Stage NSCLC

    ESMO

  3. IASLC: Staging and Management Resources

    IASLC

  4. WHO Classification of Thoracic Tumors (5th ed.)

    WHO/IARC

  5. FDA/EMA Labels for Targeted Agents and Immunotherapies

    FDA

FAQs

Which tests should every lung adenocarcinoma get at diagnosis?
  • Comprehensive molecular profiling (DNA+RNA NGS) for EGFR, ALK, ROS1, RET, MET exon 14 skipping, BRAF V600E, NTRK, ERBB2/HER2, and KRAS (esp. G12C) plus PD-L1 IHC. Use plasma ctDNA when tissue is limited; confirm negatives on tissue if feasible.
How do targeted therapies compare with chemo or immunotherapy?
  • With a druggable driver, first-line TKI usually outperforms chemo/IO for response and control. If no driver is found, PD-L1 guides IO±chemo. Combining TKIs with IO up front is generally avoided due to added toxicity.
If PD-L1 is high but I have EGFR or ALK, should I get immunotherapy first?
  • No. Targeted therapy comes first for classic drivers (EGFR, ALK, ROS1, etc.) regardless of PD-L1, as single-agent IO has low efficacy and can increase toxicity if given before some TKIs.
When is surgery or SBRT possible?
  • Early-stage disease is treated with surgery or SBRT for cure. In selected oligometastatic cases, consolidative SBRT or limited metastasectomy after good systemic response may extend control.
What happens when targeted therapy stops working?
  • Re-biopsy or ctDNA looks for resistance mechanisms (e.g., EGFR C797S, MET amplification, ALK mutations). Findings drive next-line therapy or clinical trial selection.
How are brain metastases handled?
  • Many modern TKIs have strong CNS activity. Stereotactic radiosurgery treats limited lesions; whole-brain RT is reserved for diffuse disease. Multidisciplinary review tailors the plan.
Do lifestyle changes matter?
  • Yes—smoking cessation, exercise/prehab, vaccination (flu/COVID/pneumococcal), nutrition, and symptom-triggered rapid access reduce complications and help maintain dose intensity.
Are fasting or supplements helpful?
  • Supervised fasting-mimicking diets around chemo can reduce side effects in small studies; evidence is early. Avoid high-dose antioxidants on infusion/RT days. Always review supplements for TKI/IO interactions.
Is ctDNA useful for monitoring?
  • Yes as an adjunct—helps detect resistance mutations and sometimes track response. Imaging remains the primary tool for decisions.
Which symptoms should trigger urgent contact?
  • New/worsening shortness of breath, chest pain, fever ≥100.4°F, hemoptysis, severe diarrhea, severe rash, new weakness/numbness, or confusion. See ‘Emergency Thresholds’ and ‘When to Call.’

What we don't know yet

  • Optimal sequencing/combination of TKIs after complex resistance (e.g., EGFR C797S cis/trans, polyclonal MET/HER2 amp).
  • Best IO strategies for STK11/KEAP1 co-mutated tumors.
  • ctDNA-guided perioperative/MRD strategies—prospective validation pending.
  • Durable strategies for invasive mucinous adenocarcinoma with aerogenous spread.
  • Integrative approaches (nutrition/exercise/fasting) with hard clinical endpoints in NSCLC.