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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
72 published studies that name Lung Adenocarcinoma10 human studies approved & graded (trial, observational, or meta-analysis)239 human clinical studies in the Lung Adenocarcinoma corpus2590 source documents in the Lung Adenocarcinoma corpus

last checked June 19, 2026

Why this grade?

Human trial / meta-analysisIncludes 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
  • Crizotinib
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
  • (neo)adjuvant chemotherapy
  • chemotherapy
  • concurrent chemoradiotherapy
  • stereotactic body radiation therapy
  • definitive local therapy (radiation or surgery)
  • surgery
  • stereotactic radiosurgery (SRS)
  • whole brain radiation therapy
  • memantine
  • local therapy
  • lobectomy or greater (lobectomy, pneumonectomy)
  • sublobar resection (wedge resection, segmentectomy)
  • mediastinal lymph node dissection
  • radiation therapy
  • neoadjuvant or adjuvant radiation therapy
  • adjuvant chemoradiation (combination of chemotherapy and radiation)
  • Cisplatin
  • Curcumin / Theracurmin
  • Fuzuloparib
  • Indole-3-Acetic Acid

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.

50
Interventions
23
Standard of care
6
Tested in people
4
Lab / animal
15
Named in lit.
7
Classes
Standard of care (23) Guideline option (2) Tested in people (6) Lab / animal only (4) Named in the literature (15)

Tested in people, by trial phase: phase not reported ×6

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

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 (25)
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
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
Other
Etoposide
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 (25)
Meta-analysis (6)
local therapymemantineoff-labelstereotactic radiosurgery (SRS)surgerytargeted therapy· targetable driver alterationswhole brain radiation therapy
Named in the literature
targeted therapiesadjuvant immunotherapy· Adjuvant (after surgery)immunotherapies(neo)adjuvant chemotherapy· Adjuvant (after surgery)chemotherapy· Neoadjuvant (before surgery)concurrent chemoradiotherapystereotactic body radiation therapydefinitive local therapy (radiation or surgery)surgery· Adjuvant (after surgery)lobectomy or greater (lobectomy, pneumonectomy)sublobar resection (wedge resection, segmentectomy)mediastinal lymph node dissectionradiation therapyneoadjuvant or adjuvant radiation therapy· Neoadjuvant (before surgery)adjuvant chemoradiation (combination of chemotherapy and radiation)· 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

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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 sizerisk factor for occult mediastinal nodal disease [13]
  • increases riskRadiological nodal involvementrisk 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: 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]
  • chemotherapy: 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: 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: 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): 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: 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
59
Meta-analysis
160
Systematic review
47
Randomized trial
8
Clinical trial
16
Observational
5
Case report
145
Review
2130
Preclinical
0
Other
20

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

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
1Indole-3-Acetic Acid OtherAnimal only1
2Crizotinib Targeted therapyInsufficient evidence1
3Fuzuloparib OtherInsufficient evidence1

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 · 6

EtoposideHuman · observationalReported positive1 human

Human observational evidence only — no trials.

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

Most authoritative study: Combined large cell neuroendocrine carcinoma: clinical characteristics, prognosis and postoperative management

Based on a single study.
OtherFDA approved1 studyFull profile →
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.
Other1 studyFull profile →
CisplatinInsufficient evidenceMixed results

No primary experimental studies yet.

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

No human studies yet · No numeric effect sizes reported · Based on a single study.
ChemotherapyFDA off-label1 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 →
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.
Other1 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.
Other1 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 studies8 human3 animal⚠ Conflicting evidenceMechanism (29)Trial (5)Supportive care (1)Formulation (1)

Tracking 60 published studies of Lung Adenocarcinoma: 8 in humans, 3 in animals, 49 reviews/other.

Reported direction across studies: 13 positive, 17 mixed, 30 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

Indole 3 acetic acid (1)Cisplatin (1)Curcumin (1)Etoposide (1)Fuzuloparib (1)Crizotinib (1)
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

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 590

Integrated molecular and clinical characterization of pulmonary large cell neuroendocrine carcinoma

Nature communications · Aug 2025 · cohort study (two independent clinical/genomic cohorts)

pulmonary large cell neuroendocrine carcinoma (LCNEC)small cell lung cancer (SCLC)non-small cell lung cancer (NSCLC)

The authors analyzed clinical and molecular data from 590 patients with pulmonary large cell neuroendocrine carcinoma across two cohorts. They identified two genomic subtypes (NSCLC-like with KEAP1/KRAS/STK11 mutations and SCLC-like with RB1/TP53 mutations) and report that 80% of tumors aligned with SCLC transcriptional profiles. The study found elevated FGL-1 and SPINK1 expression in NSCLC-like LCNECs and higher DLL3 in SCLC-like LCNECs, and noted fewer tumor-infiltrating lymphocytes in LCNEC compared with other lung cancers. Overall survival was comparable across chemotherapy, chemoimmunotherapy, and immunotherapy in this cohort.

Reported effect: proportion aligning with SCLC transcriptional profiles 80%, n=590

Key findings
  • Study cohort: 590 patients across two independent cohorts.
  • Comparable overall survival across treatment regimens (chemotherapy, chemoimmunotherapy, immunotherapy) without unexpected adverse events.
  • Genomic analysis identified two LCNEC subtypes: NSCLC-like (KEAP1, KRAS, STK11 mutations) and SCLC-like (RB1, TP53 mutations).
  • 80% of LCNEC tumors aligned with SCLC transcriptional profiles.
  • Serial sampling showed stable mutational landscapes but shifting transcriptomic profiles over time.
  • Elevated FGL-1 (a LAG-3 ligand) and SPINK1 expression were observed in NSCLC-like LCNECs; DLL3 levels were higher in SCLC-like LCNECs.
  • Immunofluorescence confirmed FGL-1 expression in NSCLC-like LCNECs.
  • H&E analyses indicated fewer tumor-infiltrating lymphocytes in LCNECs versus other lung cancers.
  • Authors suggest these immunogenomic features support future investigation of LAG-3, SPINK1, and DLL3-targeted approaches.
Limitations: Observational cohort design — no randomized comparison of treatments reported in the abstract.; Abstract provides no quantitative survival or subgroup outcome measures (no effect sizes or statistical details reported).; Molecular associations (expression of FGL-1, SPINK1, DLL3) are descriptive and do not demonstrate therapeutic efficacy.; Functional or clinical validation of proposed targets is not presented in the abstract.; H&E-based assessment of tumor-infiltrating lymphocytes is a histologic surrogate and may lack detailed immunophenotyping..

Identifies immunogenomic subtypes and candidate targets (FGL-1/LAG-3, SPINK1, DLL3) in LCNEC that may guide future therapeutic investigations.

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

Human · observationalSupportive careMixed resultsModerate evidenceTier 3 · early humann = 267586

Risk of atherosclerotic cardiovascular disease after cancer diagnosis: findings from 3 prospective cohort studies

Journal of the National Cancer Institute · Aug 2025 · prospective cohort study

Supportive carecervical cancerHodgkin lymphomaprostate cancerbreast cancercolorectal cancerlung cancerendometrial canceroral cavity and pharynx cancerkidney cancerovarian cancersarcomamelanomaleukemia

Researchers followed participants in three large prospective cohorts for up to 36 years to examine whether a cancer diagnosis was associated with later atherosclerotic cardiovascular disease (ASCVD). They documented 4,334 new ASCVD events among 49,603 incident cancer cases and found that cervical cancer and Hodgkin lymphoma were associated with higher ASCVD risk, prostate cancer with slightly lower risk, and that ASCVD risk trajectories over time varied by cancer type (for example, breast cancer survivors had lower ASCVD risk for the first 7.5 years, then risk increased).

Reported effects: new-onset ASCVD events among incident cancer cases 4334, n=49603 · cervical cancer HR 1.56 [1.06–2.29] · +6 more

Key findings
  • During up to 36 years of follow-up, 4,334 new-onset ASCVD events among 49,603 incident cancer cases were documented.
  • Cervical cancer was associated with increased ASCVD incidence (HR = 1.56, 95% CI = 1.06 to 2.29).
  • Hodgkin lymphoma was associated with increased ASCVD incidence (HR = 2.80, 95% CI = 1.89 to 4.15).
  • Prostate cancer was associated with lower ASCVD incidence (HR = 0.91, 95% CI = 0.85 to 0.97).
  • Breast cancer survivors experienced lower ASCVD risk during the first 7.5 years after diagnosis, but risk gradually increased afterward (Pnonlinearity = .01).
  • ASCVD risk increased over time among patients with cancers of the colorectum (P = .003), lung (P = .002), and endometrium (P = .04).
  • No statistically significant association with ASCVD risk was observed for cancers of the oral cavity and pharynx, kidney, or ovary; sarcoma; melanoma; or leukemia.
Limitations: Observational cohort design cannot establish causality.; Potential for residual confounding despite multivariable adjustment.; Cohorts consist of nurses and health professionals, which may limit generalizability to other populations.; Abstract does not report details on cancer stage or treatments, which could influence ASCVD risk..

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

ReviewFormulationReported positiveLimited evidenceTier 4 · clinical

Nanomedicine in Immunotherapy for Non-Small Cell Lung Cancer: Applications and Perspectives

Small methods · Jul 2025 · review

non-small cell lung cancer

This is a review article summarizing how nanomedicines are being developed to support immunotherapy for non-small cell lung cancer. The authors survey core features and the current clinical status of strategies such as immune checkpoint blockade, antibody-drug conjugates, cell engagers, adoptive cells, and cancer vaccines, and emphasize recent nanomedicine developments that may boost these approaches. The abstract highlights advantages of nanomedicines including tumor targeting, improved bioavailability, reduced systemic toxicity, and potential to overcome immune resistance. No new experimental data or quantitative results are reported in the abstract.

Studied with: immune checkpoint blockade, antibody-drug conjugates, cell engagers, adoptive cells, cancer vaccines.

Key findings
  • Nanomedicines may offer advantages including specific targeting of tumor cells, improved drug bioavailability, reduced systemic toxicity, and overcoming of immune resistance.
  • The review surveys the core features and current clinical status of NSCLC immunotherapy strategies: immune checkpoint blockade, antibody-drug conjugates, cell engagers, adoptive cells, and cancer vaccines.
  • Particular emphasis is placed on recent developments of nanomedicines that boost these immunotherapy strategies.
Limitations: This is a review article; no new experimental or clinical trial data are presented in the abstract.; Abstract provides no quantitative results, sample sizes, doses, or outcome metrics.; Species, specific clinical trial identifiers, and funding sources are not specified in the abstract..

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

Human · observationalMixed resultsLimited evidenceTier 3 · early humann = 11310

Epidemiology and clinical course of large cell neuroendocrine carcinoma of the lung: The Japanese lung cancer registry study

Lung cancer (Amsterdam, Netherlands) · Jun 2025 · prospective registry study (Japanese Joint Committee of Lung Cancer Registry)

large cell neuroendocrine carcinomasmall cell lung cancersquamous cell carcinomaadenocarcinoma

This prospective registry study analyzed 11,310 Japanese lung cancer patients (80 with LCNEC) from January 2012 to April 2016 to compare clinical characteristics, chemotherapy response, and survival across histologies. LCNEC patients were mostly older male smokers and had lower overall response and disease control rates to first-line cisplatin- or carboplatin-based chemotherapy in stage IV disease compared with SCLC. Three-year survival was similar between LCNEC (14.2%) and SCLC (15.9%), and Cox analysis showed no statistically significant difference in overall survival (HR 0.818, 95% CI 0.611-1.096, p = 0.178).

Reported effects: cohort_size 11310, n=11310 · LCNEC_count 80, n=80 · +9 more

Key findings
  • Total cohort: 11,310 patients from the JJCLCR database.
  • In total, 80 patients (0.7%) were diagnosed with LCNEC.
  • LCNEC patients had median age 68 years, 93.8% men, and 97.5% smokers.
  • In stage IV patients, best overall response and disease control rates for first-line cisplatin-based chemotherapy were 34.8% and 43.5% for LCNEC but 60.6% and 69.7% for SCLC.
  • For first-line carboplatin-based chemotherapy in stage IV patients, overall response and disease control rates were 29.4% and 41.2% for LCNEC, but 56.1% and 68.4% for SCLC.
  • The 3-year survival rates were 14.2% for LCNEC, 15.9% for SCLC, 17.8% for squamous cell carcinoma, and 27.1% for adenocarcinoma.
  • Cox hazard analysis comparing overall survival between LCNEC and SCLC showed hazard ratio 0.818 (95% CI 0.611-1.096, p = 0.178), not statistically significant.
Limitations: Small number of LCNEC cases (80) relative to the full registry cohort.; Observational registry design without randomized treatment assignment.; Potential heterogeneity in treatments and management across registry sites.; Follow-up limited to registry period (opened Jan 2012; completed Apr 2016) with no median follow-up duration reported in the abstract..

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

Case reportMixed resultsLimited evidenceTier 3 · early humann = 1

Tarlatamab for Large Cell Neuroendocrine Carcinoma in a Young Adult: A Case Report

JTO clinical and research reports · Jul 2024 · case report

large cell neuroendocrine carcinoma of the lung

A 20-year-old man with metastatic large cell neuroendocrine carcinoma of the lung received tarlatamab, a DLL3-targeting bispecific T-cell engager. Treatment was complicated by transient cytokine release syndrome and resulted in a partial response. The authors state that bispecific T-cell engagers may offer a novel treatment approach for this cancer.

Key findings
  • A 20-year-old man with metastatic large cell neuroendocrine carcinoma of the lung was treated with tarlatamab.
  • Treatment was complicated by transient cytokine release syndrome.
  • Treatment resulted in a partial response.
  • Authors suggest bispecific T-cell engagers may offer a novel treatment approach for large cell neuroendocrine carcinoma of the lung.
Limitations: Single-patient case report (n=1).; No control or comparator provided.; Dose, treatment schedule, and duration of follow-up are not reported in the abstract.; Findings cannot be generalized from one case.; Safety data limited to a single transient cytokine release syndrome event with no longer-term safety outcomes reported..

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

Animal studyReported positivePreclinical onlyTier 2 · animal

CDC7 inhibition impairs neuroendocrine transformation in lung and prostate tumors through MYC degradation

Signal transduction and targeted therapy · Jul 2024

lung adenocarcinomaprostate adenocarcinomasmall cell carcinoma (lung and prostate)neuroendocrine transformation

The study tested CDC7 inhibition with simurosertib in models of neuroendocrine (NE) transformation in lung and prostate tumors. In in vivo models, CDC7 inhibition suppressed NE transdifferentiation and extended responses to targeted therapy and to cytotoxic drugs by inducing proteasome-mediated degradation of the MYC oncoprotein; a degradation-resistant MYC isoform reversed this effect.

Studied with: targeted therapy (unspecified), cisplatin, irinotecan.

Key findings
  • CDC7 is upregulated during the initial steps of neuroendocrine transformation after TP53/RB1 co-inactivation.
  • CDC7 inhibition with simurosertib suppressed NE transdifferentiation and extended response to targeted therapy in in vivo models of NE transformation.
  • CDC7 inhibition induced proteasome-mediated degradation of MYC, implicated in stemness and histological transformation.
  • Ectopic overexpression of a degradation-resistant MYC isoform reestablished the NE transformation phenotype even in the presence of simurosertib.
  • CDC7 inhibition markedly extended response to standard cytotoxics (cisplatin, irinotecan) in lung and prostate small cell carcinoma models.
  • Authors propose CDC7 inhibition as a strategy to constrain lineage plasticity and to treat NE tumors; simurosertib clinical trials are ongoing (not reported in this study).
Limitations: All reported experiments are preclinical (in vivo models); no human trial data are presented in this abstract.; The abstract does not report sample sizes, doses, or detailed experimental parameters.; Species and detailed model descriptions are not specified in the abstract.; Safety, toxicity, and clinical efficacy in patients are not addressed in this study..

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

ReviewMechanismReported positivePreclinical onlyTier 4 · clinical

Extracellular vesicles in non-small cell lung cancer stemness and clinical applications

Frontiers in immunology · May 2024

non-small cell lung carcinomalung neoplasmsnon-small cell lung cancer (NSCLC)

This is a review summarizing studies on extracellular vesicles (EVs) in non-small cell lung cancer (NSCLC). It describes how EVs produced by cancer stem cells may promote stem-like traits, tumor progression and metastasis, and discusses implications for developing NSCLC biomarkers and strategies to target the cancer stem cell niche.

Key findings
  • EVs are membrane-bound nanoparticles secreted by cells that carry messages for intercellular communication.
  • Numerous studies have implicated NSCLC cancer stem cell (CSC)-derived EVs in factors associated with NSCLC lethality.
  • EV-directed cross-talk between CSCs and cells of the tumor microenvironment promotes stemness, tumor progression and metastasis in NSCLC.
  • Mechanistic studies provide insights for developing novel diagnostic and prognostic biomarkers and strategies to therapeutically target the NSCLC CSC niche.
Limitations: This article is a review and does not present new experimental data.; The abstract indicates a focus on mechanistic studies, which are likely preclinical (in vitro or animal) rather than validated clinical evidence.; The abstract does not describe clinical validation of the proposed biomarkers or therapeutic strategies..

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

ReviewTrialInconclusiveModerate evidenceTier 4 · clinical

Non-Small Cell Lung Cancer, Version 4.2024, NCCN Clinical Practice Guidelines in Oncology

Journal of the National Comprehensive Cancer Network : JNCCN · May 2024 · practice guideline

non-small cell lung cancer

This NCCN guideline update summarizes treatment recommendations for people with advanced or metastatic non-small cell lung cancer who have actionable molecular biomarkers. It notes that the panel updated the list of recommended targeted therapies based on recent FDA approvals and clinical data. The abstract does not report results from a single intervention study or any quantitative outcomes.

Key findings
  • The guideline focuses on advanced or metastatic NSCLC with actionable molecular biomarkers.
  • Recommended targeted therapies were updated based on recent FDA approvals and clinical data.
  • No specific drug, dose, or outcome data are provided in the abstract.
Limitations: This is a practice guideline summary, not an original clinical study.; The abstract does not name the specific targeted therapies or biomarkers.; No efficacy, safety, or survival results are reported in the abstract..

Provides guideline recommendations for targeted therapy in advanced/metastatic NSCLC rather than testing a single repurposed drug or natural compound.

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

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Advances in genetic profile and therapeutic strategy of pulmonary large cell neuroendocrine carcinoma

Frontiers in medicine · Feb 2024

pulmonary large cell neuroendocrine carcinoma (LCNEC)small cell lung cancer (SCLC)

This narrative review summarizes current knowledge on diagnosis, molecular characteristics, and treatment strategies for pulmonary large cell neuroendocrine carcinoma (LCNEC). The authors state LCNEC is a high-grade neuroendocrine carcinoma (about 3% of primary lung cancer) with strong invasion, high heterogeneity, and very poor prognosis, and that diagnosis and treatment remain controversial and often refer to small cell lung cancer strategies. They note recent genetic analyses and emerging clinical trials provide increasing evidence to support more precise diagnosis and therapy and outline directions for future work.

Key findings
  • LCNEC is a high-grade neuroendocrine carcinoma accounting for approximately 3% of primary lung cancer.
  • LCNEC is characterized by strong invasion, high heterogeneity, and extremely poor prognosis.
  • Diagnosis and treatment of LCNEC are controversial and currently often follow therapeutic strategies for SCLC rather than LCNEC-specific precision therapies.
  • Recent genetic analyses and clinical trials of LCNEC have begun to emerge, offering more evidence to inform precise diagnosis and treatment.
  • This review summarizes diagnosis, molecular characteristics, and treatment and suggests potential directions for future LCNEC diagnosis and treatment research.
Limitations: Narrative review article that presents synthesis rather than original experimental or clinical data.; Abstract provides no methodological details (e.g., search strategy, inclusion criteria) so it is unclear whether this is a systematic review.; No quantitative synthesis, primary outcome data, or novel trial results are reported in the abstract.; Conclusions are general and the abstract lacks specific molecular findings or treatment outcome metrics..

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

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
Etoposide11
Cisplatin1
Crizotinib1
Curcumin / Theracurmin
Fuzuloparib11
Indole-3-Acetic Acid1

Study mix

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

10 Human3 Animal59 Review/other
Reported directionReported positive15Mixed results20Reported negative1Inconclusive36

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 positive1 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 (2)
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)
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)

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 · observationalReported positive1 human

Human observational evidence only — no trials.

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

Most authoritative study: Combined large cell neuroendocrine carcinoma: clinical characteristics, prognosis and postoperative management

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.
CisplatinInsufficient evidenceMixed results

No primary experimental studies yet.

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

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.
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.

Clinical trials in Lung Adenocarcinoma

18 ongoing · 19 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
8 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 FoundationCopay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell FoundationCopay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistanceLimited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family ReachHelp with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMedsSearchable 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

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

Citations

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.