Lung Adenocarcinoma

Lung adenocarcinoma (LUAD) arises from peripheral lung epithelium and now represents the dominant subtype of non–small cell lung cancer (NSCLC). Molecular testing is foundational: many patients harbor druggable drivers (EGFR, ALK, ROS1, RET, MET exon 14 skipping, BRAF V600E, NTRK fusions, ERBB2/HER2 mutations, KRAS G12C). PD-L1 expression and tumor mutational burden guide immunotherapy strategy. Curative management at early stages centers on complete resection (or ablative SBRT) with stage-appropriate adjuvant therapy; locally advanced disease often uses multimodality regimens (chemoradiation followed by immunotherapy). Metastatic disease is increasingly treated with first-line targeted therapy for driver-positive tumors or immuno-chemotherapy for driver-negative disease. For integrative care, emphasize conditioning (prehab), symptom control, organ protection, and metabolic/behavioral levers that support dose intensity without blunting anti-tumor immunity.

• EGFR activating mutations (ex19 del, L858R; uncommon: G719X, L861Q, S768I) (common) — oncogenic driver (TKI sensitive)
• ALK fusions (e.g., EML4-ALK) (occasional) — oncogenic driver (TKI sensitive)
• ROS1 fusions (rare) — oncogenic driver
• RET fusions (rare) — oncogenic driver
• MET exon 14 skipping / MET amplification (occasional) — oncogenic driver
• BRAF V600E (rare) — oncogenic driver
• NTRK1/2/3 fusions (rare) — tumor-agnostic kinase driver
• ERBB2 (HER2) mutations (exon 20 ins and others) (occasional) — oncogenic driver
• KRAS (esp. G12C; others G12D/V/R) (common) — oncogenic driver (historically ‘undruggable’)
• PD-L1 (TPS) (variable) — immune checkpoint biomarker
• TMB (tumor mutational burden) (variable) — immunotherapy biomarker
• MSI/MMR (rare) — DNA repair biomarker
• STK11/LKB1, KEAP1, TP53 (co-mutations) (common) — prognostic/biologic context
• ALK/ROS1/RET false-positive pitfalls (IHC only) (variable) — preanalytic/analytic caveat

• RTK–RAS–RAF–MEK–ERK (MAPK) — growth factor
• PI3K–AKT–mTOR — growth factor
• EGFR signaling (driver subset) — growth factor
• EMT/AXL/TGF-β program — lineage/emt
• Angiogenesis (VEGF/VEGFR) — angiogenesis
• Immune evasion (PD-1/PD-L1 axis) — immune
• Metabolic rewiring (glycolysis/FAO/PPP/redox) — metabolic

• Agents Database
• Protocols
• Alternative Therapies Guide
• Glossary
• Fasting / FMD (supervised)
• Omega-3 (EPA/DHA)
• Melatonin
• G-CSF (filgrastim/pegfilgrastim)
• Folate + Vitamin B12 with pemetrexed
• Pulmonary prehab / rehab
• Ginger (standardized extract)
• Acupuncture
• Smoking cessation program
• Vaccination (influenza, pneumococcal, COVID-19 per season)

• rarity: Common; most prevalent NSCLC histology worldwide.
• medianAge: Mid-60s (broad range); rising incidence in never-smokers and women.
• annualIncidence: Highest of lung histologies; contributes the majority of the ~2.2M lung cancer cases globally.
• sex: Affects all sexes; slight female predominance among never-smokers.
• geographicVariation: Driver mutation prevalence varies by region (e.g., EGFR higher in East Asia).
• riskFactors:
  • Tobacco smoke (active and secondhand).
  • Radon and occupational exposures (silica, asbestos, diesel).
  • Air pollution (PM2.5).
  • Genetic susceptibility; family history.
  • Preexisting lung disease (fibrosis/ILD).
  • Prior chest radiation.
• prognosis: Stage drives outcomes. Early-stage resection/SBRT can be curative. In metastatic disease, matched targeted therapies dramatically improve PFS/OS; IO±chemo benefits driver-negative disease. Brain/CNS activity of systemic agents and control of oligometastatic sites extend survival. Co-mutations (STK11/KEAP1) and performance status influence prognosis.
• trends:
  • Shift toward never-smoker LUAD; increased detection of druggable drivers.
  • Perioperative IO ± chemo, and adjuvant targeted therapy (driver-specific) reshaping early-stage care.
  • Broader use of ctDNA for resistance and MRD research.
  • Stereotactic approaches for oligometastatic consolidation.

• Gland-forming adenocarcinoma with acinar, papillary, lepidic, micropapillary, and/or solid patterns (often mixed).
• IHC: TTF-1+, Napsin A+ (typical); CK7+; helps distinguish from squamous/colorectal primaries.
• Mucin production in invasive mucinous adenocarcinoma; KRAS mutations common; aerogenous spread pattern.
• Molecular: frequent oncogenic drivers (EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, ERBB2/HER2, KRAS including G12C).
• PD-L1 expression variable; TMB often lower in never-smokers/driver+ tumors; MSI rare.
• Co-mutations (STK11/LKB1, KEAP1, TP53) influence biology and IO responsiveness.

• Persistent cough, dyspnea on exertion, chest discomfort.
• Incidental pulmonary nodule on imaging.
• Hemoptysis (variable volume).
• Unintentional weight loss, fatigue, anorexia.
• Recurrent pneumonia or nonresolving infiltrates.
• Bone pain/pathologic fracture, neurologic symptoms (brain mets), or new headaches.
• Hoarseness (recurrent laryngeal nerve involvement), SVC syndrome (central disease).

• Hematogenous: brain, bone, liver, adrenal glands.
• Lymphatic: hilar, mediastinal, supraclavicular nodes.
• Pleural: effusion, pleural nodularity.
• Aerogenous spread: especially invasive mucinous subtype with multifocal/lobar involvement.
• Chest wall/mediastinal invasion in locally advanced tumors.

• TNM (8th edition): size, nodal map, and metastatic burden determine stage.
• Baseline workup: contrast CT chest/upper abdomen; PET-CT for staging; brain MRI for stage II–IV or neuro symptoms.
• EBUS/EUS or mediastinoscopy for nodal staging when results change management.
• Pulmonary function testing and quantitative perfusion for surgical candidates.
• Perioperative approaches: neoadjuvant chemo-IO (driver-negative) and adjuvant targeted therapy (driver-specific) per stage and biomarkers.
• Oligometastatic disease: consider local consolidative therapy (SBRT/SRS/surgery) after systemic control.

• EGFR, ALK, ROS1, RET, METex14, BRAF V600E, NTRK, HER2: prioritize matched TKIs with CNS-active options where possible.
• KRAS G12C: G12C inhibitors active; co-mutations (STK11/KEAP1) shape IO benefit.
• PD-L1 high driver-negative disease: consider IO monotherapy; otherwise IO-chemotherapy.
• Avoid initiating IO just before TKIs with high pneumonitis/hepatitis overlap; sequence thoughtfully.
• Re-biopsy/ctDNA at progression to reveal on-target mutations (e.g., EGFR C797S) or bypass (MET/HER2 amp) for next-line strategy.
• Combinations to overcome resistance (TKI + MET/MEK/other) best pursued on trials.

• Clinic: symptoms (dyspnea, cough, chest pain, hemoptysis), performance, weight, nutrition.
• Labs: CBC/CMP/TSH (IO), glucose/lipids (steroids), hepatic panel for TKIs/chemo.
• Imaging: CT chest/abdomen every 8–12 weeks on active therapy; brain MRI per symptoms or CNS-risk biology.
• Toxicity surveillance: IO irAEs (skin, GI, endocrine, lung), TKI AEs (rash, diarrhea, liver enzymes, ILD), chemo AEs (myelosuppression, neuropathy).
• Bone health and VTE vigilance; prompt evaluation of unilateral leg swelling or pleuritic chest pain.
• Use consistent imaging protocols to compare response over time.

• 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.

• Avoid initiating IO immediately before/after certain TKIs due to additive pneumonitis/hepatitis risk; plan sequencing.
• Strong CYP3A4/P-gp modulators can alter TKI levels; review med list carefully (azole antifungals, macrolides, rifamycins, anticonvulsants, St. John’s wort, grapefruit/Seville orange).
• Anti-angiogenic agents: hold peri-operatively and with uncontrolled hypertension/bleeding risk.
• High-dose antioxidants on chemo/RT days may blunt cytotoxic efficacy.
• Live vaccines contraindicated during active cytotoxic therapy; coordinate in household contacts.
• QT prolongation risks with some TKIs plus antiemetics/antibiotics—obtain baseline/interval ECG when indicated.

• Fever ≥ 100.4°F (38.0°C) during chemotherapy or while neutropenic.
• Severe chest pain, acute pressure, or sudden/worsening shortness of breath.
• Coughing up ≥1 teaspoon of bright red blood (hemoptysis) or any rapid, ongoing bleeding.
• Oxygen saturation <92% at rest or rapid drop from baseline despite usual oxygen.
• New focal neurologic deficit, seizure, severe confusion, or sudden disabling headache (possible brain metastasis/bleed).
• Severe allergic/infusion reaction: wheezing, facial or tongue swelling, hives, dizziness/fainting.
• Shaking chills/rigors, mottled skin, or very low blood pressure—concern for sepsis.
• Acute facial/neck swelling with venous distension and dyspnea—concern for SVC syndrome.
• Pleuritic chest pain, tachycardia, or syncope—concern for pulmonary embolism.
• Rapidly worsening cough or dyspnea after starting immunotherapy or radiation—possible pneumonitis.
• Severe diarrhea (≥6 stools/day), bloody stools, or severe abdominal pain—possible IO colitis or neutropenic enterocolitis.
• Inability to keep liquids down >12 hours, continuous vomiting (>4 episodes in 6 hours), or minimal urine output.
• Back pain with leg weakness/numbness, saddle anesthesia, or bladder/bowel dysfunction—possible spinal cord compression.
• Uncontrolled pain not relieved by prescribed medications.

• New or worsening cough, chest discomfort, wheeze, or shortness of breath—even if mild.
• Low-grade fevers, chills, or night sweats lasting >48 hours.
• New blood-streaked sputum or persistent hoarseness.
• Progressive fatigue, appetite loss, or unintentional weight loss >5% in a month.
• Rash, mouth sores, or skin breakdown that affects eating or medications.
• New diarrhea, constipation, or abdominal pain—especially on immunotherapy or pemetrexed.
• Symptoms of endocrine irAEs (IO): heat/cold intolerance, palpitations, tremor, fatigue, dizziness.
• Peripheral neuropathy (numbness, tingling, weakness) or balance issues/falls.
• Worsening bone pain, new focal spine pain, or gait changes.
• Wound/port issues (erythema, drainage, fever) or arm swelling on the port side.
• Urinary burning/urgency/flank pain or markedly decreased output.
• Dark urine, pale stools, jaundice, generalized itching, or RUQ discomfort (TKI/chemo hepatotoxicity).
• Planned dental work/surgeries/invasive procedures—confirm timing with anti-angiogenic agents and chemo.
• Any new OTC/herbal/supplement—check interactions before starting.
• Medication/supplement changes or adherence challenges; ask for simplification/support.

• Contrast-enhanced CT chest/upper abdomen for baseline and response.
• PET-CT for staging and to evaluate occult metastases.
• Brain MRI (baseline for stage II–IV or neuro symptoms; surveillance per risk).
• Low-dose chest CT for higher-cadence thoracic follow-up when needed.
• Targeted MRI (spine/liver) for symptom-driven evaluation.

• TNM stage and metastatic burden (esp. brain, liver, bone).
• Driver status and access to CNS-active TKIs.
• PD-L1 level in driver-negative disease.
• Co-mutations (STK11/KEAP1/TP53) and performance status.
• Depth/duration of first-line response and control of oligometastases.
• Ability to maintain dose intensity and promptly manage toxicity.

• Curative intent: surgery or SBRT for early-stage; perioperative IO/chemo or adjuvant targeted therapy as indicated.
• Disease control: first-line targeted therapy or IO±chemo with consolidation to oligomet sites when feasible.
• Symptom-led focus with palliative measures when appropriate.
• Trial-first strategy at resistance or when biomarkers match novel agents.
• Response-adapted plan with pre-agreed switch rules at radiologic progression.

• Analgesia optimization (WHO ladder); consider palliative RT for painful bone/chest wall lesions.
• Dyspnea relief: titrated opioids, fan therapy, pulmonary rehab, and oxygen if hypoxemic; evaluate for reversible causes (effusion, PE, airway obstruction).
• Malignant pleural effusion: therapeutic thoracentesis → indwelling pleural catheter and/or talc pleurodesis for recurrence.
• Malignant airway obstruction/hemoptysis: urgent bronchoscopy for debulking/stent; consider endobronchial RT or bronchial artery embolization for bleeding.
• Brain mets symptoms: corticosteroids for edema, antiepileptics for seizures, and SRS/WBRT per pattern; prioritize CNS-active TKIs when driver-positive.
• Fatigue/anemia support, exercise/rehab, psychosocial care; screen/treat depression, anxiety, and insomnia early.
• Bone/spine disease: SBRT for pain/local control; vertebroplasty/kyphoplasty when indicated; urgent pathway for cord compression signs.
• Liver-dominant symptoms: consider ablation/embolization consults for pain or cholestasis relief when systemic control is limited.
• Cough management: antitussives, gabapentinoids for neuropathic cough, and reflux/post-nasal drip control.
• Appetite/weight: dietitian input, short trials of appetite stimulants when appropriate; address early satiety/constipation.
• VTE prevention/treatment education with clear ED triggers (unilateral leg swelling, pleuritic chest pain, hemoptysis).
• Early palliative care co-management improves symptom control and treatment deliverability; escalate before crises.

• Platinum + Pemetrexed (± Pembrolizumab) — first-line driver-negative non-squamous (Standard induction (4 cycles) followed by maintenance pemetrexed ± pembrolizumab; folate/B12 + steroid premed required.)
• Platinum + Taxane (± Pembrolizumab/Bevacizumab) — first-line non-squamous alternative (Useful when pemetrexed contraindicated; consider bevacizumab if no bleeding/hemoptysis or recent surgery.)
• Single-agent Pemetrexed Maintenance — post-induction (Non-squamous maintenance option; continue until progression/toxicity; add IO per initial plan.)
• Docetaxel (± Ramucirumab) — subsequent line (Post–IO/chemo progression; monitor for neutropenia, mucositis, edema; ramucirumab adds VEGF-related AEs.)
• Gemcitabine/Vinorelbine/Other Doublets — selected cases (Alternatives when standard options exhausted/contraindicated; response rates modest.)

• Comprehensive NGS (DNA+RNA) on tumor ± plasma ctDNA — Identifies EGFR, ALK, ROS1, RET, MET exon 14 skipping, BRAF V600E, NTRK fusions, ERBB2/HER2 mutations, KRAS (esp. G12C) to select matched TKIs/ADCs and trial arms.
• PD-L1 IHC (TPS) — Guides immunotherapy intensity in driver-negative disease (IO monotherapy vs IO-chemotherapy).
• Brain MRI (with contrast) — Detects occult CNS metastases to select CNS-active TKIs and SRS vs WBRT.
• EBUS/EUS nodal sampling (when indicated) — Pathologic staging that changes surgery/RT fields and systemic strategy.
• MSI/MMR — Rare in LUAD; if positive, enables tumor-agnostic PD-1 therapy.
• TMB (large panel/WES) — Contextual biomarker for IO benefit in select settings; integrate with PD-L1 and driver status.
• ctDNA at progression — Noninvasive capture of resistance mechanisms (e.g., EGFR C797S, MET/HER2 amplifications, ALK mutations) to guide next-line therapy/trials.
• HER2 IHC/ISH (contextual) — Less predictive than mutation status but may contribute to ADC eligibility patterns in select regions/trials.
• Smoking status verification (CO level if needed) — Alters TKI exposure (e.g., erlotinib) and perioperative/RT risk; guides cessation supports.

• metastatic lung adenocarcinoma
• oligometastatic NSCLC consolidation
• perioperative immunotherapy lung cancer
• adjuvant targeted therapy EGFR ALK
• EGFR C797S combination trial
• EGFR plus MET amplification trial
• ALK resistance mutation next-gen ALK inhibitor
• ROS1 solvent-front mutation inhibitor
• RET inhibitor next-gen resistance
• MET exon 14 skipping inhibitor trial
• BRAF V600E NSCLC combination trial
• HER2 (ERBB2) mutant NSCLC ADC
• NTRK fusion TRK inhibitor NSCLC
• KRAS G12C inhibitor combination
• PD-1 PD-L1 CTLA-4 lung adenocarcinoma
• STK11 KEAP1 NSCLC immunotherapy combination
• TMB-high NSCLC basket
• SBRT oligometastatic NSCLC
• SRS brain metastases NSCLC
• ctDNA-guided NSCLC management trial

• EGFR resistance (C797S; MET-amplification combinations).
• ALK next-generation inhibitors for specific resistance mutations; CNS-optimized ALK TKIs.
• ROS1/RET solvent-front mutation inhibitors.
• MET exon 14 skipping inhibitors (first-line and resistance settings).
• BRAF V600E + MEK inhibitor combinations in NSCLC.
• HER2-mutant (ERBB2) ADCs/TKIs (exon 20 insertions and others).
• NTRK fusion TRK inhibitors (tumor-agnostic).
• KRAS G12C inhibitor combinations (SHP2/MEK/IO).
• STK11/KEAP1-co-mutated IO-combination strategies.
• Perioperative immunotherapy ± chemotherapy for resectable NSCLC.
• Oligometastatic consolidation (SBRT/SRS/metastasectomy) after systemic response.
• ctDNA-guided MRD/relapse-interception protocols.

Active systemic therapy: CT chest/abdomen every 8–12 weeks (6–8 weeks for aggressive biology, heavy symptom burden, or early post-switch checks). Brain MRI baseline for stage II–IV or neuro symptoms; repeat per symptoms or high CNS-risk biology. Early objective response check after 2–3 cycles (or ~6–8 weeks on TKIs) to trigger escalation/switch if inadequate. IO monitoring: exam each cycle; TSH/free T4 every 6–12 weeks; watch for pneumonitis/colitis/hepatitis/endocrinopathies. TKI monitoring: LFTs and AE check at 2–4 weeks after start/change, then each visit; ILD vigilance. Stable disease/response: extend to every 3–4 months; faster if new symptoms. Post-local consolidation (SBRT/SRS/metastasectomy): site-directed imaging at ~6–8 weeks, then rejoin routine cadence.

• Pemetrexed: start folic acid and vitamin B12 ≥7 days before first dose; continue through treatment; steroid premed as labeled.
• Plan immunotherapy labs (TSH/T4, LFTs) every 6–12 weeks; educate on irAE symptom timing (often weeks 6–12 but can be earlier/later).
• Space TKI initiation several weeks after checkpoint inhibitor when switching sequences that raise pneumonitis/hepatitis risk.
• Coordinate dental/invasive procedures away from bevacizumab/VEGF-TKI windows (hold pre/post per label) and away from neutropenia nadirs.
• Book brain MRI slots early for driver-positive disease with CNS risk to prevent delays in stereotactic radiotherapy.
• If using contrast CT close to cisplatin or ifosfamide days (mixed histologies), separate by ≥48–72h and hydrate.
• Map nadirs (days 7–14) for cytotoxics; schedule travel/procedures outside nadirs; plan G-CSF 24–72h post-chemo when indicated.
• For smoking cessation pharmacotherapy starts, align quit date before thoracic surgery/RT to improve outcomes.

• High-dose antioxidants on chemo/RT days—may blunt ROS-dependent efficacy.
• Bevacizumab/VEGF TKIs with recent major surgery, uncontrolled hypertension, or significant hemoptysis—hold/avoid per label.
• Strong CYP3A4/P-gp modulators with TKIs (azole antifungals, macrolides, rifampin, St. John’s wort) without pharmacist review.
• Acid suppressants with acid-dependent TKIs (erlotinib/gefitinib): separate or avoid PPI; prefer H2 blocker timed apart.
• Grapefruit/Seville orange products with many TKIs—CYP3A4 effects.
• Chronic high-dose steroids started just before IO—can blunt efficacy; taper to physiologic if possible.
• Live vaccines during active cytotoxic therapy or high-dose steroids; coordinate household vaccine plans.

• Early dietitian referral; protein target ~1.2–1.5 g/kg/day when feasible; track weight and lean mass.
• Small, frequent, energy-dense meals for early satiety; oral nutrition supplements if intake falls.
• Hydration focus with diarrhea-prominent TKIs; loperamide protocol and electrolyte replacement.
• Manage reflux and dysgeusia that suppress intake; zinc and oral care bundles as appropriate.
• Avoid restrictive diets in frail/underweight patients; any fasting/ketogenic approach must be supervised to preserve dose intensity.
• Food-safety counseling during neutropenia (no unpasteurized dairy, raw sprouts, undercooked meats).
• Bone health: vitamin D/calcium sufficiency; weight-bearing activity; consider DEXA with steroids or hypogonadism.

• Indwelling pleural catheter: infection prevention, drainage schedule, skin protection; know when to attempt pleurodesis.
• Central venous port: watch for erythema, tenderness, or arm swelling—evaluate for catheter-associated DVT when symptomatic.
• Airway stents: coordinate with interventional pulmonology; humidification and secretion management.
• Pacemaker/ICD: confirm MRI compatibility; respect RT dose constraints and magnet precautions in the vault.
• Orthopedic hardware/spine instrumentation: anticipate imaging artifacts; collaborate for RT planning and positioning.
• Home oxygen: safety counseling (fire risks), humidification to reduce mucosal dryness; arrange portable tanks for rehab.

• Platinum/pemetrexed: myelosuppression—CBC nadir planning; renal function for cisplatin; folate/B12 adherence.
• Docetaxel (± ramucirumab): neutropenia, mucositis, edema—CBC and LFT surveillance; VEGF-related hypertension/proteinuria with ramucirumab.
• EGFR TKIs: LFTs, rash/diarrhea monitoring; watch for ILD/pneumonitis—new dyspnea warrants urgent evaluation.
• ALK/ROS1/RET TKIs: LFTs, CPK (some agents), bradycardia/QT; ocular/neurologic AEs with select agents.
• MET inhibitors: edema, LFTs; interstitial lung disease vigilance.
• KRAS G12C inhibitors: LFTs, GI AEs; drug–drug interaction review.
• HER2-directed ADCs (e.g., T-DXd): ILD/pneumonitis risk—promptly evaluate cough/dyspnea; baseline and periodic imaging review.
• Immunotherapy: TSH/free T4 q6–12w; LFTs; cortisol/ACTH if symptomatic; monitor for colitis, hepatitis, pneumonitis, endocrinopathies.
• Bevacizumab/VEGF TKIs: BP each visit; urine protein/creatinine ratio; hematuria/bleeding review.
• Corticosteroids (supportive or for brain mets): glucose, mood, infection risk; taper thoughtfully.

• driver-status
• pd-l1-strategy
• tki-sequencing
• cns-plan
• oligomet-consolidation
• io-toxicity-plan
• bev-eligibility
• dose-intensity
• gcsf-plan
• nutrition-plan
• rehab/prehab
• ctdna-trending
• re-biopsy-at-progression
• trial-eligibility
• expanded-access

• 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.

• 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?

• https://clinicaltrials.gov/search?cond=Non-Small-Cell+Lung+Carcinoma
• https://www.cancer.gov/about-cancer/treatment/clinical-trials/search
• https://www.iaslc.org/patient-resources/clinical-trials

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

• Alternative Therapies Guide
• Agents Database
• Protocols

• Educational resource; not medical advice. Coordinate decisions with thoracic oncology, radiation oncology, interventional pulmonology, and palliative care.
• Highlight clinical trials at baseline and every progression—driver status and resistance mechanisms change options.