Overview
Lung cancer is not one disease but a family of biologically distinct tumours.
Roughly 85 % of all lung cancers fall into the non-small-cell group, the rest being
small-cell type.
Within NSCLC, the three main histologies are adenocarcinoma, squamous-cell
carcinoma, and large-cell carcinoma.
Two decades ago, treatment meant the same chemotherapy for everyone.
Today, thanks to genomic research, NSCLC is a molecularly driven illness.
When we identify the specific mutation powering a tumour, we can often match it to
an oral targeted drug or immunotherapy that dramatically improves outcomes.
At Coimbatore Cancer Clinic, every patient is offered comprehensive molecular
testing before starting therapy. This ensures a truly personalised
approach—maximising benefit, minimising toxicity, and giving patients years of
high-quality life that were once impossible.
Risk Factors & Causes
● Smoking: the dominant cause (about 80 %).
● Second-hand smoke: risk rises even in lifelong non-smokers.
● Air pollution & biomass fuel exposure: important in India; associated with
EGFR-mutant adenocarcinoma in never-smokers and women.
● Occupational hazards: asbestos, chromium, nickel, arsenic, diesel exhaust.
● Radiation exposure or prior chest radiotherapy.
● Genetic predisposition: familial clustering; germline EGFR T790M or TP53.
● Age > 50 years and male sex remain traditional demographic risks.
Pathologic Types
Symptoms & Warning Signs
● Persistent or worsening cough
● Blood in sputum (hemoptysis)
● Chest or shoulder pain
● Shortness of breath or wheezing
● Hoarseness (recurrent-laryngeal-nerve involvement)
● Weight loss, fatigue, loss of appetite
Metastatic symptoms: headaches or seizures (brain), bone pain, jaundice,
abdominal distension, or back pain.
Because many of these mimic ordinary lung infections, delayed diagnosis is
common—underscoring the value of early imaging and screening.
Diagnostic Evaluation
1️⃣Imaging
● CT Chest with contrast – defines tumour size and nodes.
● PET-CT – detects hidden spread; now standard for staging.
● Brain MRI – mandatory for stage III/IV or neurologic symptoms.
2️⃣Tissue Diagnosis
● Bronchoscopy for central lesions.
● CT-guided core needle biopsy for peripheral nodules.
● EBUS-TBNA for mediastinal nodes.
● VATS / surgical biopsy if minimally invasive options fail.
3️⃣Pathology & IHC
● TTF-1 / Napsin A → adenocarcinoma.
● p40 / CK5/6 → squamous.
● PD-L1 immunostaining → guides immunotherapy.
4️⃣Molecular Profiling (Next-Generation Sequencing)
Every non-squamous NSCLC—and many squamous cases in non-smokers—should
be tested for a panel of actionable alterations:
Liquid-biopsy cfDNA testing complements tissue analysis when samples are small.
Stage Classification (AJCC 8ᵗʰ)
● Stage I–II: confined to lung ± small nodes.
● Stage III: mediastinal or chest-wall involvement but no distant spread.
● Stage IV: metastatic to opposite lung, bone, brain, liver, adrenals.
Stage-wise Treatment Approach (2025)
Stage I–II (Localized Disease)
Goal → Cure
● Surgery: lobectomy or segmentectomy + systematic node dissection. Minimally invasive (VATS/robotic) preferred.
● Adjuvant Chemotherapy: Cisplatin + Pemetrexed / Vinorelbine for stage II or node positive.
● Adjuvant Targeted Therapy:
.
o EGFR-mutant: Osimertinib for 3 years (adjuvant ADAURA protocol).
o ALK-positive: Alectinib under study (SALSA trial).
● Adjuvant Immunotherapy: Atezolizumab for PD-L1 ≥ 1% post-chemo (IMpower010).
● Surveillance: CT every 6 months × 2 years then yearly.
Stage III (Locally Advanced)
Goal → Cure or Long-term Control
Options depend on resectability:
● Stage IIIA (resectable):
.
o Neoadjuvant chemo ± immunotherapy (Pembrolizumab + Cisplatin doublet).
.
o Surgery → Adjuvant targeted or immunotherapy based on biomarkers.
● Unresectable Stage III (N2 / N3):
.
o Concurrent Chemoradiation (Cisplatin + Etoposide or Pemetrexed + Radiation 60 Gy).
.
o Durvalumab consolidation for 1 year (PACIFIC trial) improves 5-year OS to 43%.
Stage IV (Metastatic)
Goal → Disease control, symptom relief, prolonged survival
Treatment is now entirely biomarker-driven.
1️⃣ Targetable Driver Mutations
Sequential re-biopsy or liquid biopsy is recommended when progression occurs to
identify resistance mutations (e.g., EGFR C797S).
2️⃣ PD-L1 Expression / Immunotherapy
Immunotherapy achieves durable responses lasting years in a subset of patients
with high PD-L1 or inflamed tumours.
3️⃣ Chemotherapy for Driver-Negative Disease
● Non-squamous: Carboplatin + Pemetrexed ± Pembrolizumab.
● Squamous: Carboplatin + Paclitaxel ± Pembrolizumab.
Maintenance Pemetrexed or Pembrolizumab after 4–6 cycles.
4️⃣ Oligometastatic Disease
● Local ablation (SBRT or surgery) for limited metastases can prolong survival.
● Continue targeted therapy throughout.
5️⃣ Brain Metastases
● Modern TKIs (Osimertinib, Lorlatinib, Selpercatinib) cross the blood–brain
barrier.
● SRS (Stereotactic Radiosurgery) preferred over whole-brain RT.
Resistance & Subsequent Therapy
Most patients on targeted therapy eventually develop resistance.
Common mechanisms include:
● EGFR T790M → treated with Osimertinib.
● ALK G1202R → Lorlatinib.
● MET amp or HER2 bypass → switch to appropriate targeted agent.
● Histologic transformation (adenocarcinoma → small-cell) → treat as SCLC.
ctDNA testing helps detect these changes non-invasively and guide next steps.
Recent Advances (2024 – 2025)
● Peri-operative Immunotherapy: neoadjuvant Nivolumab + Chemo (CHK 8
trial) improves pathologic response.
● Adjuvant Osimertinib data (ADAURA update) shows 5-year DFS > 70 %.
● Antibody–Drug Conjugates (ADCs): Patritumab Deruxtecan for
EGFR-resistant cases; Datopotamab Deruxtecan for TROP2-positive
tumours.
● ctDNA MRD tracking predicts recurrence months earlier than scans.
● AI-guided radiomics for therapy response assessment.
Supportive Care & Quality of Life
● Symptom control: breathlessness, pain, cough managed by integrated
palliative care.
● Nutrition & exercise programmes maintain muscle mass during therapy.
● Smoking cessation and lung rehabilitation reduce toxicity.
● Psychological support for anxiety and fear of recurrence.
Our Expertise @ Coimbatore Cancer Clinic
● Complete diagnostic work-up including bronchoscopy, EBUS and biopsy on
site.
● NGS panel testing for all actionable mutations (EGFR, ALK, ROS1, MET,
RET, KRAS, HER2, PD-L1).
● Access to targeted and immunotherapy agents through patient-assistance
programmes in India.
● Tumour-board discussion for every case to design a personalised plan.
● Seamless referral to CAR-T and cell-therapy trials at partner centres when
indicated.
When to Consult
Any persistent cough, unexplained breathlessness or blood in sputum should prompt
a chest CT and specialist evaluation — early diagnosis can save lives
Frequently Asked Questions
Is NSCLC curable?
Yes, when caught early. Even stage IV disease can often be controlled for years with
targeted or immune therapy.
Do all patients need chemotherapy?
No. Many receive oral targeted therapy alone if a driver mutation is found.
Are targeted drugs available in India?
Yes — most agents (EGFR, ALK, ROS1, RET, MET, KRAS inhibitors and
immunotherapies) are approved and accessible through support programs.
How long will treatment continue?
Targeted and immunotherapies are continued until progression or intolerance; some
patients remain stable > 5 years.
Disclaimer
This page is for educational information only. Treatment should be individualised by
qualified oncologists based on complete clinical and molecular evaluation.
Small Cell Lung Cancer (SCLC)
Overview
Small Cell Lung Cancer (SCLC) is a fast-growing form of lung cancer that originates
from neuro-endocrine cells lining the bronchi.
It represents about 15 % of all lung cancers but causes a disproportionately high
number of deaths because of its aggressive biology and early spread.
Unlike Non-Small Cell Lung Cancer (NSCLC), SCLC usually responds dramatically
to initial chemotherapy and radiation, yet it tends to relapse within months.
Recent advances—including immunotherapy, maintenance strategies, and novel
antibody–drug conjugates—are improving both survival and quality of life.
At Coimbatore Cancer Clinic, we combine rapid diagnosis, state-of-the-art staging,
and NCCN-aligned multimodality therapy to ensure that every patient receives the
most effective and least disruptive treatment possible.
Causes & Risk Factors
● Cigarette smoking – present in > 95 % of cases; cumulative exposure is the
major determinant.
● Second-hand smoke – increases risk for household contacts.
● Occupational exposure – asbestos, arsenic, diesel exhaust.
● Radon gas – naturally occurring radioactive gas trapped in poorly ventilated
areas.
● Genetic susceptibility – rare germline variants in TP53 or RB1.
Pathology & Biology
Microscopically, SCLC cells are small with scant cytoplasm, finely granular
chromatin, and high mitotic rate.
They express neuro-endocrine markers (Synaptophysin, Chromogranin A, CD56)
and often produce hormones causing paraneoplastic syndromes (SIADH, ectopic
ACTH, Lambert-Eaton myasthenic syndrome).
Biologically, almost all SCLCs show loss of TP53 and RB1.
Molecular subsets defined by transcription factors (ASCL1, NEUROD1, POU2F3,
YAP1) may soon guide personalised therapy.
Symptoms & Presentation
● Persistent cough or chest pain
● Shortness of breath or wheezing
● Coughing up blood
● Rapid weight loss, fatigue
● Facial swelling or distended neck veins (superior vena cava syndrome)
● Neurologic or metabolic abnormalities from paraneoplastic hormones
Because it spreads early, one-third of patients already have distant metastases at
diagnosis.
Diagnostic Evaluation
1️⃣ Imaging & Staging
● CT Chest + Abdomen for initial assessment.
● PET-CT for metabolic staging when available.
● Brain MRI mandatory at baseline — brain metastases occur in up to 25%.
● Bone scan if PET not available.
2️⃣ Tissue Diagnosis
● Bronchoscopic biopsy (endobronchial or EBUS).
● Core-needle biopsy for peripheral lesions or metastases.
Histopathology distinguishes pure SCLC from combined SCLC + NSCLC, which has treatment implications.
3️⃣ Staging Systems
Although AJCC TNM 8ᵗʰ is now recommended, clinicians still classify disease as:
● Limited-Stage (LS-SCLC) – confined to one hemithorax and regional nodes, treatable within a single radiation field.
● Extensive-Stage (ES-SCLC) – spread beyond those limits (contralateral chest, distant organs).
Treatment Approach
Limited-Stage Disease (LS-SCLC)
Goal → Cure
1. Concurrent Chemoradiation
● Platinum (Cisplatin or Carboplatin) + Etoposide × 4 cycles with thoracic RT (45 Gy twice-daily or 60 Gy daily).
● Starting radiation within the first or second chemo cycle gives the best survival.
2. Prophylactic Cranial Irradiation (PCI)
● Reduces brain metastases by > 50%.
● Recommended for good-response patients ≤ 70 years with ECOG 0–2.
3. Maintenance / Consolidation
● No standard targeted agent yet, but trials using immunotherapy consolidation are ongoing.
Outcomes: 5-year survival 30–35% (double that achieved in the 1990s).
Extensive-Stage Disease (ES-SCLC)
Goal → Long-term Control, Symptom Relief
1️⃣ First-Line Therapy
● Chemo-Immunotherapy Combination (Standard of Care 2025):
o Atezolizumab + Carboplatin + Etoposide (IMpower133)
o Durvalumab + Carboplatin + Etoposide (CASPIAN trial)
o 4 cycles followed by maintenance immunotherapy until progression.
→ Median OS ≈ 15–17 months vs 10 months with chemotherapy alone.
2️⃣ Second-Line / Relapsed Therapy
● Lurbinectedin (transcription-inhibitor) – response ≈ 35%.
● Topotecan – long-used alternative where Lurbinectedin unavailable.
● Platinum re-challenge – for relapses > 6 months after initial therapy.
● Clinical trials / ADCs – e.g., DLL3-targeted Tarlatamab showing encouraging results.
3️⃣ Local Treatment
● Thoracic RT to residual chest lesion after good chemo-response.
● Palliative RT for bone, brain, or airway symptoms.
Immunotherapy & Biomarkers
Unlike NSCLC, PD-L1 expression and TMB are not reliable biomarkers in SCLC;
all-comer immunotherapy is used.
Checkpoint inhibitors (Atezolizumab, Durvalumab) enhance survival modestly but
meaningfully.
Research into novel immune targets—TIM-3, TIGIT, CTLA-4—is ongoing.
Emerging Targets and Precision Therapies
● DLL3 (Delta-Like Ligand 3): over-expressed in > 80 % of SCLCs; targeted
by Tarlatamab (BiTE) and Rovalpituzumab tesirine (ADC).
● PARP inhibitors for homologous-recombination-deficient tumours.
● Epigenetic modifiers (EZH2, BET inhibitors) reversing neuro-endocrine
phenotype.
● Molecular subtyping (ASCL1, NEUROD1, POU2F3, YAP1) guiding trial
enrolment.
Supportive & Palliative Care
Because of the disease’s pace, supportive care is integral from day 1:
● Anti-nausea, appetite stimulants, and pain control.
● Early palliative-care involvement improves survival and quality of life.
● Psychosocial and smoking-cessation counselling.
● Nutritional support to maintain weight during therapy.
Follow-Up
● Clinical review and CT chest every 3 months for 2 years, then 6-monthly.
● Brain MRI every 6–12 months for patients who declined PCI.
● Manage late effects: fatigue, cognitive changes, hearing loss, neuropathy.
Our Expertise @ Coimbatore Cancer Clinic
● Rapid same-day diagnostic pathway (CT, bronchoscopy, EBUS).
● Multidisciplinary tumour board for combined chemo-radiation planning.
● Availability of Atezolizumab / Durvalumab / Lurbinectedin through assistance
programmes.
● Precision radiation facilities with image guidance and conformal dosing.
● Dedicated survivorship and neuro-cognitive rehabilitation support after PCI.
When to Consult
● Any chronic smoker with new cough, hoarseness, or facial swelling should
undergo CT chest immediately.
● Early detection during screening can convert an otherwise fatal disease into
one with curative potential.
Frequently Asked Questions
Is SCLC curable?
Yes, if confined to the chest (limited stage) and treated early with chemo-radiation.
Does immunotherapy help?
Adding Durvalumab or Atezolizumab to first-line therapy extends life by several months and produces long-term survivors in about 15%.
Will I lose my hair?
Temporary hair loss is common with Etoposide and Platinum but reversible after therapy.
Can SCLC come back?
Relapse is frequent; however, newer drugs like Lurbinectedin and Tarlatamab offer effective second-line options.
Disclaimer
This information is for patient education only. Individual treatment must be decided
by qualified oncologists based on stage, organ function, and patient preference.
Malignant Mesothelioma (Pleural & Peritoneal)
Overview
Malignant mesothelioma is an uncommon but devastating cancer of the mesothelial
cells—the delicate lining that covers the lungs (pleura), abdomen (peritoneum),
heart (pericardium), and testis (tunica vaginalis).
Nearly 90 % of cases involve the pleura. The disease is almost always linked to
asbestos exposure, sometimes decades earlier.
Although mesothelioma historically carried a grim outlook, survival is improving
dramatically in the modern era through early multidisciplinary evaluation, tailored
surgery, precision chemotherapy, and immune checkpoint inhibitors.
At Coimbatore Cancer Clinic, every patient is assessed by a thoracic oncology
board to individualize care — balancing tumor control, lung preservation, and quality
of life.
Disease Biology & Pathogenesis
● Asbestos fibers (chrysotile, amosite, crocidolite) are inhaled and embed
within the pleura or peritoneum.
● Chronic inflammation and oxidative DNA injury cause mutations in BAP1,
NF2, CDKN2A, and TP53.
● Mesothelial cells undergo malignant transformation, forming diffuse, sheet-like
tumors encasing the lung or abdominal organs.
● The latency period averages 30–40 years after exposure, explaining why
incidence continues to rise despite asbestos bans.
Risk Factors
● Occupational exposure: shipyard, textile, brake-lining, insulation, construction.
● Secondary household exposure (washing asbestos-laden clothes).
● Radiotherapy to the chest.
● Genetic predisposition: germline BAP1 mutation increases lifetime risk.
● Male gender, age > 60 years.
Symptoms & Warning Signs
● Persistent shortness of breath
● Chest or shoulder pain, often dull or diffuse
● Recurrent pleural effusion (fluid around lungs)
● Fatigue, loss of appetite, weight loss
● Persistent cough or hoarseness
● For peritoneal disease: abdominal distension, pain, or early satiety
Because these symptoms mimic benign pleural disease, many patients are
diagnosed late.
Diagnosis & Investigations
1. Imaging
o CT Chest/Abdomen → shows irregular pleural thickening, nodules, or encasement of lung.
o PET-CT → differentiates benign from malignant and maps metastases.
o MRI → superior for chest-wall, diaphragmatic, or pericardial invasion.
2. Fluid Analysis
o Pleural tapping (thoracentesis) rarely diagnostic — sensitivity < 30%.
o If cytology positive, immunocytochemistry (Calretinin+, WT-1+, CK5/6+) confirms mesothelial origin.
3. Tissue Biopsy (Gold Standard)
o Video-Assisted Thoracoscopic Surgery (VATS) or medical thoracoscopy yields ample tissue for histologic and molecular study.
o Subtyping: Epithelioid (70%, best prognosis), Sarcomatoid, Biphasic.
4. Staging
o AJCC 8ᵗʰ Edition TNM:
▪ T: pleural surface involvement
▪ N: ipsilateral vs contralateral nodes
▪ M: distant metastasis
o Accurate staging determines operability.
Management Strategy
1️⃣ Multimodality Approach
The best outcomes occur in experienced centers combining surgery + chemotherapy ± radiation.
A. Surgery
Two principal operations:
Post-operative 30-day mortality is < 5% in expert hands.
Lung-sparing P/D is increasingly favored for better function and similar control.
B. Chemotherapy
● Cisplatin + Pemetrexed (standard of care; 3-weekly × 4–6 cycles).
● Carboplatin can replace cisplatin for renal impairment.
● Addition of Bevacizumab improves median survival by 2–3 months.
● Vitamin B₁₂ + Folate supplementation mandatory to reduce toxicity.
C. Immunotherapy
● Nivolumab + Ipilimumab dual checkpoint blockade — first-line for unresectable disease (CheckMate 743).
o Median overall survival ≈ 18 months vs 14 months with chemo.
o Works best in non-epithelioid variants where chemo is less effective.
● Pembrolizumab or Durvalumab used in selected PD-L1–positive cases.
D. Radiation Therapy
● Adjuvant hemithoracic IMRT after EPP reduces local recurrence.
● Palliative RT (20–30 Gy) for pain, nerve compression, or chest-wall invasion.
E. Emerging Options
● Tumor Treating Fields (TTF): wearable electrical-field device disrupting cancer cell division.
● Mesothelin-directed Antibody–Drug Conjugates and CAR-T therapy under active trials.
● Maintenance immunotherapy under study (DREAM3R, BEAT-meso trials).
2️⃣ Peritoneal Mesothelioma
● Cytoreductive Surgery + HIPEC (Hyperthermic Intraperitoneal Chemotherapy):
Heated cisplatin/pemetrexed perfusion directly in abdomen after complete visible tumor removal; median OS > 5 years in selected patients.
● Systemic chemo or immunotherapy for unresectable cases.
● Supportive management: ascitic drainage, paracentesis, albumin replacement, pain control, nutritional rehabilitation.
3️⃣ Symptom Control & Supportive Care
● Recurrent effusion → Indwelling pleural catheter for at-home drainage.
● Breathlessness → supplemental oxygen, breathing exercises.
● Pain → multimodal analgesia, intercostal nerve blocks.
● Psychological counselling and palliative-care integration from diagnosis.
Recent Advances (2024 – 2025)
● Genomic subclassification (BAP1, NF2, CDKN2A) predicting IO response.
● Personalized multimodal algorithms improving 3-year survival to ~30 %.
● Artificial-intelligence imaging for earlier diagnosis.
● Ongoing Indian trials evaluating cost-effective immunotherapy combinations.
Our Expertise at Coimbatore Cancer Clinic
● In-house diagnostic thoracoscopy and image-guided pleural biopsy.
● Collaboration with thoracic-surgical and HIPEC teams.
● Access to Pemetrexed, Bevacizumab, Nivolumab, and Ipilimumab locally.
● Comprehensive respiratory physiotherapy and palliative-care programs.
● Long-term follow-up with serial imaging and functional assessment.
When to Seek Evaluation
Persistent pleural effusion, chest heaviness, or unexplained breathlessness in
anyone with past asbestos exposure warrants immediate CT and oncology review
FAQs
Is mesothelioma always fatal?
No. With early detection, lung-sparing surgery and immunotherapy can achieve multi-year control.
Can immunotherapy replace chemotherapy?
For non-epithelioid disease or patients unfit for chemo, yes — dual IO is now first-line.
How common is recurrence after surgery?
About 50% within 2 years; continued surveillance and early IO salvage improve outcomes.
Are treatments available in India?
All standard chemotherapy and immunotherapy agents are accessible through assistance programs.
Disclaimer
Information for patient education; individual management must be planned by
qualified oncologists.
Thymomas and Thymic Carcinomas
Overview
The thymus sits behind the breastbone and plays a vital role in immune-cell
maturation.
Thymic epithelial tumors (TETs) are rare, but crucial because many are curable
when detected early.
They span a spectrum:
● Thymoma: indolent, often linked with autoimmune diseases (notably
myasthenia gravis).
● Thymic carcinoma: histologically malignant, higher metastatic potential.
At Coimbatore Cancer Clinic, each case is reviewed by a multidisciplinary thoracic
team ensuring radical resection whenever feasible and meticulous management of
associated autoimmune disorders.
Epidemiology & Etiology
● Incidence ≈ 1.5 per million / year.
● Peak 40–60 years; equal in men and women.
● Etiology unknown; no smoking correlation.
● Strong autoimmune association:
o Myasthenia gravis (~30 %)
o Pure red-cell aplasia, thyroiditis, lupus, or hypogammaglobulinemia.
Pathology & Molecular Insights
● Classified (WHO 2021) as A, AB, B1, B2, B3 (thymoma) and Type C
(thymic carcinoma).
● GTF2I mutation is characteristic of indolent type A/AB; KIT, PI3K, EGFR
alterations occur in carcinoma.
● PD-L1 over-expression common in carcinoma (potential IO target).
Clinical Presentation
● Often discovered incidentally on chest imaging.
● Symptoms due to compression:
o Chest pain, cough, breathlessness.
o Hoarseness, facial swelling (SVC obstruction).
● Autoimmune manifestations: muscle weakness, ptosis, diplopia.
Diagnosis & Staging
1. Contrast CT / MRI Chest: defines size, invasion of vessels or pericardium.
2. Biopsy: core-needle or thoracoscopic.
3. Myasthenia evaluation: anti-AChR or anti-MuSK antibodies.
4. Staging:
o Masaoka-Koga (I–IV) remains practical for prognosis.
o TNM 8ᵗʰ Edition increasingly used in international studies.
Treatment
1️⃣ Surgery (Cornerstone of Cure)
● Complete R0 thymectomy including perithymic fat.
● Approaches: median sternotomy, VATS, or robotic.
● For invasive tumors, en bloc removal of pericardium or lung segments may be required.
● Post-operative myasthenia improvement seen in 80%.
2️⃣ Adjuvant / Post-operative Therapy
3️⃣ Unresectable / Metastatic
● First-line: CAP regimen (Cisplatin + Adriamycin + Cyclophosphamide) or Cisplatin + Etoposide.
● Second-line: Gemcitabine, Pemetrexed, or Paclitaxel.
● Targeted therapy:
o Sunitinib and Lenvatinib (multi-TKIs) active in refractory disease.
o Imatinib for KIT-mutated carcinomas.
● Immunotherapy: Pembrolizumab effective in PD-L1 ≥ 50% thymic carcinoma; caution in thymoma due to higher autoimmune toxicity (myositis, hepatitis).
4️⃣ Recurrent / Disseminated
● Surgical re-resection when feasible.
● Local RT or radiofrequency ablation for isolated pleural nodules.
● Systemic therapy as above for widespread disease.
Supportive & Autoimmune Management
● All thymoma patients screened and managed for myasthenia gravis in
collaboration with neurology.
● Pre-operative optimization with anticholinesterases, corticosteroids, or
plasmapheresis prevents crisis.
● Endocrine, thyroid, and hematologic evaluations periodically.
● Long-term follow-up with annual CT scans for ≥ 10 years (late recurrences
possible).
Recent Advances
● Robotic thymectomy provides equivalent oncologic outcomes with smaller
incisions and faster recovery.
● Next-generation sequencing of thymic carcinoma enables targeted therapy
trials.
● Combination IO + TKI strategies under exploration.
● Indian collaborative registry data now improving local evidence and
outcomes.
Our Expertise @ Coimbatore Cancer Clinic
● Advanced imaging and thoracoscopic biopsy facilities.
● Collaboration with thoracic surgeons skilled in robotic and extended
thymectomy.
● Full suite of chemo, radiotherapy, and targeted drugs on-site.
● Integrated care with neurology for myasthenia and autoimmune control.
● Long-term survivorship tracking with multidisciplinary support.
When to Consult
Any anterior mediastinal mass or unexplained weakness, drooping eyelids, or double
vision should prompt a CT chest and thymic evaluation.
Frequently Asked Questions
Can thymoma recur after many years?
Yes, hence prolonged surveillance is vital.
Is radiation always necessary after surgery?
Only if margins are close or tumor invades surrounding tissue.
Can I receive immunotherapy safely if I have myasthenia?
Caution is advised; your oncologist and neurologist will jointly decide.
Are robotic surgeries available locally?
Yes, through partner thoracic-surgical centers affiliated with our clinic.
Disclaimer
This information is meant for educational purposes only; management must be tailored by qualified specialists.
