The treatment landscape for EGFR-mutated metastatic non-small cell lung cancer (mNSCLC) has evolved significantly with multiple combination regimens demonstrating superiority over single agent Osimertinib over the past two years. Recent trials such as FLAURA2 and MARIPOSA have explored intensified front-line regimens, with FLAURA2 demonstrating improvement in PFS with the addition of chemotherapy to Osimertinib and MARIPOSA, showing both a PFS and OS benefit with a novel combination regimen of Amivantamab and Lazertinib. However, these regimens are associated with significantly higher toxicity to patients and pose a huge financial and logistical burden to the health care system; therefore, treatment selection must therefore be individualized, considering disease biology, patient fitness, and toxicity burden. Post-progression strategies remain challenging due to resistance mechanisms like EGFR C797S mutations and MET amplification and the lack of data post-progression on novel first-line combinations. Ongoing trials are investigating fourth-generation EGFR TKIs, MET inhibitors, antibody–drug conjugates, and bispecific antibodies in subsequent lines. While regimens like Amivantamab-Lazertinib show promise even in second-line settings, toxicity, cost, and access remain barriers. As therapeutic options expand, biomarker-driven sequencing and personalized care will be critical to optimizing long-term outcomes in EGFR-mutated mNSCLC.

Management of multiple myeloma has transformed care of patients in high-income countries. Use of proteasome inhibitor-immunomodulator (IMiD) triplets and anti-CD38–based quadruplets and routine use of front-line autologous stem-cell transplantation (ASCT) as consolidation have extended survival beyond a decade for most newly diagnosed cases. However, in low- and middle-income countries (LMICs), care delivery is constrained by high out-of-pocket expenditure, limited transplant center infrastructure, erratic drug supply, and inequities in diagnostic access. This review aims to contextualize global advances within resource-limited settings in India and to provide a pragmatic, evidence-informed framework for optimizing outcomes where cost and capacity are major determinants of care. We integrate evidence from pivotal phase II/III international trials and real-world cohorts evidence from local studies and expert consensus to evaluate therapeutic choices across the disease continuum. Bortezomib, lenalidomide, and dexamethasone (VRd) remains the most cost-effective induction regimen, whereas CD38-based quadruplets offer incremental benefit but are often limited by affordability in LMIC settings. Early or frontline use of ASCT significantly deepens response and extends progression-free survival at a fraction of the cost of continuous use of monoclonal antibody therapy. At relapse, antibody-sparing triplets such as pomalidomide-bortezomib-dexamethasone or carfilzomib-dexamethasone are effective alternatives, whereas alkylator-based regimens and salvage ASCT remain valuable when novel agents are inaccessible. Emerging immunotherapies remain largely inaccessible in LMIC settings. The review emphasizes the need for the development of equitable access strategies, government procurement initiatives, and patient-assistance programs to translate global therapeutic advances into real-world benefits in resource-constrained settings. By systematically integrating clinical evidence with local economic considerations and health system realities, this review provides a roadmap for delivering high-value care in LMICs, balancing efficacy, affordability, and equity.

The treatment landscape for EGFR-mutated metastatic non-small cell lung cancer (mNSCLC) has evolved significantly with multiple combination regimens demonstrating superiority over single agent Osimertinib over the past two years. Recent trials such as FLAURA2 and MARIPOSA have explored intensified frontline regimens with FLAURA2 demonstrating improvement in PFS with addition of chemotherapy to Osimertinib and MARIPOSA showing both a PFS and OS benefit with a novel combination regimen of Amivantamab and Lazertinib. However, these regimens are associated with significantly higher toxicity to patients and pose a huge financial and logistical burden to the health care system, therefore, treatment selection must therefore be individualized, considering disease biology, patient fitness, and toxicity burden. Post-progression strategies remain challenging due to resistance mechanisms like EGFR C797S mutations and MET amplification and lack of data post progression on novel 1st line combinations. Ongoing trials are investigating fourth-generation EGFR TKIs, MET inhibitors, antibody-drug conjugates, and bispecific antibodies in subsequent lines. While regimen like Amivantamab-Lazertinib show promise even in second-line settings, toxicity, cost, and access remain barriers. As therapeutic options expand, biomarker-driven sequencing and personalized care will be critical to optimizing long-term outcomes in EGFR-mutated mNSCLC.

Paraneoplastic neurological syndromes (PNS) associated with triple-negative breast carcinoma (TNBC) are exceptionally rare. We report a case of fulminant encephalitis in a middle-aged woman with TNBC presenting with concurrent PNMA2 (Ma2/Ta), ZIC4 and recoverin antibody positivity. The patient initially developed a subacute cerebellar syndrome characterised by downbeat nystagmus, gait ataxia and diplopia. Comprehensive evaluation revealed FDG-avid left axillary lymphadenopathy and biopsy confirmed high-grade TNBC with PD-L1 CPS of 77. She received neoadjuvant chemo-immunotherapy as per standard institutional protocol (paclitaxel, carboplatin, epirubicin, cyclophosphamide and pembrolizumab). Following the sixth cycle, she developed refractory focal seizures progressing to status epilepticus with MRI findings consistent with cortical encephalitis. Despite aggressive immunosuppression including corticosteroids, intravenous immunoglobulin and rituximab, her condition proved refractory. She ultimately succumbed despite maximal supportive care. This case illustrates a rare paraneoplastic overlap syndrome combining PNMA2-associated encephalitis and ZIC4-associated cerebellar degeneration in TNBC, highlights diagnostic challenges when immune checkpoint inhibitors may amplify pre-existing onconeural immunity and underscores the dismal prognosis of intracellular antibody-mediated neurological syndromes despite aggressive immunotherapy.