Some of the hardest lung cancers to treat carry two co-occurring mutations — KRAS and LKB1. This study asked why that combination is so aggressive, and found that those tumors have a metabolic blind spot: they can't compensate when their energy pathways are disrupted. Blocking a specific enzyme (HDAC6) exploits exactly that weakness, and pairing it with a second inhibitor makes the effect stronger. A potential treatment path for a subtype that currently has very few options.

KMT2D is an epigenetic regulator frequently mutated in lung squamous cell carcinoma — but this study showed that losing it doesn't just contribute to cancer, it creates a specific exploitable weakness. When KMT2D is gone, EGFR and ERBB2 receptors become hyperactivated through a chromatin-level change. That overactivation is the vulnerability: combining two targeted inhibitors shut down tumor growth in mouse models and patient-derived tumors carrying the mutation. An epigenetic defect that inadvertently hands you a drug target.

Some lung cancer patients respond remarkably well to immunotherapy. Others don't respond at all. This study found that mutations in TSC1 or TSC2 are a genetic signature for the responders — they increase PD-L1 expression, create a more inflammatory tumor environment, and in both mouse models and real patients, dramatically improved survival with anti-PD-1 therapy. A way to predict, before treatment, who is likely to benefit from checkpoint blockade.

Small cell lung cancer is one of the most aggressive cancers and responds poorly to most treatments. This study tested nemvaleukin alfa — an engineered version of IL-2, a cytokine that activates immune cells — in mouse models of SCLC. On its own, modest effects. Combined with chemotherapy, it dramatically improved survival by expanding NK cells and cytotoxic T-cells inside the tumor. A preclinical case for pairing this immune activator with standard chemotherapy in clinical trials.

Tumors don't just grow — they learn to hide. One way they do this is by suppressing their own antigens, turning invisible to immune cells that would otherwise attack them. This study used a CRISPR screen to find the genes responsible and identified a two-protein complex (Atf7ip-Setdb1) as the key switch. Disrupting it forced tumors back into visibility — restoring antigen expression, triggering interferon responses, and flooding the tumor with T-cells. A potential strategy for making 'cold' tumors responsive to immunotherapy.

A specific HER2 mutation — exon 20 insertions — affects a subset of lung cancer patients who had historically very few targeted options. This study tested mobocertinib, a drug designed to lock onto that mutation specifically. In mouse models it achieved complete sustained responses in some tumor types and partial in others. The more surprising finding: combining it with T-DM1 didn't just add their effects — it triggered an immune response, recruiting macrophages and T-cells to attack the tumor. A targeted drug that also turns on the immune system.

Catching breast cancer early is the difference between a manageable and a devastating diagnosis. This study looked at a protein called PIP and found that its levels drop dramatically in cancerous tissue — 93-fold in advanced grades, 22-fold in triple-negative tumors. Run across 190 qPCR samples and 517 tissue specimens, the findings suggest PIP could give pathologists a reliable molecular signal to confirm early-stage diagnoses rather than relying on morphology alone.

Before the oncology lab, there was this — a field study on whether tablet-based telehealth could close the healthcare access gap between low and high income older adults. Participants had their blood pressure, oxygen saturation, and weight monitored biweekly through a telehealth platform called VICS. The finding: it helped both communities, but made the biggest difference for low-income residents who had the least existing access. An early look at technology as an equalizer in healthcare, funded by a NYC Economic Development Corporation grant.