Oncology

A 3-year-old with chemotherapy-resistant metastatic hepatoblastoma had complete regression after two infusions of GPC3-targeted CAR T cells engineered to express IL-15 and IL-21. The response lasted at least 12 months.

Loss of TET2 leaves single-stranded gaps behind DNA replication and makes cells more vulnerable to PARP inhibition. The study traces a possible path from altered DNA chemistry to breaks in the genome.

Breast fat cells produce the lipid signal 9S-HODE, which can drive ferroptosis in cancer cells. In obesity, this signal is reduced, potentially removing one of the local restraints on breast tumor growth.

Researchers identified PLA2G2D as an immune brake concentrated in tumour-draining lymph nodes. Blocking it expanded tumour-specific T cells and slowed tumour growth in mouse models, including alongside anti-PD-1 treatment.

PRMT7 acts as an internal restraint on antitumor CD8+ T cells. Removing it enhanced T-cell activation and tumor control in mice, while an experimental PRMT7 degrader produced similar effects in human cells.

In mouse models of ovarian cancer, early disseminating tumor cells disproportionately seeded later metastases and helped cells arriving afterward establish themselves. Tumor-intrinsic IFNγ signaling was a key part of this early adaptation.

Tumors can use the antioxidant enzyme PRDX1 as an immune suppressor, removing reactive oxygen species that T cells need for signaling. In mouse models, loss of PRDX1 strengthened antitumor immunity and improved responses to checkpoint therapy.

Loss of the actin regulator CRACD triggers a signaling cascade that raises PD-L1 and weakens antitumor immunity. The mechanism was demonstrated in organoids and mice, with a CRACD–PD-L1 association also found in human tumors.

Mycobacterium abscessus in non-small cell lung tumors was associated with an APOBEC mutational signature. Experimental models traced the effect to bacterial NDK, IRF3 signaling, and sustained APOBEC3A activation.

A study of hundreds of meningiomas identified a DNA methylation signature linked to progression risk and connected it mechanistically to epigenetic silencing of clustered protocadherins and β-catenin localization.

Cas12a2 was programmed to recognize mutant RNA and then damage chromatin inside the same cell. The system selectively impaired cancer cells carrying certain EGFR and TP53 mutations and showed antitumor activity in mice.

In an analysis of more than 572,000 people with pancreatic cancer risk factors, GLP-1 users had fewer diagnoses of the disease. The association was substantial, but the observational design cannot establish a preventive effect.

Certain TP53 mutations may help tumors hide from innate immunity. The study links mutant p53 to RBM28, reduced double-stranded RNA, weaker interferon signaling, and resistance to immune checkpoint blockade.

An experimental mutant-KRAS vaccine was tested in 20 people at inherited high risk of pancreatic cancer. Ninety percent developed a specific T-cell response, with some vaccine-induced T-cell clones persisting for up to two years.

In mouse models, alcohol changed the cellular origins and immune state of liver cancer arising with metabolic disease. Tumors followed different developmental routes and responded differently to PD-1 blockade.

In experimental models, astrocytes transferred mitochondria to glioblastoma cells. The exchange helped dormant tumor cells re-enter the cell cycle while making them more resistant to immune attack.

Isoleucine and valine feed a metabolic signalling pathway in prostate cancer cells that increases cholesterol and androgen production and may help tumours adapt to androgen deprivation.

In COMMIT, adding mFOLFOX6 chemotherapy and bevacizumab to atezolizumab improved disease control in dMMR/MSI-H metastatic colorectal cancer, but substantially increased serious toxicity.

In an observational cohort, 122 participants reported an 84.4% clinical benefit rate after six months on ivermectin plus mebendazole. But without a control group, verified imaging, and with substantial loss to follow-up, the study cannot establish efficacy.

In the phase 3 RASolute 302 trial, daraxonrasib was compared with standard chemotherapy in 500 patients with previously treated metastatic pancreatic cancer. Median overall survival was 13.2 months versus 6.7 months.

Liquid biopsy does not sample the genome uniformly. Across 317 cfDNA samples, researchers mapped reproducible “penumbra” regions with reduced representation that may weaken signals from clinically relevant cancer loci.

The FDA has granted accelerated approval to a genetically engineered HSV-1 oncolytic therapy combined with nivolumab for advanced melanoma after anti-PD-1 treatment failure. The regulatory efficacy analysis showed a 24.2% response rate.

A dCas13-based system lengthened the regulatory tail of SPSB1 mRNA, restored MHC-I on tumour cells and improved checkpoint therapy responses in two mouse models of prostate cancer.

Focused ultrasound can mechanically destroy small liver tumors without an incision or thermal ablation. One-year HOPE4LIVER data reveal both the potential of histotripsy and important limitations, including an unexpected challenge in interpreting follow-up imaging.

Circular DNA outside chromosomes can assemble into nuclear clusters. A polymer model and experiments in colorectal cancer cells show how these structures selectively strengthen regulatory contacts involving MYC.

In mouse models, pregnancy raised adenosine levels and created an immunosuppressive environment in the lungs and liver that favored metastasis. Similar blood changes appeared in healthy pregnant women, but cancer patients were not studied.

Gedatolisib combined with endocrine therapy extended median progression-free survival from 2.0 months to 7.4–9.3 months. The FDA has approved it for advanced breast cancers without a detected PIK3CA mutation.

New cancer drugs can extend survival while safety systems remain better at detecting acute severe events than months of rash, diarrhea, fatigue, impaired daily functioning and emotional distress.

A subset of pancreatic tumours uses GSK3β–NFATc1 signalling to activate DNA repair. The subtype was linked to early recurrence and platinum resistance, but the treatment evidence remains preclinical and the patient cohort was small.

An antisense oligonucleotide reduced GFRAL in the hindbrain of tumor-bearing mice. The animals retained more muscle and fat, recovered strength, and survived longer, although the drug was delivered directly into the brain.

Gut microbes altered how liver macrophages captured nanoparticle drugs. In mice, microbiome remodeling prolonged circulation, increased tumor delivery and strengthened responses to nanomedicine-based chemotherapy.

Fat accumulation in the liver may steer colorectal cancer metastases toward a more aggressive replacement growth pattern. The study links this effect to MYC stabilization, proline synthesis and collagen production, primarily in preclinical models.

Cas12a2 does not behave like a conventional gene editor: it recognizes tumour-associated RNA and triggers chromatin destruction in the same cell. The method reduced tumour burden in mice but remains an early experimental platform.

An analysis of two CAR T-cell trials links inherited variants in STXBP2, ADAMTSL3, and PTPN22 to inflammatory toxicity and the expansion of therapeutic cells after infusion.

Engineered CAR T cells were given an extra defence against an immune-suppressing signal from liver tumours. The phase I trial showed tumour shrinkage, but responses were often brief.

Across 611 childhood tumour genomes, researchers identified mutational scars left by earlier treatment. Platinum drugs produced the clearest imprint, sometimes detectable within three months.

Thymulin, a peptide produced by the thymus, reduced age-related myeloid inflammation in mice, slowed mammary tumor growth, and restored responsiveness to anti-PD-L1 therapy. Human evidence was limited to observational and ex vivo analyses.

TNG961 degraded HBS1L and caused tumor regression in preclinical models of FOCAD-deleted cancer, including a PRMT5 inhibitor-resistant model.

An experimental antibody blocked a tumour-promoting receptor mechanism and reduced prostate cancer growth and metastasis in mice. Human testing has not yet been performed.

Two years after surgery for pancreatic cancer, a three-centimeter mass appeared in the wall of a 70-year-old woman’s stomach. It sat precisely where a biopsy needle had previously passed.…

CAR T cells were engineered to resist liver cancer’s stop signal A solid tumour can display a convenient target to immune cells while simultaneously telling them to stand down. That…

Pancreatic cancer has a molecular engine found in almost every tumor: RAS. For decades, the protein was considered exceptionally difficult to drug. Its surface offered few pockets where a…

Glioblastoma is difficult to treat not only because it grows rapidly. Most drugs penetrate the brain poorly because it is protected by the blood–brain barrier — a tightly sealed cellular…