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Oncology

Tumor biology and anticancer therapy: from mechanism papers to pivotal readouts and launches.

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401–420 of 665
Sep 15Tue
  1. 顶刊论文(社媒热度)69

    Magnetically actuated nanoantennas for wireless glioblastoma therapy.

    Wireless bioelectric therapy HITMAN uses magnetically actuated nanoantennas to convert low-frequency (≤200 kHz) magnetic fields into localized electric fields that kill glioblastoma cells through protein unfolding, membrane disruption and ER stress. In drug-resistant patient-derived GBM cells it cut viability by 52.2% versus 10% with temozolomide, while sparing neurons and astrocycytes. In orthotopic mouse models it inhibited tumor growth, extended median survival by more than 50%, and showed no systemic toxicity.

    Why it matters: Wireless electric-field therapy outperformed temozolomide in drug-resistant GBM with no systemic toxicity in mice.

  2. BioCentury59

    AZ’s camizestrant miss narrows oral SERD treatment settings

    AstraZeneca's camizestrant missed its primary endpoint of progression-free survival in the Phase III SERENA-4 trial in first-line HER2-negative, estrogen receptor-positive breast cancer, where it was combined with the CDK4/6 inhibitor palbociclib. This is the second Phase III setback this year for oral SERDs in an early-line breast cancer setting, and both results suggest proving efficacy may require focusing on patients with ESR1 mutations.

    Why it matters: A second Phase III oral SERD failure narrows where the class can compete and points to ESR1-mutant selection.

  3. Cell65

    Copper ion-induced MYH9 polymerization executes cuproptosis.

    MYH9 (myosin heavy-chain 9) acts as an executioner of cuproptosis: copper binding induces MYH9 polymerization, which disrupts the actin cytoskeleton and causes cuproptotic cell death. The compound HThPA triggers this process by binding the nuclear receptor Nur77, depleting the copper chelate glutathione and releasing free copper from intracellular stores. Physiological copper levels were higher in drug-resistant tumor cells and clinical samples, increasing their susceptibility to HThPA-induced cuproptosis, suggesting a treatment strategy for drug-resistant tumors.

    Why it matters: It names a protein executing cuproptosis and links elevated copper in drug-resistant tumors to a candidate treatment strategy.

  4. 顶刊论文(社媒热度)57

    Estimating the carcinogenesis timelines in early-onset versus late-onset cancers and changes across birth cohorts.

    A tumor kinetic model combined with long-term cancer registry data estimates when mutational transitions occur in breast, colorectal, and thyroid cancers. Malignant transitions occur about 10 years earlier in early-onset versus late-onset breast and colorectal cancers, in the late 30s versus late 40s to 50s, while thyroid cancer transitions occur in the late 20s regardless of onset age. More recent birth cohorts, from 1950-1954 to 1980-1984, show accelerated progression and earlier malignancy.

    Why it matters: It dates the hidden mutational steps of early-onset cancers, informing when prevention and detection should act.

Sep 14Mon
  1. Nature63

    A serpin-myeloid axis in pancreatic cancer heterogeneity and immune evasion.

    SERPINE1 (PAI1) and SERPINB2 (PAI2) act as dominant organizers of immune evasion in pancreatic ductal carcinoma, building fibrin-rich extracellular matrix niches that programme macrophages toward immunosuppressive states and exclude cytotoxic T cells. Perturb-map spatial genomics in mice traced this remodelling to early gene-driven changes that precede spatial clonal dominance. Loss of either serpin, or pharmacological inhibition of PAI1 or CD18, improved tumour control and synergized with anti-PD-1, while patient tumour analysis showed immunosuppressive niches around rare SERPIN-expressing subpopulations dominated by SPP1+/MARCO+ macrophages.

    Why it matters: It links spatial clonal heterogeneity to local immune suppression and names a targetable serpin axis that sensitizes PDAC to anti-PD-1.

  2. WeChat71

    TAISHAN-302 Trial Sets New Benchmark for Second-Line Treatment of Relapsed Small Cell Lung Cancer

    The TAISHAN-302 study, led by Professor Zhang Li's team, was presented at the WCLC plenary session and published in the New England Journal of Medicine. It tested a drug named only in Chinese in the source material as second-line therapy for relapsed small cell lung cancer, a setting where nearly all patients relapse after first-line platinum-based chemotherapy with immunotherapy and effective options are scarce. The report names no efficacy figures.

    Why it matters: A WCLC plenary and New England Journal of Medicine publication on second-line therapy for relapsed small cell lung cancer, a major unmet need.

  3. Fierce Biotech35

    Cellectis cans allogeneic CAR-Ts to hop aboard in vivo bandwagon

    French biotech Cellectis has discontinued its allogeneic CAR-T pipeline and pivoted to in vivo CAR-T therapies. The company began the year claiming the allogeneic CAR-T field would see "huge momentum," but ultimately made a strategic shift in the face of the overwhelming advantage of in vivo therapies.

    Why it matters: Cellectis dropped its allogeneic CAR-T programs and pivoted to in vivo CAR-T development.

  4. WeChat71

    Ivonescimab Beats Pembrolizumab on Overall Survival in First-Line PD-L1-Positive Advanced NSCLC

    Ivonescimab significantly extended overall survival versus pembrolizumab as first-line treatment for PD-L1-positive advanced NSCLC, meeting the prespecified statistical bar for significance. At a median follow-up of 36 months as of August 20, 2026, 234 overall survival events had occurred and median overall survival reached 30.8 months. Prespecified subgroup analyses showed a consistent survival benefit, most pronounced in patients with high PD-L1 expression.

    Why it matters: Head-to-head overall survival win over pembrolizumab in first-line PD-L1-positive advanced NSCLC changes the standard-of-care discussion.

  5. Fierce Biotech50

    Roche, MediLink notch phase 3 lung cancer win but trail GSK on cross-trial survival

    A phase 3 trial of the Roche-partnered, B7-H3-directed antibody-drug conjugate from MediLink hit its primary endpoint in small-cell lung cancer. The median overall survival benefit, however, fell short of the cross-trial bar set by GSK's rival B7-H3 asset, positioning MediLink and Roche behind GSK in this setting.

    Why it matters: First phase 3 readout positioning a Roche-partnered B7-H3 ADC against GSK's rival in small-cell lung cancer.

  6. WeChat74

    Trastuzumab Deruxtecan Extends Median PFS to 14.3 Months as First-Line Therapy in HER2-Mutant Advanced NSCLC

    In the phase III DESTINY-Lung04 trial, first-line trastuzumab deruxtecan (Enhertu) gave a median progression-free survival of 14.3 months in patients with HER2-mutant advanced non-small cell lung cancer, versus 8.3 months with pembrolizumab plus chemotherapy. It is the first HER2-targeted therapy to show superiority over standard treatment in this setting.

    Why it matters: First HER2-targeted therapy to beat standard first-line care in HER2-mutant advanced NSCLC in phase III.

  7. WeChat61

    AstraZeneca Oral SERD Camizestrant Misses PFS Primary Endpoint in Phase 3 SERENA-4 First-Line Breast Cancer Trial

    Camizestrant plus the CDK4/6 inhibitor palbociclib missed the primary endpoint of progression-free survival compared with anastrozole plus palbociclib in the phase 3 SERENA-4 trial, AstraZeneca announced on September 11. The randomized, double-blind study enrolled 1371 patients with ER-positive, HER2-negative advanced breast cancer receiving no prior systemic therapy for advanced disease, including 194 in mainland China, across 263 sites. The result weakens the case for the oral SERD as a first-line endocrine partner to palbociclib.

    Why it matters: Phase 3 miss for camizestrant in first-line ER-positive, HER2-negative advanced breast cancer.

  8. WeChat68

    Enhertu Extends PFS in DESTINY-Lung04 but Early Overall Survival Signals 15% Higher Death Risk

    Enhertu posted strong progression-free survival in the DESTINY-Lung04 trial presented at WCLC 2026: median PFS of 14.3 months, 6 months longer than control, with a 37% reduction in risk of disease progression or death and an ORR of 70% versus 44.5%. Preliminary overall survival did not favor the drug: 115 deaths (50.7%) on Enhertu versus 98 (43.2%) on control, median OS 29.3 versus 33.1 months, a 15% higher risk of death.

    Why it matters: A widely used ADC shows a clear PFS gain in lung cancer while preliminary OS runs against it.

  9. WeChat74

    Ivonescimab Beats Pembrolizumab on Overall Survival in PD-L1-Positive NSCLC in HARMONi-2

    Ivonescimab monotherapy as first-line treatment for PD-L1-positive non-small cell lung cancer achieved a median overall survival of more than 30 months, extending survival by over 8 months compared with pembrolizumab. The phase 3 HARMONi-2 trial, led by Professor Zhou Caicun of Shanghai East Hospital and presented at the 2026 World Conference on Lung Cancer, is the first randomized double-blind phase 3 trial to show positive results for both overall survival and progression-free survival against pembrolizumab.

    Why it matters: First randomized phase 3 trial to beat pembrolizumab on both OS and PFS in first-line PD-L1-positive NSCLC.

  10. WeChat69

    Parallel Phase III Trials Show B7-H3 ADCs Cut Death Risk in Relapsed Small Cell Lung Cancer

    Two Phase III trials of B7-H3 antibody-drug conjugates in second-line relapsed small cell lung cancer, TAISHAN-302 and ARTEMIS-008, both hit their primary overall survival endpoint against topotecan, and TAISHAN-302 was published simultaneously in the New England Journal of Medicine. Reported back to back at WCLC 2026, the trials yielded identical OS hazard ratios of 0.46 (95% CI 0.35-0.62), providing independent, replicable Phase III evidence that B7-H3 ADCs beat current standard treatment in this setting.

    Why it matters: Two independent Phase III trials produced the same OS hazard ratio of 0.46 for B7-H3 ADCs in relapsed SCLC.

  11. medRxiv45

    Matched marrow and blood profiling reveals compartment- and feature-specific liquid-biopsy signals in multiple myeloma

    Peripheral-blood cfDNA matched or exceeded marrow-plasma cfDNA as a liquid biopsy for multiple myeloma, despite the tumor's marrow confinement. In 74 patients profiled across 372 cfDNA time points, blood cfDNA recovered marrow-defined CNAs and mutations at 77.4% vs 72.0% and 69.2% vs 65.4%, and at high tumor fraction adverse-lesion sensitivity reached 100% in both compartments. Marrow cfDNA did show distinct, handling-sensitive fragmentomic architecture (LOOCV AUC=0.910), so compartment, biomarker class, tumor fraction and processing all shape liquid-biopsy performance.

    Why it matters: It shows a simpler blood draw is not inferior to marrow-derived cfDNA for myeloma genomic profiling, with practical processing caveats.

  12. medRxiv51

    Glycovariants of CA-125 in the early detection of ovarian cancer

    The Sialyl-Thomsen-nouveau (STn) glycovariant of CA-125 predicted ovarian cancer years before clinical diagnosis, whereas conventional CA-125, HE4 and MGL-detected glycovariants did not. In a case-control study of 82 incident ovarian cancer cases matched 1:3 to controls from the Malmö Diet and Cancer cohort, CA-125-STn had an AUC of 0.68 for cases within 5 years of blood draw, and 49% of those cases fell in the top 20% of CA-125-STn levels. The finding suggests a marker that may detect ovarian cancer earlier than conventional CA-125 screening, which two randomized trials showed does not reduce mortality.

    Why it matters: It identifies a CA-125 glycovariant that may detect ovarian cancer years before conventional markers fail.

  13. Cell55

    Copper ion-induced MYH9 polymerization executes cuproptosis

    Copper binding drives polymerization of MYH9, causing cytoskeletal collapse and executing cuproptosis. HThPA depletes glutathione to release intracellular copper, exploiting this pathway as a therapeutic vulnerability in drug-resistant tumors. The work identifies MYH9 polymerization as the mechanistic link between copper accumulation and cuproptotic cell death.

    Why it matters: Defines the molecular executor of cuproptosis and a way to trigger it in drug-resistant tumors.

  14. medRxiv40

    Dosimetric Impact of Residual Intrafraction Motion in Gated MR-Guided Prostate SBRT With Focal Dose Intensification

    Residual intrafraction motion during gated MR-guided prostate SBRT with simultaneous integrated boost caused directionally asymmetric coverage loss, hitting the boosted GTV hardest: per-fraction median GTV deviations were −1.2% for D95 and −5.6% for V45Gy across 150 fractions in 30 patients. Motion-inclusive dose reconstruction yielded asymmetric internal target volume margins (2/2/1/2/1/2 mm for GTV) that achieved sufficient coverage in about 94% of fractions per direction, at the cost of an average 6.9 ± 4.7% reduction in gating duty cycle.

    Why it matters: Provides concrete population-based margins that trade a small loss of delivery efficiency for robust GTV coverage in gated MR-guided prostate SBRT.

  15. medRxiv42

    Germline Variants Absent from Global Reference Databases in Malawian DLBCL Patients: Implications for Variant Interpretation in African Genomic Medicine

    Whole-exome sequencing of 55 Malawian patients with diffuse large B-cell lymphoma identified 332 germline variants (0.26% of 127,456 PASS-filtered variants) absent from gnomAD, ExAC, and 1000 Genomes, distributed across 289 genes. Database-absent variants were enriched for predicted loss-of-function consequences (16.9% vs 7.8%; OR 2.41) and a substantial share occurred in HLA class I loci. The results show that global reference databases miss variants present in this population, creating uncertainty in clinical variant interpretation for African patients.

    Why it matters: Quantifies how many Malawian DLBCL germline variants are missing from gnomAD, ExAC, and 1000 Genomes, with loss-of-function and HLA enrichment.

  16. 顶刊论文(社媒热度)48

    Widespread atypical UV-induced mutations form in single-stranded DNA.

    UV light induces an extended array of noncanonical mutations in single-stranded DNA, including AT>AM, GT>GV, AC>AA, AT>TT, and TA>TT substitutions that resist photo-reversion and likely originate from atypical photoproducts. The work coupled temperature-induced telomeric end resection in yeast with serial UV irradiation and whole-genome sequencing. These ssDNA-specific lesions offer an additional damage-mediated route to oncogenic melanoma mutations such as BRAF V600E, which involves a GT>GA substitution.

    Why it matters: It explains how UV light can generate melanoma-driver mutations that canonical SBS7-type lesions do not account for.

CBACBA Frontier Insights (CFI)Chinese Biopharmaceutical Association (CBA)www.cba-usa.org