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Normal view

  • ✇Nature Cancer
  • A breakthrough in p53-targeted therapy Klas G. Wiman
    Nature Cancer, Published online: 01 October 2026; doi:10.1038/s43018-026-01254-8TP53 gene alterations are common cancer drivers and a focus of intense translational and clinical research. However, effective p53-targeted therapies remain elusive. This Clinical Outlook examines the evolving clinical landscape, highlighting recent advances and emerging strategies for improving outcomes in TP53-mutated malignancies.
     

A breakthrough in p53-targeted therapy

1 October 2026 at 08:00

Nature Cancer, Published online: 01 October 2026; doi:10.1038/s43018-026-01254-8

TP53 gene alterations are common cancer drivers and a focus of intense translational and clinical research. However, effective p53-targeted therapies remain elusive. This Clinical Outlook examines the evolving clinical landscape, highlighting recent advances and emerging strategies for improving outcomes in TP53-mutated malignancies.
  • ✇Nature Cancer
  • From task-specific tools to a universal foundation model for cytology
    Nature Cancer, Published online: 29 September 2026; doi:10.1038/s43018-026-01239-7Cytology is required for cancer screening and cancer diagnosis, yet most artificial intelligence systems assist cytology at individual tasks and specific specimen types. We developed CROWN, a universal foundation model for cytology that has the potential to support a broad spectrum of diagnostic applications across organs, diseases and clinical settings.
     

From task-specific tools to a universal foundation model for cytology

29 September 2026 at 08:00

Nature Cancer, Published online: 29 September 2026; doi:10.1038/s43018-026-01239-7

Cytology is required for cancer screening and cancer diagnosis, yet most artificial intelligence systems assist cytology at individual tasks and specific specimen types. We developed CROWN, a universal foundation model for cytology that has the potential to support a broad spectrum of diagnostic applications across organs, diseases and clinical settings.

Unraveling the lexicon of complex mutational phenomena in human cancers

Nature Cancer, Published online: 25 September 2026; doi:10.1038/s43018-026-01242-y

Alexandrov and colleagues summarize the current understanding of complex mutational phenomena in human cancers and their associations with therapy and clinical outcomes.

Stroke drives glioma progression through the emergence of tumor-associated astrocytes with reduced Ca<sup>2+</sup> activity

Nature Cancer, Published online: 25 September 2026; doi:10.1038/s43018-026-01238-8

Lee and colleagues report that ischemic stroke induces the generation of an astrocytic population that, through reduced calcium signaling, favors the recruitment of tumor-associated macrophages, thereby promoting glioma invasion in preclinical models.
  • ✇Nature Cancer
  • Next-generation cancer therapeutics
    Nature Cancer, Published online: 23 September 2026; doi:10.1038/s43018-026-01244-wCancer therapies have evolved substantially in recent decades; however, there remains a pressing need for new therapeutic options. Our Series on Next-Generation Cancer Therapeutics presents commissioned Reviews and opinion pieces on the latest therapeutic approaches and their implementation in the existing clinical landscape.
     

Next-generation cancer therapeutics

23 September 2026 at 08:00

Nature Cancer, Published online: 23 September 2026; doi:10.1038/s43018-026-01244-w

Cancer therapies have evolved substantially in recent decades; however, there remains a pressing need for new therapeutic options. Our Series on Next-Generation Cancer Therapeutics presents commissioned Reviews and opinion pieces on the latest therapeutic approaches and their implementation in the existing clinical landscape.
  • ✇Nature Cancer
  • Adipocyte methionine reduction promotes cancer cachexia Stefan Offermanns
    Nature Cancer, Published online: 22 September 2026; doi:10.1038/s43018-026-01202-6Cancer cachexia is a common wasting syndrome in individuals with cancer that involves activation of PKA in white adipose tissue, but the mechanisms that control PKA activity are unclear. A study now identifies iron-activated MSRA as a regulator of PKA in cancer cachexia, which reduces oxidized PKA and thereby increases PKA activity.
     

Adipocyte methionine reduction promotes cancer cachexia

22 September 2026 at 08:00

Nature Cancer, Published online: 22 September 2026; doi:10.1038/s43018-026-01202-6

Cancer cachexia is a common wasting syndrome in individuals with cancer that involves activation of PKA in white adipose tissue, but the mechanisms that control PKA activity are unclear. A study now identifies iron-activated MSRA as a regulator of PKA in cancer cachexia, which reduces oxidized PKA and thereby increases PKA activity.

An iron-regulated methionine redox axis governs adipose browning and cancer cachexia

Nature Cancer, Published online: 22 September 2026; doi:10.1038/s43018-026-01234-y

Chio and colleagues describe an iron-dependent pathway with a role in the induction of cancer cachexia-linked events such as adipose browning and identify methionine sulfoxide reductase A as an important and targetable factor in this process.

A universal visual foundation model for computational cytopathology

Nature Cancer, Published online: 18 September 2026; doi:10.1038/s43018-026-01240-0

Zheng, Zheng, Wang, Zhang et al. developed CROWN, a universal visual foundation model for cytopathology, which they benchmarked on more than 200 real-world cytology tasks across cohorts, including lymph node metastasis and cervical screening datasets.
  • ✇Nature Cancer
  • Targeting valine metabolism and ferroptosis to overcome chemoresistance in PDAC
    Nature Cancer, Published online: 14 September 2026; doi:10.1038/s43018-026-01235-xWe identified a metabolic signaling axis that enables pancreatic cancer cells to survive chemotherapy by suppressing ferroptosis. Targeting of the valine catabolism enzyme MMSDH reverses this chemoresistance and shows promise as a potential component of combination strategies against refractory tumors.
     

Targeting valine metabolism and ferroptosis to overcome chemoresistance in PDAC

14 September 2026 at 08:00

Nature Cancer, Published online: 14 September 2026; doi:10.1038/s43018-026-01235-x

We identified a metabolic signaling axis that enables pancreatic cancer cells to survive chemotherapy by suppressing ferroptosis. Targeting of the valine catabolism enzyme MMSDH reverses this chemoresistance and shows promise as a potential component of combination strategies against refractory tumors.

MMSDH facilitates ACSL4 propionylation to counteract ferroptosis upon hypoxia and impairs PDAC chemotherapy efficacy

Nature Cancer, Published online: 11 September 2026; doi:10.1038/s43018-026-01236-w

Zheng et al. describe how hypoxia-induced methylmalonate semialdehyde dehydrogenase lactylation promotes acyl-CoA synthetase long-chain family member 4 propionylation and degradation, thereby suppressing ferroptosis induced by chemotherapy, and develop a blocking peptide that increased chemotherapy efficacy in pancreatic ductal adenocarcinoma.

Commensal <i>Nakaseomyces glabratus</i> migrates into prostate tumors to accelerate cancer progression

Nature Cancer, Published online: 09 September 2026; doi:10.1038/s43018-026-01229-9

Lai et al. show that Nakaseomyces glabratus is enriched in fecal and tumor samples of patients with castration-resistant prostate cancer and that administration of the fungus accelerates cancer progression in prostate cancer-bearing castrated mice.
  • ✇Nature Cancer
  • <span>l</span>-Glutamine’s potential to enhance chemotherapy efficacy in advanced pancreatic cancer
    Nature Cancer, Published online: 01 September 2026; doi:10.1038/s43018-026-01231-1The addition of oral l-glutamine to first-line gemcitabine plus nab-paclitaxel appears safe and is associated with improved survival outcomes and tumor responses compared with historical benchmarks in untreated advanced pancreatic cancer. The beneficial effects of l-glutamine may be mediated through modulation of intermediary metabolism, gut microbial function, inflammatory responses and gut barrier integrity.
     

<span>l</span>-Glutamine’s potential to enhance chemotherapy efficacy in advanced pancreatic cancer

1 September 2026 at 08:00

Nature Cancer, Published online: 01 September 2026; doi:10.1038/s43018-026-01231-1

The addition of oral l-glutamine to first-line gemcitabine plus nab-paclitaxel appears safe and is associated with improved survival outcomes and tumor responses compared with historical benchmarks in untreated advanced pancreatic cancer. The beneficial effects of l-glutamine may be mediated through modulation of intermediary metabolism, gut microbial function, inflammatory responses and gut barrier integrity.

SlideChat is a multimodal generative artificial intelligence assistant for whole-slide computational pathology across cancer types

Nature Cancer, Published online: 01 September 2026; doi:10.1038/s43018-026-01220-4

Chen et al. have developed SlideChat, a multimodal generative artificial intelligence assistant, which they benchmark on 27 pathology tasks across 33 cancer types. Expert pathologists rated the assistant as clinically relevant and accurate.

<span>l</span>-Glutamine in combination with first-line gemcitabine and nab-paclitaxel in advanced pancreatic ductal adenocarcinoma: an open-label, single-arm, phase 1 GlutaPanc trial

Nature Cancer, Published online: 31 August 2026; doi:10.1038/s43018-026-01225-z

In this open-label, single-arm, phase 1 GlutaPanc trial, Gong and colleagues report the safety and feasibility of l-glutamine in participants with advanced pancreatic ductal adenocarcinoma and determine the recommended phase 2 dose of l-glutamine in combination with gemcitabine and nab-paclitaxel.

Author Correction: Low-protein diet enhances antitumor immunity in pancreatic cancer through microbiota-derived UDP-galactose

Nature Cancer, Published online: 25 August 2026; doi:10.1038/s43018-026-01241-z

Author Correction: Low-protein diet enhances antitumor immunity in pancreatic cancer through microbiota-derived UDP-galactose

Galanin impairs tumor immunity in glioblastoma by promoting infiltration and ferroptosis resistance of myeloid-derived suppressor cells

Nature Cancer, Published online: 25 August 2026; doi:10.1038/s43018-026-01221-3

Chen and colleagues report that the neuropeptide galanin impairs antitumor immunity in glioblastoma by interacting with its receptor GALR3 on monocytic myeloid-derived suppressor cells, promoting their infiltration and ferroptosis resistance.
  • ✇Nature Cancer
  • Coming full circle Paul S. Mischel
    Nature Cancer, Published online: 21 August 2026; doi:10.1038/s43018-026-01219-xPaul Mischel obtained his MD from Cornell University Medical College, trained in anatomic and neuropathology at UCLA and did post-doctoral research training in Louis Reichardt’s lab at HHMI/UCSF. He is the Fortinet Founders Professor, vice chair for research for the department of pathology, and deputy director of translational science and an institute scholar at Sarafan ChEM-H, Stanford University. Mischel leads Team
     

Coming full circle

21 August 2026 at 08:00

Nature Cancer, Published online: 21 August 2026; doi:10.1038/s43018-026-01219-x

Paul Mischel obtained his MD from Cornell University Medical College, trained in anatomic and neuropathology at UCLA and did post-doctoral research training in Louis Reichardt’s lab at HHMI/UCSF. He is the Fortinet Founders Professor, vice chair for research for the department of pathology, and deputy director of translational science and an institute scholar at Sarafan ChEM-H, Stanford University. Mischel leads Team eDyNAmiC of the Cancer Grand Challenges Program. He is a member of the National Academy of Medicine, a fellow of the AACR Academy, and past president of the American Society for Clinical Investigation.

Copper depletion boosts CNS leukemia therapy by inhibiting nucleotide synthesis through impairment of mitochondrial complex IV activity

Nature Cancer, Published online: 25 May 2026; doi:10.1038/s43018-026-01177-4

Wong et al. uncover a nutritional dependency for acute lymphoblastic leukemia cells that spread to the central nervous system and propose using copper restriction to impair leukemia progression by disrupting nucleotide synthesis through the inhibition of electron transport chain activity.
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