Trends in Cancer

There's still time to submit your abstract to @CellPressEvents #CSHallmarks2026 and join award-winning scientists, including @CharlesSwanton, @deVisserKarin, @michelle_monje and many more. Submit here: hubs.li/Q04nKZQ80

Discover how AI is transforming cancer research. Join Kun-Hsing Yu @kunhsingyu at #CSHallmarks2026 in Sitges, Spain, and hear his talk “From morphology to molecular insights: AI-enabled discovery in cancer pathology. Abstracts due this Friday! 🔗hubs.li/Q04mr0HY0

Cuproptosis-immunity crosstalk informs strategy to overcome immunotherapy resistance @CellCellPress cell.com/cell/fulltext/… @BoyiGan @MDAndersonNews

Excited to see the @CellPressNews #HallmarksOfCancer Symposium 2026 bring together such an exceptional group of scientists and clinicians in Sitges, Spain From tumor evolution and microenvironment to AI, spatial biology, and translational cancer science, this looks like a timely and important meeting for the field. #CancerResearch #Oncology cell-press-symposia.com/hallmarksofcan…

Online Now: High-plasticity oncofetal cell states in early pre-metastatic colorectal cancer dlvr.it/TT51Kg

Join @leeat_keren at the upcoming @CellPressEvents #CSHallmarks2026 and hear her talk “Phenotypic, microenvironmental, and genetic crosstalk shapes pancreatic cancer organization.” Abstract deadline: June 26, 2026

Dissecting the cellular architecture of breast cancer brain metastases reveals prognostically distinct immune landscapes dlvr.it/TSz5Qh

Excited to hear María Casanova Acebes @Casanova_Acebes present her talk "Decoding time: Circadian and longitudinal myeloid landscapes in lung cancer" @CellPressEvents #CSHallmarks2026 Submit an abstract for a chance to join her: hubs.li/Q04l2dn50

Don't miss @UCSanDiego Theodore Alexandrov's talk "High-throughput spatial single-cell metabolomics: decoding metabolism one cell at a time" @CellPressEvents #CSHallmarks2026 in Sitges, Spain, Nov 1–3, 2026. Submit an abstract before June 26: hubs.li/Q04k93tp0)

A holy grail for our lab has been tracking myeloid cells in human tumors in the same way that we track T and B cells with TCR/BCR. @vincentzliu and @CalebLareau solved it! We developed Mitotrek using scATAC-seq + mitochondrial DNA to do exactly this. Using Mitotrek, we find that new myeloid cells clones constantly infiltrate the tumor via circulating monocytes — and that their macrophage or dendritic cell fate is epigenetically programmed before tumor entry. @10xGenomics @parkerici @CancerResearch @TheMarkFdn cell.com/cancer-cell/fu…

Can ctDNA transform the management of biliary tract cancers? Our new @trendscancer forum paper outlines the promise, limitations, and path toward clinical implementation. Grateful to all collaborators who made this work possible. @PrecisionBTCnet @atuvibi cell.com/trends/cancer/…

Online Now: Endocytic evasion confers resistance to antibody-drug conjugates therapy in cancer dlvr.it/TSghCJ

Be part of the Hallmarks of cancer legacy. Join our distinguished keynote speakers Johanna Joyce @Joycelab & Faisal Mahmood @AI4Pathology in Sitges, Spain, November 1–3, 2026. Abstract deadline: June 26, 2026 🔗hubs.li/Q04h4PzV0 @CellPressEvents #CSHallmarks2026

Interested in #DNAmethylation predictors of #cancer response to #immune checkpoint inhibitors, #targetedtherapy, and #chemotherapy? 🔎 Our recent Trends in Cancer @TrendsCancer @CellPressNews article summarizes the field : Don’t miss Table 1 for a comprehensive list! sciencedirect.com/science/articl…

🚨 Out today in Cell! @CellCellPress Path2Space: #AI that predicts spatial transcriptomics (ST) from H&E pathology, enabling spatial biomarker discovery in #BreastCancer at scale. 📄 doi.org/10.1016/j.cell… 🧵1/8

🧬 #ScienceSaturday ❓ What if cancer treatment could target not only tumor cells, but also the tumor’s stromal support: non-malignant, non-cancerous cells within the tumor microenvironment, that actively help cancer grow, spread, and resist treatment? ➡️ In a new study published in @CellCellPress, researchers identified uPAR, a cell-surface protein linked to aggressive tumor behavior, as a marker found on both solid tumor cells and the fibrotic, immune-suppressive environment that helps sustain them. ➡️ The team developed uPAR-targeted CAR T cells that attacked both tumor cells and their supportive stroma, leading to durable tumor regression across multiple cancer models, including metastatic disease. ➡️ They also found that senescence-inducing therapies, like chemotherapy, increased uPAR expression and made tumors even more vulnerable to CAR T cell treatment. 🌟 This dual-targeting strategy could help overcome some of the biggest barriers to CAR T therapy in solid tumors, including immune suppression and treatment resistance. 🔗 Read the study: cell.com/cell/fulltext/… @ZedaZhang @Aveline_Filliol @LoweLabMSKCC

See what the organizers have to say about @CellPressEvents #CSHallmarks2026 and join them in Spain, Nov 1–3, 2026, to celebrate the convergence of basic and translational science, spark new connections, and shape the future of precision oncology. hubs.li/Q04fDr7q0

Daraxonrasib in Previously Treated Advanced RAS-Mutated #PancreaticCancer (Phase 1-2 study) nejm.org/doi/pdf/10.105… @RevMedicines @salmanpunekar

Conventional type-1 DC density is associated with checkpoint inhibitor response across multiple types of cancer @jclinicalinvest @DrIgMelero @ClinicaNavarra @CIMA_unav jci.org/articles/view/… 🇪🇸

New @Cancer_Cell paper on mechanisms of resistance to @RevMedicines Daraxonrasib Disrupted molecular glue complex drives RAS inhibitor resistance cell.com/cell/fulltext/… 18/40 genomic alterations in RAS pathway (👇🏽) Recurrent RAS Y64 alteration attenuates tri-complex formation