Trends in Cancer

Thrilled to share our new review article on #p53 and #plasticity in @trendscancer - p53: defender of lineage fidelity and foe of plasticity in cancer and regeneration @arati_rajeevan sciencedirect.com/science/articl…

Two cancer associated fibroblast (CAF) papers in #PancreaticCancer A: In @Cancer_Cell Reticular CAFs (rCAFs) facilitating tertiary lymphoid structures (TLS) cell.com/cancer-cell/fu… B: In @CD_AACR senescent CAFs (senCAFs) promoting lymph node metastases aacrjournals.org/cancerdiscover…

Abstracts are invited for @CellSymposia Hallmarks of cancer 📆 Nov 1–3, 2026 📍Sitges, Spain Submit by June 26 for the chance to share your insights with a global audience committed to translating science into life-saving therapies. 👉hubs.li/Q045lFmY0 #CSHallmarks2026

#ScienceSaturday ❓ Can your own brain and nervous system promote cancer growth? ➡️ A new study in Nature reveals a hidden “conversation” between lung tumors and the brain that shuts down the immune system. ➡️ Researchers discovered lung cancer can act like a puppet master, using a specific nerve pathway called the vagal sensory-sympathetic axis to protect itself. ➡️ Here’s how this “secret circuit” works: • The Signal: Lung tumors release growth factors that attract and activate “sensing” nerves called vagal sensory neurons. 
• The Brain Connection: These nerves send a distress signal from the tumor all the way to the brainstem. 
• The Command: The brain responds by sending a message back down through sympathetic nerves, releasing noradrenaline directly into the tumor. 
• The Sabotage: Noradrenaline flips a switch (the ADRB2 receptor) on immune cells called macrophages, turning them suppressive and blocking killer T cells from attacking. ➡️ Why does this matter? When researchers broke this circuit, by silencing the nerves or blocking the noradrenaline switch, the immune system “woke up,” and tumor growth slowed significantly. ➡️ This discovery is a game changer because it shows cancer isn’t just a local problem, it can hijack our own nervous system to survive. Targeting this tumor-brain circuit could open new doors for future therapies. 🌟 Shoutout to the research team led by Haohan K. Wei and Chuyue D. Yu for uncovering how our own nerves can be “tricked” by tumors! 👏🔬 
@Nature @YaleMed @PennMedicine 🔗 Read the full study: doi.org/10.1038/s41586…

⭐️Lung cancer in never smokers: from early detection to prevention- Nice review on this by @CharlesSwanton & colleagues @trendscancer @CellCellPress 👉Lung cancer in never smokers (LCINS) now accounts for a growing proportion of lung cancer cases, with distinct demographics and biology. 👉Identifying risk factors for LCINS remains challenging. The most well-established factors—germline variants, clonal hematopoiesis, and environmental exposures—currently lack validated screening tests @OncoAlert cell.com/trends/cancer/…

In a new @CellCellPress review, pioneer Douglas Hanahan @Ludwig_Cancer shows how the Hallmarks of cancer framework has evolved over the last 25 years: hubs.li/Q041kd5R0 We'll discuss this in depth @CellSymposia #CSHallmarks2026, Nov 1–3, Sitges. hubs.li/Q041k73p0

#ScienceSaturday ❓ Why does immunotherapy work incredibly well for some melanoma patients, but not for others? ➡️ A new study in Cancer Cell takes a closer look at the immune cells that matter most during immunotherapy. Researchers tracked melanoma-specific CD8+ T cells (the immune system’s cancer killers) in patients receiving anti-PD-1 treatment before surgery. ➡️ They found that not all T cells are created equal. Patients who responded best had a special group of T cells marked by a protein called T-bet. These cells weren’t “burned out,” but they weren’t fully fresh either, instead, they were in a powerful in-between state that allowed them to expand, stay active, and attack tumors when PD-1 therapy removed the brakes. ➡️ In contrast, patients who didn’t respond had more terminally exhausted T cells, immune cells that were too worn down to bounce back, even with immunotherapy. ➡️ The team also discovered that these fate decisions start early, in the lymph nodes, before T cells ever reach the tumor. And importantly, ongoing exposure to tumor antigens helped sustain effective immune responses, helping explain why neoadjuvant (pre-surgery) immunotherapy can be so effective. ➡️ Together, these findings show that which T cells are present, not just how many, can predict response to immunotherapy, and could guide better biomarkers and treatment strategies in the future. 🌟 Kudos to the researchers for uncovering how immune cell “identity” shapes success with cancer immunotherapy! @Cancer_Cell @lynn_schuchter @PennMedicine @AmaravadiRavi @PennCancer 🔗 Read more in Cancer Cell: doi.org/10.1016/j.ccel…

The preliminary program for Cell Symposia: Hallmarks of cancer is now live! Explore cutting-edge sessions spanning AI and technology, tumor immunology, system oncology, microbiome, & cancer neuroscience. hubs.ly/Q040R_Fl0 @CellSymposia #CSHallmarks2026 #Sitges Nov 1–3, 2026

New @CellCellPress The hallmarks of cancer, refined from the original concepts 25 years ago, as an outgrowth of our expanding knowledge base cell.com/cell/fulltext/…

Beautiful work from all 3 labs describing how the transcription factor BACH2 enforces stemness programs in a time- and dose-dependent manner. Congrats!

Tired - Iron; Wired - Copper Cuproptosis in cancer: from molecular mechanisms to therapeutic intervention sciencedirect.com/science/articl… New @trendscancer review from my @MDAndersonNews colleagues (@ACKoongMDPhD @BoyiGan @Dadi_Jiang)

Now online! Mapping cellular targets of covalent cancer drugs in the entire mammalian body dlvr.it/TPyfL6

Join our editor Dr. Danielle Loughlin at @KeystoneSymp's, Spotlight on the Cancer Cell: Intrinsic Properties and Vulnerabilities for Therapeutics. The poster abstract deadline is January 6, 2026! Register today: hubs.li/Q03Yc4Kg0 #KSCancerCell26

In the latest issue! Macrophage-targeted immunocytokine leverages myeloid, T, and NK cell synergy for cancer immunotherapy dlvr.it/TPqZ8H

How exercise decreases the risk of cancer and cancer- related mortality by reducing immunosenescence and inflammaging sciencedirect.com/science/articl…

Now online! HLA export by melanoma cells decoys cytotoxic T cells to promote immune evasion dlvr.it/TPs7v4

The Rudensky lab at @MSKCancerCenter examined the heterogeneity of tumoral Treg cells in colorectal cancer and identified two distinct tumoral #Treg subsets with differential Il10 expression. See the abstract in @CellPressNews: bit.ly/4q0bSC9

Viral mimicry in cancer therapy cell.com/trends/cancer/… How can we make the body's immune system sense tumors (and precancers) like it senses and targets pathogenic viruses? Lots of great science happening in this space of tumor selective transposable element (TE) re-expression.

MED1-driven ecDNA super-enhancers in cancer dlvr.it/TPnYJQ

Nature research paper: Somatic evolution following cancer treatment in normal tissue go.nature.com/4q3ps7h