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Oct 15Thu
  1. biorxiv.org49

    Pervasive expression of early embryonic programs in cancer has stage-dependent survival impact

    Early embryonic gene expression programs are widespread in human tumours, and transcriptional similarity to distinct preimplantation stages independently predicts overall survival beyond age, sex, mutational status and molecular subtype. Similarity to zygote and 2-cell embryo stages predicted improved survival, driven in kidney cancer by stromal and immune cells, while trophectoderm-associated programs in tumour cells predicted worse survival in breast cancer and melanoma and were linked to MYBL2 and FOXM1 dependencies.

  2. biorxiv.org42

    Tobacco Carcinogen Induces Persistent DNA Damage and Homologous Recombination Dysregulation in Pancreatic Ductal Carcinogenesis

    The tobacco carcinogen NNK produces a biphasic DNA damage response in human pancreatic ductal epithelial cells: 5 days of exposure induced double-strand breaks with ATM-γH2AX activation and RAD51/BRCA2 recruitment, while 50 days caused persistent damage signaling, upregulation of HR genes (RAD51, BRCA1, BRCA2, FANCD2, PLK1), altered RAD51 localization, and chromosomal instability. In human PDAC tissue microarrays and TCGA-PAAD data, increased γH2AX correlated with tumor progression and poor overall survival, and elevated RAD51 with adverse outcomes, positioning γH2AX as a candidate prognostic biomarker in tobacco-associated PDAC.

  3. biorxiv.org61

    A microbiota-driven neuroepithelial feed-forward circuit drives gastroesophageal junction tumorigenesis

    Bile acid remodeling enriches the oral commensal Prevotella melaninogenica at the gastroesophageal junction, where bacterial succinate activates vagal sensory neurons and SUCNR1-expressing tuft cells. Tuft cells release 15-d-PGJ2 to sensitize sensory neurons, while neuronal CGRP drives expansion and tuft-cell differentiation of neuro-responsive epithelial progenitors through RAMP1, forming a self-reinforcing microbiota-neuron-epithelium circuit that promotes dysplastic progression. Genetic or pharmacological disruption of the circuit, including with the approved CGRP antagonist rimegepant, suppresses tumor development.

  4. doi.org51

    Structural and Mechanistic Insights Into GSDME Pore Formation and Functional Regulation

    Cryo-EM structures of gasdermin E pores, with oligomeric stoichiometries ranging from 23 to 29 protomers, expose how pore assembly works. Mutagenesis, liposome leakage assays and cancer-associated mutation analysis identified residues governing membrane binding, shallow membrane insertion and oligomerization via three interfaces, while molecular dynamics simulations showed anionic TMCL2 recruited by basic residues to aid membrane penetration. The work supports a stepwise, time-dependent mechanism of GSDME pore assembly.

  5. doi.org41

    Dynamic changes of claudin 18.2 expression after systemic therapy in gastric and esophagogastric junction cancer

    Claudin 18.2 (CLDN18.2) expression in advanced gastric/esophagogastric junction adenocarcinoma changes frequently during systemic therapy. In paired samples from 155 patients, positivity rose from 54 (34.84%) before treatment to 61 (39.35%) after (p < .001); overall, 131 patients (84.52%) showed altered expression. Conversion rates did not differ between chemotherapy alone and chemotherapy plus immunotherapy, supporting CLDN18.2 reassessment before targeted therapy.

  6. Nat Biotechnol69

    Engineering bispecific exosome activators of T cells to target immune checkpoint inhibitor-resistant metastatic melanoma.

    An inhalable exosome system called BEAT co-displays PD-1 and FZD8 in a uniform 1:1 ratio to block PD-L1 and Wnt7b, overexpressed in immune checkpoint inhibitor-resistant melanoma. BEAT recruited and activated CD8+ T cells, reprogramming the tumor microenvironment and producing robust antitumor activity in mouse models of lung metastases, outperforming a linked dual antibody against PD-L1 and Wnt7b in vivo.

  7. medrxiv.org40

    Choroid plexus asymmetry on routine MRI as an imaging signature of breast cancer brain metastasis

    Choroid plexus asymmetry on routine contrast-enhanced brain MRI is associated with breast cancer brain metastasis. In 1,000 women with breast cancer, 190 with brain metastasis, a deep-learning-derived Choroid Plexus Asymmetry Index was elevated in metastasis cases (median 0.088 vs 0.059; adjusted OR 1.58 per +1 SD, 95% CI 1.32-1.88), independent of peripheral inflammation markers, histological grade, tumour laterality and metastasis side. Total choroid plexus volume did not differ between groups, pointing to asymmetry rather than size as the relevant signature.

  8. biorxiv.org49

    AMPK Signalling Rewires WWP1 mediated RUNX1 Ubiquitination in CML Progression

    The E3 ubiquitin ligase WWP1 binds the PPxY motif of RUNX1 and catalyzes K63-linked polyubiquitination that stabilizes the protein and drives chronic myeloid leukemia cell growth. AMPK phosphorylates WWP1 at Thr692, sending it to lysosomal degradation, and also phosphorylates RUNX1 to curb its leukemogenic activity. Metformin activated this AMPK-WWP1-RUNX1 axis in leukemia cell lines, primary CML patient-derived cells, and xenograft tumors, pointing to WWP1 as a therapeutic vulnerability.

  9. biorxiv.org40

    A Multi-Kinase Inhibitor Screen Identifies mTOR Signaling as a Vulnerability in Advanced Prostate Cancer.

    Loss of the receptor tyrosine kinase AXL is linked to treatment resistance, aggressive phenotypes, and shorter overall survival in prostate cancer. Screening isogenic CRISPR-generated AXL-knockout cells against 1,814 kinase inhibitors identified Torin-2, which showed an ~18-fold lower IC50 in AXL-knockout than AXL-wildtype cells. PRISM/DepMap analysis confirmed a selective vulnerability to PI3K/AKT/mTOR pathway inhibition, pointing to mTOR inhibition as a therapeutic strategy for AXL-deficient prostate cancer.

  10. biorxiv.org42

    Spatial Tumour Tissue Distribution Dynamics of a Bicycle Peptide-MMAE Toxin Conjugate Profiled by Targeted Mass Spectrometry

    Laser capture microdissection coupled to targeted LC-PRM mass spectrometry maps the spatial distribution of MMAE released from the NECTIN-4-binding Bicycle Drug Conjugate zelenectide pevedotin (BT8009) at sub-tissue resolution in mice. The method showed progressive accumulation and sustained retention of MMAE in tumour tissues over 24 h, while levels in plasma, liver and muscle declined after early exposure, and revealed heterogeneous MMAE distribution between tumour cell-rich and stroma-rich regions with distinct temporal patterns.

  11. nature.com64

    Divergent genomic evolution in astrocytomas and oligodendrogliomas

    Astrocytomas and oligodendrogliomas develop treatment resistance through different genomic routes, longitudinal analyses of patient tumours show. Astrocytomas accumulate copy-number alterations and markers of chromosomal instability, whereas oligodendrogliomas acquire new driver mutations. The finding separates the two tumour types by evolutionary mechanism rather than by histology alone.

Oct 14Wed
  1. Mol Cell65

    A feedback mechanism of m6A via PARP1-mediated ADP ribosylation of METTL3/METTL14.

    The m6A reader IGF2BPs recruits PARP1 to m6A-modified RNAs and stimulates its activity, leading to ADP ribosylation of the m6A writer METTL3/METTL14, which impairs its RNA-binding capability and reduces m6A deposition in human cell lines. This "read-orchestrate-write" negative feedback loop expands the regulatory paradigm of m6A methylation beyond the writer/eraser/reader system. Combining PARP inhibitor therapy with inhibition of IGF2BP2 or METTL3 produced synergistic anti-tumor effects.

  2. Mol Cell68

    Transposable element splicing reveals a tumor-enriched class of gene-independent transcripts.

    A pan-cancer analysis defines TEtrans, a splice-resolved class of transposable element-derived transcripts that are tumor-enriched and gene-independent. An endogenous retrovirus-derived TEtrans promotes colorectal cancer growth by enhancing topoisomerase I-mediated DNA relaxation, and a subset encodes shared tumor antigens that elicit cytotoxic T cell responses, with a murine TEtrans-like transcript mediating antigen-dependent tumor control in vivo. The work adds spliced TE transcripts to the roster of oncogenic drivers and actionable tumor antigens.

  3. biorxiv.org52

    Co-targeting KRAS and BCL-2 induces pyroptosis and antitumor tertiary lymphoid structures

    Co-targeting KRAS and BCL-2 synergistically triggers GSDME-mediated pyroptosis in KRAS G12D-mutant lung tumors, which are metabolically vulnerable through weakened HK1 interaction and reduced spare respiratory capacity compared with G12C. The combination induces functional tertiary lymphoid structures in vivo, and depletion experiments show the antitumor efficacy depends on B cells. It also drives membrane attack complex deposition in situ and elicits memory antitumor responses.

  4. biorxiv.org52

    Microglia-derived Small Extracellular Vesicles Promote Bone Marrow Monocyte Expansion and Recruitment in Glioblastoma.

    Tumor-associated microglia in glioblastoma release small extracellular vesicles that traffic to the bone marrow, where they selectively target monocytes and their progenitors. Internalization of these vesicles activates MAPK signaling and inflammatory transcriptional programs, driving differentiation and expansion of inflammatory monocytes that are then recruited into the tumor microenvironment. The work identifies a communication route between the glioblastoma TME and the peripheral immune system that helps establish the immunosuppressive TME driving GBM progression.

  5. biorxiv.org52

    Trp53 heterozygosity defines novel states impacting tumor plasticity and progression in Kras-initiated non-small cell lung cancer

    Trp53 single-allele loss expands transcriptional plasticity and increases genomic instability relative to complete Trp53 loss in KrasG12D-driven murine lung tumors, while K and KP+/- mice live longer than KP mice, matching clinical survival patterns. Murine KP+/- signatures and copy-number profiles appear in human NSCLC datasets, and two signatures correlate with better and worse patient survival, respectively. TP53 heterozygosity therefore defines a distinct genomic landscape that should inform therapeutic strategy in KRAS-mutant lung cancer.

  6. biorxiv.org48

    Oncogenic ETS factors expressed from fusion genes utilize EWSR1 to associate with the paraspeckle and regulate transcription.

    Oncogenic ETS fusion proteins ERG and EWSR1::FLI1 associate with the paraspeckle scaffold long non-coding RNA NEAT1_2, linking them to this EWSR1-containing nuclear organelle. Disrupting paraspeckles in prostate cancer and Ewing sarcoma cell lines disrupted oncogenic phenotypes and, in Ewing sarcoma cells, produced transcriptional profiles similar to loss of EWSR1::FLI1. The work identifies the paraspeckle as a transcriptional regulator and potential drug target in ETS fusion cancers.

  7. biorxiv.org45

    A multimodal precision oncology platform integrating genomics,single-cell transcriptomics, and functional drug screening expandstherapeutic options in pediatric brain tumors

    A tiered precision oncology framework combining deep whole-genome sequencing, single-cell RNA sequencing, and ex vivo functional drug screening was applied to 17 children with malignant CNS tumors. Functional screening gave every patient at least one high-confidence targeted-therapy or chemotherapy nomination, single-cell RNA sequencing found an average of 37 druggable gene targets per patient, and high-confidence targeted-therapy recommendations rose fourfold. Functional classifications matched outcomes in 8 of 10 evaluable cases.

  8. biorxiv.org50

    Biomarker-driven and gene-enhanced viral therapy for malignant peripheral nerve sheath tumor

    Loss of the PRC2 histone mark H3K27me3, common in high-grade MPNST, sensitizes tumors to the oncolytic HSV G47Δ, but also triggers a compensatory integrated stress response that blunts viral protein translation. Engineers built G47Δ² with tumor-regulated ICP34.5 expression (BIRC5-driven), limiting daily xenograft tumor-volume growth to 0.6% (95% CI -2.9–4.2%) versus 8.3% for G47Δ² and 22.5% for controls, though murine gastrointestinal toxicity reduced event-free survival.

  9. biorxiv.org40

    Predicting resistance to synthetic lethal therapies in cancer

    Resistance to synthetic lethal cancer therapies can be predicted from molecular network features. A random forest model combining protein-protein interaction, co-expression and essentiality data, trained on CRISPR-Cas9 resistance screens across ten SL biomarker-target pairs, achieved a mean AUROC of 0.72 under leave-one-SL-pair-out validation (range 0.57-0.91) and independently predicted resistance to the MTAP-PRMT5 and ATM-ATR therapies now in trials. The work gives a computational way to anticipate resistance mechanisms before they emerge.

  10. Nat Med69

    A health-system-scale, episode-resolved multimodal atlas of cancer cachexia.

    Longitudinal clinicogenomic data from 52,236 patients with cancer profiled by MSK-IMPACT (2010-2024) show that cachectic weight loss episodes cluster near disease progression, worsen outcomes across nearly all cancer types, and carry a consistent serologic signature of lower albumin and hemoglobin with higher liver enzymes. Tumor genotypes including TP53 mutation were linked to more frequent episode onset. A model predicting impending cachectic weight loss in lung, colorectal and prostate cancer was validated in an external Dana-Farber cohort of 5,785 patients.

    Why it matters: It shows routine clinicogenomic data can identify cachexia drivers and predict weight loss risk at health-system scale.

  11. nature.com50

    Personalized neoantigen-targeting cancer vaccines in ovarian cancer: a phase 1 trial

    Personalized neoantigen vaccines combined with PD-1 blockade were feasible in patients with high-grade serous ovarian cancer in a phase 1 trial. Many patients mounted tumor-specific immune responses. Cell-free DNA analysis identified putative resistance mechanisms related to antigen presentation. The trial establishes feasibility of this approach in ovarian cancer and points to antigen presentation as a resistance pathway.

  12. medrxiv.org41

    MRI Biomarkers for Brain Metastases in Lung Cancer Using Machine Learning

    MRI-derived radiomic features improved prognostic stratification beyond clinical variables in 103 patients with brain metastases from lung cancer. The combined clinical-imaging DeepSurv model reached a concordance index of 0.728 for overall survival, and risk groups separated median overall survival at 26.7 versus 9.1 months. Imaging-only high-risk patients were less likely to have tumor-infiltrating lymphocytes and PD-L1 expression of at least 50%, linking the biomarkers to the tumor immune microenvironment.

  13. Sci Adv59

    Citron kinase activity controls alternative splicing events that drive prostate cancer growth.

    Citron (CIT) kinase drives prostate cancer growth by phosphorylating the RNA splicing regulator THRAP3, controlling its binding to pre-messenger RNA targets and producing transcripts that stimulate growth of prostate cancer cell lines, xenografts, patient-derived organoids, and PDX-derived organoids. An antisense oligonucleotide blocking THRAP3 recruitment to a CIT-dependent RNA binding site prevented production of these transcripts and inhibited growth of cell lines and PDX-derived organoids across prostate cancer stages and lineages, but not of benign cells. The work identifies CIT-mediated alternative splicing as a therapeutic strategy in treatment-resistant prostate cancer.

    Why it matters: It offers an indirect way to hit CIT kinase, for which no selective inhibitors exist, via a splicing antisense oligonucleotide.

  14. biorxiv.org57

    An RFX-driven ciliogenic cell state defines ex vivo FGFR-inhibitor sensitivity in colorectal cancer

    An RFX-driven ciliogenic cell state marked by upregulation of cilia-related genes predicts selective sensitivity to the FGFR inhibitor erdafitinib in colorectal cancer. Image-based ex vivo drug profiling with matched transcriptomics of 127 patient biopsies linked the signature to poor progression-free survival (hazard ratio 2.28; adjusted p=0.0098), even in early-stage disease, and knockdown of RFX2 and RFX3 attenuated erdafitinib sensitivity. The work offers a patient-stratified route to FGFR inhibition beyond current CRC treatment paradigms.

  15. biorxiv.org47

    Tumour-derived factors prime microglia for immune checkpoint-mediated T-cell regulation

    Soluble tumour-derived factors, not direct tumour contact, drive early microglial activation: quantitative proteomics showed extensive remodelling of the microglial proteome after exposure to tumour-conditioned media, with coordinated upregulation of MHC-I, PD-L1 and Galectin-9. Flow cytometry in murine and human cell models confirmed increased PD-L1 and MHC-I, and these microglia induced PD-1 and TIM-3 on cocultured T-cells. Single-cell RNA sequencing datasets from brain tumour patients recapitulate the same immune-regulatory program.

  16. biorxiv.org58

    Catabolism of extracellular glutathione is a driver of metastasis formation

    Cancer cells forming liver metastases can catabolize extracellular glutathione via gamma-glutamyl-transferase to obtain cysteine, sustaining proliferation and preventing ferroptosis when cystine is absent from the liver microenvironment. The mechanism was independent of system Xc- but required glutamate-cysteine ligase activity. GGT1 expression correlated with poor survival and was upregulated in liver metastases of human breast cancer patients, and Ggt1 overexpression in murine breast cancer cells enhanced liver colonization and lung metastases after orthotopic implantation.

    Why it matters: It identifies extracellular glutathione catabolism via GGT as a mechanism driving metastatic colonization of cystine-poor organs.

  17. biorxiv.org46

    THERAPY RESISTANCE IN MELANOMA DRIVES CILIOGENESIS AND GLUTAMINE/ASPARTATE METABOLISM DEPENDENCY

    Drug resistance in BRAF melanoma enhances primary ciliogenesis, and this cilia formation is required for cells to respond and survive combination therapy. Using in vitro and in vivo models of target therapy resistance, the authors identified a translational program supporting ciliogenesis in resistant melanoma. Knocking out IFT88 to impair cilia formation rewired glutamine and aspartate metabolism, defining a metabolic mechanism underlying therapy resistance.

  18. biorxiv.org53

    FLASH X-rays preserve neutrophil chromatin to boost antitumor immunity

    FLASH X-rays at 8 Gy, unlike an equal conventional dose-rate dose, triggered a robust abscopal antitumor effect with anti-PD-1 in a bilateral subcutaneous tumor model in mice. The ultrashort dose delivery conserved neutrophil chromatin compaction, inhibiting neutrophil extracellular trap formation and reversing NET-mediated CD8+ T-cell exclusion, while conventional or split-dose FLASH caused chromatin hyper-relaxation and NETosis. Radiation-induced chromatin relaxation in neutrophils emerges as a determinant of radioimmunotherapy outcome.

  19. biorxiv.org45

    Cyclic Hypoxia drives Wnt5a-ROR1 stroma-tumor crosstalk promoting breast cancer growth

    Cyclic hypoxia, unlike stable hypoxia, reprograms the triple-negative breast cancer microenvironment in a cell type specific way: it reverses chronic hypoxia-induced cell cycle arrest and a stabilized WNT5A+/COL6+ mesenchymal subpopulation, activates fibroblasts, and suppresses MSC proliferation. Single cell RNA and ATAC sequencing of a multicellular TNBC co-culture traced the effect to paracrine WNT5A/B-ROR1 signaling between fibroblasts and cancer cells. Blocking this crosstalk in a mouse CAF-TNBC co-xenograft model reduced tumor growth in vivo.

  20. biorxiv.org50

    PIEZO1 marks a low neuroendocrine state and supports cisplatin tolerance in small cell lung cancer

    PIEZO1 marks a low neuroendocrine cell state and supports cisplatin tolerance in small cell lung cancer. Its upregulation accompanied loss of NE markers in chemoresistant H69AR cells, with reduced cisplatin sensitivity in H446DDP cells, and patient multiomics, single-cell and spatial data linked PIEZO1 to low NE activity. PIEZO1 depletion lowered cisplatin IC50 and raised drug-induced apoptosis, while Yoda1 increased calcium signals and cisplatin tolerance, supporting an actomyosin-YAP-linked mechanism.

  21. biorxiv.org63

    Glyceraldehyde-3-phosphate sensing by SOS1 and RAS sustains a self-reinforcing oncogenic metabolic-signaling circuit

    The glycolytic intermediate glyceraldehyde-3-phosphate (GA3P) directly binds SOS1 and RAS, enhancing their interaction and sustaining hyperactivated RAS signaling in RAS-mutant cancer cells. GA3P accumulates through MAZ-dependent transcriptional upregulation of GLUT6, an atypical class III glucose transporter. Suppressing MAZ or GLUT6 selectively inhibits RAS-mutant cancer cells in vitro and in vivo, and GLUT6 expression is elevated in clinical RAS-mutant human malignancies.

    Why it matters: Identifies GA3P-SOS1-RAS as a metabolic activation loop and MAZ-GLUT6 as a synthetic-lethal target in RAS-mutant cancers.

  22. biorxiv.org51

    CCR2 is a potential biomarker and therapeutic target in Group 3 medulloblastoma

    High CCR2 expression correlates with dissemination and reduced survival in Group 3 medulloblastoma, across 1094 primary tumor samples, and CCR2 protein rises in recurrent/metastatic tumors versus paired primaries. Overexpression of CCR2 in ONS76 and UW228 cells drove proliferation and migration, and CCR2-driven mouse xenografts showed aggressive disease and decreased survival. The CCR2 antagonist Cenicriviroc suppressed CCR2-mediated signaling and showed therapeutic efficacy against established tumors in vivo.

  23. biorxiv.org41

    Spatial transcriptomics reveals interferon pathway enrichment in early relapsing serous carcinoma

    Spatial transcriptomics of matched treatment-naive adnexal and omental tumors from nine high-grade serous carcinoma patients found that short platinum-free interval tumors show an interferon-driven inflammatory phenotype at both sites. C3, IFI27 and BST2 were consistently associated with short PFI across sites and validated by RNA in-situ hybridization; in two public ovarian cancer cohorts, high C3 expression was significantly associated with shorter platinum-free survival. The work nominates C3 as a candidate prognostic biomarker and potential therapeutic target.

  24. medrxiv.org52

    Beyond ERBB2 amplification: RNA and proteomic HER2 assessment for pan-tumor treatment stratification

    RNA-based and proteomic HER2 screening identified HER2-enriched tumors beyond ERBB2 amplification in a pan-tumor cohort of 1,331 biopsies, with validation in 3,898 external biopsies. All six objective responses among 51 treated patients occurred in tumors positive by ERBB2 mRNA and the combined RNA-signature. ERBB2 mRNA positivity was linked to longer time on treatment (hazard ratio 0.42) and overall survival (0.41), supporting prospective evaluation for treatment selection.

  25. biorxiv.org43

    p53 activity links chromosomal instability to pro-migratory extracellular vesicles

    Acute chromosomal instability in p53-proficient NIH/3T3 cells splits cells into two p21-RFP populations with distinct fates: p21-RFPLOW cells re-enter the cell cycle after short arrest, while p21-RFPHIGH cells show persistent arrest with a senescence-like state. Late-stage p21-RFPHIGH-derived extracellular vesicles are enriched for ECM-, adhesion-, and cytoskeleton-associated proteins and confer increased migration on recipient cells, linking p53 activity to pro-migratory paracrine signaling.

Oct 13Tue
  1. Mol Cell60

    PHYHD1-mediated translational control regulates renal cell carcinoma progression.

    PHYHD1 acts as a tumor suppressor in renal cell carcinoma by restraining protein translation. Progressive PHYHD1 loss predicts poor prognosis, while restoring it suppresses tumor growth in RCC cell and patient-derived xenograft models independently of its dioxygenase activity. Mechanistically, PHYHD1 binds eEF1A1, alters its ribosome association, and limits translation of ceramide transporter CERT1, whose targeting impairs proliferation of PHYHD1-deficient cells.

    Why it matters: It defines a translational control axis and names CERT1 as a candidate therapeutic target in PHYHD1-deficient RCC.

  2. biorxiv.org51

    Spatial context of cellular heterogeneity in triple-negative breast cancer reveals actionable subtypes

    Bulk and spatial transcriptomics with cellular mapping of breast tissue from a large patient cohort identified three reproducible TNBC ecosystem subtypes with distinct spatial tumor-microenvironment architectures and treatment-response phenotypes: an immune-exhausted subtype associated with immune checkpoint therapy, a fibrotic/hypoxic subtype, and a metabolically reprogrammed subtype driven by nuclear-receptor and fatty-acid signaling. Multiplexed imaging independently confirmed the immune-infiltrated versus stromal-excluded architectures, and subtype-specific markers offer a basis for subtyping and candidate therapeutic vulnerabilities.

  3. biorxiv.org44

    Pan-cancer remodeling of reactive oxygen species homeostasis: distinct roles of the ROS-generation and antioxidant arms in immune context and outcome

    Pan-cancer analysis of a 107-gene ROS program shows both ROS-generation and antioxidant arms are coordinately up-regulated in tumors, but carry distinct meanings. The composite balance score tracked reduced immune infiltration, driven by low generation-arm activity in immune-cold tumors, while adverse outcome was attributable to the antioxidant arm and generation was null. In cohort-held-out validation, redox programs outperformed generic programs in separating tumors from adjacent normal tissue across cancer types.

  4. nature.com66

    Characterizing the onset and progression of cancer cachexia using routine clinical data

    In 52,236 patients with cancer, cachectic weight loss episodes coincided with disease progression, were linked to lower survival rates, and shared a consistent serological signature across routine laboratory markers. TP53 mutations and other specific tumor genotypes were positively associated with cachexia risk, and statistical models were trained to predict impending cachexia risk.

    Why it matters: Links routine clinical data to cachexia onset and progression at scale, with a predictive model clinicians could use.

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