204 papers
Cancer biology explores the complex ways cells grow out of control, investigating the genetic mutations and environmental factors that drive tumor formation. This field seeks to understand how healthy cells transform into malignant ones and how these rogue cells spread throughout the body. By decoding these fundamental mechanisms, researchers aim to develop more effective treatments that target the disease at its source while sparing healthy tissue.
At Gist.Science, we process every new preprint published in this category directly from bioRxiv to ensure you stay ahead of the curve. Our team provides both accessible plain-language overviews and detailed technical summaries for each study, bridging the gap between raw research data and practical understanding. Whether you are a specialist or a curious reader, our goal is to make these critical findings clear and actionable.
Below are the latest papers in cancer biology, offering fresh insights into the ongoing fight against this disease.
This study identifies SRRM1 as a key splicing regulator that, often in concert with SRSF11, drives the expression of oncogenic protein isoforms—including those of NUMB and other signaling or cytoskeletal genes—to promote tumor growth, proliferation, and stemness in multiple cancer types, thereby highlighting its potential as a therapeutic target.
This study demonstrates that combining untargeted long-read transcriptome sequencing with in vivo functional validation in Drosophila reveals novel, oncogenic gene fusions in gliomas that are missed by standard targeted short-read fusion panels.
The paper introduces SubNetDL, a robust and interpretable deep learning framework that integrates subclonal mutation profiles with protein-protein interaction networks via network propagation to accurately predict cancer therapy responses and identify novel biomarkers across diverse cancer types and treatment modalities.
This study integrates a spatially resolved agent-based model with an interpretable machine learning surrogate to demonstrate that combination therapy targeting both HER2-positive and HER2-negative cell populations effectively overcomes phenotypic plasticity-driven resistance in heterogeneous breast cancer, offering a scalable framework for predicting and optimizing treatment strategies.
This study demonstrates that the protein phosphatase activity of PTEN, distinct from its lipid phosphatase function, is essential for normal embryonic development and tumor suppression in mice, as evidenced by the embryonic lethality and increased tumorigenesis observed in mice expressing a mutant PTEN lacking protein phosphatase activity.
This study identifies the POLQ-driven MMEJ Deletion Footprint (MDF) as a key genomic marker in homologous recombination-deficient pancreatic cancer that promotes immunogenicity by increasing neoantigens, remodeling myeloid cells to enhance antigen presentation, and fostering productive T-cell interactions, thereby linking specific DNA repair mechanisms to favorable clinical responses to immunotherapy.
This paper presents a piecewise-linear mathematical model of a three-transcription-factor gene regulatory network to demonstrate how strong intercellular signaling drives travelling waves of gene expression, ultimately determining the dominant cell-state characteristic in melanoma populations.
This study utilizes cell-surface capture mass spectrometry to profile the MPNST proteome, revealing that PRC2 loss drives the upregulation of specific surface proteins and identifying PTK7 as a promising therapeutic target for antibody-drug conjugates in treating these aggressive tumors.
This study systematically demonstrates that while ferroptosis induction via the GPX4 axis fails to impact established tumors in vivo, inhibiting cytosolic thioredoxin reductase or GCLC triggers potent tumor regression through a distinct, non-ferroptotic cell death mechanism, revealing that standard cell culture models significantly overestimate the therapeutic potential of ferroptosis.
This study establishes a mutation-resolved therapeutic atlas for NRAS-mutant melanoma using a saturation mutagenesis screen, revealing that tri-complex RAS(ON) inhibitors exhibit genotype-selective efficacy across most variants while identifying adaptive STAT3 signaling as a critical resistance mechanism that can be targeted to enhance therapeutic outcomes.