256 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 introduces the KaryoTME framework to demonstrate that specific aneuploidies, particularly chromosome 1q gain, drive immune evasion and serve as independent, robust predictors of poor response to immunotherapy in melanoma patients.
This study demonstrates that oncogenic KRAS drives NF-kB-mediated CCL20 expression in pancreatic ductal adenocarcinoma, creating a pharmacologically reversible mechanism of immune evasion that can be targeted by blocking CCL20-CCR6 signaling to enhance immune cell recruitment.
This study utilizes a novel antibody to demonstrate that Sialyl-Tn (sTn) is frequently upregulated in prostate cancer, correlates with poor patient survival, and is present in metastatic and xenograft models, thereby establishing it as a promising prognostic biomarker and therapeutic target for advanced disease.
This study reveals that Menin acts as a context-dependent regulator of enhancer-promoter architecture, where its inhibition causes broad transcriptional dysregulation and disrupts enhancer connectivity specifically in MLL-rearranged leukemia but not in NPM1-mutant leukemia, thereby identifying enhancer-promoter interactions as a selective therapeutic vulnerability in the former.
This study reveals that despite widespread chromosomal copy number reductions in various cancers, a small subset of genes (less than 10%)—including the pro-tumorigenic transcription factor TGIF1 and mitotic regulators—exhibits paradoxically increased expression driven by key transcriptional programs, suggesting these genes as promising therapeutic targets.
This study reveals that branched actin-driven membrane protrusions (BAMPs) function not merely as downstream outputs but as active positive feedback regulators of oncogenic KRAS signaling, where they enhance KRAS-TIAM1 interactions to inactivate the merlin tumor suppressor and drive proliferation independently of the MAPK pathway.
By applying the MeRLin single-cell lineage tracing platform to a spontaneous melanoma model, this study reveals that metastatic progression is driven by the selective expansion of pre-existing polyclonal subpopulations that maintain distinct neural crest-like and lipid metabolism transcriptional programs across organs, with specific spatial localization at invasive fronts.
This study identifies EZH1 upregulation as a resistance mechanism to PI3K inhibition in acute myeloid leukemia leukemic stem cells and demonstrates that combining a PI3K inhibitor with an EZH1/2 dual inhibitor overcomes this resistance to effectively target the disease in preclinical models.
This study utilizes single-cell and multi-omics analyses to reveal that while BRCA1 and BRCA2 somatic mutations in lung adenocarcinoma drive distinct transcriptional programs and immune microenvironment alterations—such as differential T cell activation and tissue-resident memory T cell expansion—they collectively predict improved responses to immune checkpoint blockade despite being associated with genomic instability and poor prognosis.
This study reveals that antibodies against a specific enterovirus epitope (CE1) protect against hepatocellular carcinoma by cross-reacting with the tumor-associated protein ASPH via molecular mimicry, thereby triggering NK cell-mediated tumor destruction.