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 utilizes integrated single-cell and spatial transcriptomics to map distinct, tumor-specific MMP expression patterns across colorectal cancer cell types, revealing that specific MMP-expressing fibroblast and cancer cell subpopulations are spatially organized to potentially drive tumor progression and metastasis.
This study reveals that histidine serves as a critical bidirectional substrate for the LAT1 transporter, sustaining mTORC1 signaling and tumor proliferation in glutamine-addicted breast cancers, thereby identifying histidine restriction as a potential therapeutic strategy to enhance LAT1 inhibition.
By integrating bulk and single-nucleus RNA sequencing of human fallopian tubes and high-grade serous ovarian cancer (HGSOC) tumors, this study identifies OVGP1/RNPC3 progenitors as the most plausible cellular precursors of HGSOC, revealing key transcriptional regulators and stromal factors that could inform earlier detection and prevention strategies.
This study demonstrates that while stabilizing oncogenic mutations increase target protein levels without altering the minimum steady-state achievable by PROTACs, transcriptional upregulation raises both baseline and post-treatment protein levels, revealing a synthesis-dependent ceiling on degrader efficacy.
Through a large-scale positive selection screen of natural product mixtures using mammalian cells, researchers identified a compound that inactivates oncogenic β-catenin by activating novel protein kinase Cs to relocate the protein to juxtamembrane vacuolar structures, demonstrating the potential of phenotypic screening to target previously undruggable cancer drivers.
This study identifies Bone Morphogenetic Protein 7 (BMP7) as a master regulator of gastric cancer-associated cachexia that drives muscle wasting and poor survival by upregulating GDF11 and GDF15, highlighting its potential as a therapeutic target.
By re-evaluating the relationship between dog breed size and at-risk cell numbers, this study proposes that canine carcinogenesis typically requires only a single driver mutation and is driven by increased somatic mutation rates in larger breeds, while also quantifying the distinct contributions of somatic divisions and inherited recessive mutations to cancer mortality.
By applying 13C metabolic flux analysis to slice cultures of pancreatic ductal adenocarcinoma tumors, this study reveals that metabolic salvage and acyl-chain remodeling within the tumor microenvironment are critical for glycosphingolipid synthesis, specifically highlighting the role of PIKfyve in ganglioside homeostasis.
This study reveals that KIF18A-dependent chromosomal instability (CIN) tumor cells rely on the kinesin motor to restrain excessive microtubule polymerization, thereby maintaining kinetochore-microtubule attachments and preventing mitotic failure.
This study evaluates the utility of Imaging Mass Cytometry (IMC) as a multiplexed, unbiased tool for characterizing single and clustered circulating tumor cells in preclinical mouse xenograft models to investigate metastasis and treatment resistance.