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Colon cancer is the disease characterized by the development of malignant cells in the lining or epithelium of the first and longest portion of the large intestine.
Relentless accumulation of somatic mutations renders mismatch repair (MMR)-deficient cancers immunogenic. The evolutionary strategies that these hypermutator tumors use to drive immune evasion remain unknown. We identify repetitive homopolymer sequences in MMR genes as genetic ON/OFF switches, which vary mutation rate and bias during tumor evolution to fuel intratumor heterogeneity.
RAS mutations have been shown to be lost after first line treatment for metastatic colorectal cancer. Here, the authors leverage the GOZILA study to identify these patients and identify their association with other risk factor.
Upon inflammation and targeted gene mutation, some fully differentiated secretory and postmitotic intestinal epithelial lineages dedifferentiate to acquire stem-like features and promote tumor formation.
The molecular mechanisms underlying metabolic remodelling in colorectal cancer (CRC) are not completely elucidated. Here, they authors show that the oncogenic protein MYG1 promotes CRC progression not only through regulating mitochondrial activity, but also through activating a nuclear-associated pathway for glycolysis increase.
Relentless accumulation of somatic mutations renders mismatch repair (MMR)-deficient cancers immunogenic. The evolutionary strategies that these hypermutator tumors use to drive immune evasion remain unknown. We identify repetitive homopolymer sequences in MMR genes as genetic ON/OFF switches, which vary mutation rate and bias during tumor evolution to fuel intratumor heterogeneity.
In a recent study published in Nature, Goto et al. explore mechanisms of immune evasion in early colorectal cancers and adenomas and identify SOX17 to be crucial for immune escape through suppression of interferon-γ signalling.
Self-renewing cancer stem cells drive tumor initiation and progression and represent a major target for therapeutic development. A study now shows that vanoxerine, a dopamine transporter antagonist, precisely inhibits this cell population in colorectal cancer, which leads to attenuation of tumor initiation and increased infiltration by immune cells.