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p53 wild-type colorectal cancer cells that express a fetal gene signature are associated with metastasis and poor prognosis
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p53 wild-type colorectal cancer cells that express a fetal gene signature are associated with metastasis and poor prognosis
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Journal Article
p53 wild-type colorectal cancer cells that express a fetal gene signature are associated with metastasis and poor prognosis
2022
Overview
Current therapy against colorectal cancer (CRC) is based on DNA-damaging agents that remain ineffective in a proportion of patients. Whether and how non-curative DNA damage-based treatment affects tumor cell behavior and patient outcome is primarily unstudied. Using CRC patient-derived organoids (PDO)s, we show that sublethal doses of chemotherapy (CT) does not select previously resistant tumor populations but induces a quiescent state specifically to
TP53
wildtype (WT) cancer cells, which is linked to the acquisition of a YAP1-dependent fetal phenotype. Cells displaying this phenotype exhibit high tumor-initiating and metastatic activity. Nuclear YAP1 and fetal traits are present in a proportion of tumors at diagnosis and predict poor prognosis in patients carrying
TP53
WT CRC tumors. We provide data indicating the higher efficacy of CT together with YAP1 inhibitors for eradication of therapy resistant
TP53
WT cancer cells. Together these results identify fetal conversion as a useful biomarker for patient prognosis and therapy prescription.
The failure of chemotherapy in colorectal cancer is currently unclear. Here, the authors show that upon sub-lethal dose of chemotherapy wild-type p53 colorectal cancers acquire a quiescence-like phenotype and a YAP-dependent fetal-like intestinal stem cell state associated with a higher metastatic activity and poor prognosis in patients.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/95
/ 49
/ 49/91
/ 64
/ 64/60
/ 692/4028
/ Cancer
/ Colorectal Neoplasms - drug therapy
/ Colorectal Neoplasms - genetics
/ Colorectal Neoplasms - pathology
/ Damage
/ DNA
/ Fetuses
/ Humanities and Social Sciences
/ Humans
/ Patients
/ Science
/ Tumor Suppressor Protein p53 - genetics
/ Tumor Suppressor Protein p53 - metabolism
/ Tumors
