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Record W3007141947 · doi:10.1093/jcag/gwz047.030

A31 ALTERED SMALL INTESTINAL EPITHELIAL HOMEOSTASIS AND CELL FATE DECISION UPON LOSS OF TRP53 IN KRT15+ INTESTINAL STEM CELLS

2020· article· en· W3007141947 on OpenAlexaff
Anand Prakash Dubey, Véronique Giroux

Bibliographic record

VenueJournal of the Canadian Association of Gastroenterology · 2020
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCancer Research and Treatments
Canadian institutionsUniversité de Sherbrooke
Fundersnot available
KeywordsLGR5Stem cellBiologyCancer stem cellStem cell markerAdult stem cellCryptCell biologyMultipotent Stem CellIntestinal epitheliumColorectal cancerCancer researchCellular differentiationImmunologyCancerEpitheliumEndocrinologyProgenitor cellGenetics

Abstract

fetched live from OpenAlex

Abstract Background Intestinal homeostasis is mainly maintained by two groups of stem cells: Lgr5+ stem cells and reserve stem cells. Recently, we reported that Krt15+ cells are present in small intestinal and colon epithelia, and harbor self-renewal, multipotent and regenerative capacities. Initiation of sporadic colorectal cancer has been described in Krt15+ stem cells, Lgr5+ stem cells and reserve stem cells following the loss of Apc. While these intestinal stem cell (ISC) populations can act as tumor-initiating cells in sporadic colon cancer, little is known about the cell-of-origin of colitis-associated colon cancer. TP53 alteration is reported as an early event in colitis-associated colon cancer cases. Therefore, we hypothesize that Trp53 loss specifically in Krt15+ stem cells will perturb the epithelial homeostasis and lead to tumor formation Aims Identify if Krt15+ cells may act as the cell-of-origin in colitis-associated colorectal cancer. Methods To induce Trp53 loss specifically in Krt15+ cells, we generated Krt15-CrePR1;Trp53fl/fl (Krt15△Trp53) mice, induced Cre recombination by injecting RU486 (PR agonist) and euthanized the mice after 12 months following recombination. Histological analysis was performed on small intestinal tissues. Results Results: Trp53 loss in Krt15+ cells severely perturbed small intestinal morphology. Increased crypt (proliferative compartment) length correlated with no proliferation changes surprisingly but higher number of Paneth cells and abnormal presence of goblet cells. Interestingly, we also observed the presence of cells expressing both Paneth and goblet cells markers suggesting a deregulation of secretory cell fate decision. Decreased expression of Hes1 and increased β-catenin nuclear expression in the small intestinal crypt of Krt15△Trp53 mice suggest altered Notch and Wnt signaling. Furthermore, villi (differentiated compartment) were significantly wider and shorter, and showed accumulation of activated fibroblasts. Finally, we observed inflammatory lesions as well as adenomas in the small intestine of Krt15△Trp53 mice which remain to be further characterized Conclusions Conclusion: In summary, Trp53 loss specifically in Krt15+ cells impaired cell fate decision, induced inflammation and initiated tumor formation. Overall, these results suggest that Krt15+ cells could act as the cell-of-origin of colitis-associated colon cancer. Funding Agencies Cancer Research Society, CRC Tier 2

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.006

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0020.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.013
GPT teacher head0.233
Teacher spread0.220 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

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Citations0
Published2020
Admission routes1
Has abstractyes

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