MétaCan
Menu
Back to cohort
Record W1519693764

Oncogenic pathways in breast cancer downstream of Pten

2006· article· en· W1519693764 on OpenAlexaff
Rajwinder Lehal, Ming‐Sound Tsao, Tak W. Mak, Eldad Zacksenhaus

Bibliographic record

VenueCancer Research · 2006
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicPI3K/AKT/mTOR signaling in cancer
Canadian institutionsUniversity of TorontoOntario Institute for Cancer Research
Fundersnot available
KeywordsPTENCancer researchCancerBiologyBreast cancerPopulationPI3K/AKT/mTOR pathwayMedicineSignal transductionCell biologyGenetics
DOInot available

Abstract

fetched live from OpenAlex

3987 The tumor suppressor protein Pten is commonly inactivated in human malignancies, including breast cancer. Pten has lipid phosphatase activity that antagonizes the function of PI3K and affects the PKB pathway. Comparative studies on breast cancer mouse models, MMTV-Wnt1 and MMTV-neu tumors show induction of both cyclinD1 and D2 in MMTV-Wnt1 tumors, but not in MMTV-neu tumors (Yu et al., Nature, 2001). Accordingly, MMTV-Wnt1, but not MMTV-neu tumor development is independent of cyclinD1. Li et. al. (2003) has shown that MMTV-Wnt1 tumors consists of both myo- and luminal- epithelial cells. These tumors also exhibit an expansion of Sca-1 and keratin 6 positive cell population suggesting stem cell origins of these tumors. On the other hand, MMTV-neu tumors do not possess these properties. To elucidate the oncogenic pathways downstream of Pten in breast cancer and the role of D-type cyclins in cancer progression, We are analyzing mouse mammary tumors in conditionally knock-out Wap-Cre:Ptenf/f mice. Preliminary data suggest that both cyclinD1 and D2 are induced in some of the Pten mutant tumors. To further elucidate the importance of cyclinD1 in tumor initiation and progression downstream of Pten, Wap-Cre:Ptenf/f mice were crossed with CyclinD1 -/- mice to generate Wap-Cre:Ptenf/f:CyclinD1 -/- mice; incidence of tumor is monitored. Histological analyses revealed that mutations in Pten give rise to at least two types of tumors: adenocarcinoma and adenosarcoma. Immunostaining of these tumors show the presence of both myo- and luminal epithelial cells and keratin6 positive cells in a fraction of these tumors. FACS analyses of Pten tumors also suggest an expansion of Sca-1 positive cells compared to mammary gland from virgin or pregnant mice. These observations suggest that aberrant signaling of Pten may induce at least two distinct oncogenic pathways, one of which like MMTV-Wnt1 tumors, may target the stem cell population and the other pathway, like MMTV-neu tumors, may targets more committed progenitor cells. To further analyze oncogenic pathways downstream of Pten, we have generated tumorspheres from Pten mutant tumors. These tumourspheres can be propagated in ultra-low attachment plates in DMEM/F12 media supplemented with EGF, FGF and B-27. These tumorspheres express both luminal and myo-epithelial cell markers when plated on collagen-coated slides. Understanding Pten-dependent tumor initiation may open new avenues for therapeutic interventions for breast cancer treatment.

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 score0.003
Threshold uncertainty score0.012

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0010.001
Science and technology studies0.0000.000
Scholarly communication0.0010.000
Open science0.0000.001
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0030.001

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 head0.040
GPT teacher head0.364
Teacher spread0.325 · 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".

Quick stats

Citations0
Published2006
Admission routes1
Has abstractyes

Explore more

Same venueCancer ResearchSame topicPI3K/AKT/mTOR signaling in cancerFrench-language works237,207