Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Probing tumorigenic potentials of the genetic interactions reconstituted in murine fallopian tube organoids

ABSTRACT: Despite histological diversity in the subcutaneous nodules and tumors, the derived tumor-derived organoids stereotypically exhibited cystic featuresTo clarify molecular differences among the p53-null falopian tube-derived tumors driven by KrasG12D, Pik3caH1047R, and Apc580D, the transcriptome across tumor-derived organoidss, originating organoids before inoculation, p53-null organoids without driver mutations, and organoids without recombination as a reference were compared.

ORGANISM(S): Mus musculus

PROVIDER: GSE175511 | GEO | 2021/06/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Probing tumorigenic potentials of the genetic interactions reconstituted in murine fallopian tube organoids

Project description:Probing tumorigenic potentials of the genetic interactions reconstituted in murine fallopian tube organoids

| PRJNA732676 | ENA

An organoid-based transplantation model reveals genetic interactions potentiating niche-independent gastric carcinogenesis

Project description:Despite distinct genetic aberrations introduced and diverse tumor histology, the derived tumor-derived organoids stereotypically exhibited cystic features. To clarify distinct genotype-dependent properties of p53-null tumor-derived organoids, seven tumor-derived organoids and organoids with pLKO.1 and shLuc were compared.

2022-12-31 | GSE192604 | GEO

Mutant p53 R270H induces invasion and metastasis of mouse intestinal tumor organoids through gain-of-function mechanism

Project description:Apc(D716) mutant mice develop benign intestinal adenoma, while Apc(D716) and p53 R270H compound mutant mice develop invasive adenocarcinoma in the intestine. We examined expression profile of tumor-derived organoids using Apc(D716), Apc(D716) p53 Null, Apc(D716) p53 R270H mutant mice by RNA sequencing, and identified mutant p53-induced gene set.

2017-02-01 | GSE81441 | GEO

CDK12 Loss Promotes Prostate Cancer Development While Exposing Vulnerabilities to Paralog-Based Synthetic Lethality [RNA-Seq]

Project description:Biallelic loss of cyclin-dependent kinase 12 (CDK12) defines a unique molecular subtype of metastatic castration resistant prostate cancer (mCRPC). It remains unclear, however, whether CDK12 loss per se is sufficient to drive prostate cancer development—either alone, or in the context of other genetic alterations—and whether CDK12-mutant tumors exhibit sensitivity to specific pharmacotherapies. Here, we demonstrate that tissue-specific Cdk12 ablation is sufficient to induce preneoplastic lesions in the mouse prostate. Allograft-based CRISPR screening demonstrated that Cdk12 loss is positively associated with p53 inactivation, but negatively associated with Pten inactivation—similar to what is seen in human mCRPC. Consistent with this, ablation of Cdk12 in prostate organoids with concurrent p53 loss promotes their proliferation and ability to form tumors in mice, while Cdk12 knockout in the Pten-null prostate cancer mouse model abrogates tumor growth. Bigenic CDK12 and p53 loss allografts represent a new syngeneic model for the study of prostate cancer. Cdk12-null organoids (either with or without p53 co-ablation) and patient-derived xenografts from tumors with CDK12 inactivation are highly sensitive to inhibition or degradation of its paralog kinase, CDK13. Together, these data identify CDK12 as a bona fide tumor suppressor gene with impact on tumor progression and paralog-based synthetic lethality is a promising strategy for treating CDK12 mutant mCRPC.

2024-04-17 | GSE254388 | GEO

CDK12 Loss Promotes Prostate Cancer Development While Exposing Vulnerabilities to Paralog-Based Synthetic Lethality [scRNA-Seq]

2024-04-17 | GSE254387 | GEO

Probing the luminal microenvironment of reconstituted epithelial microtissues.

Project description: Not available

| S-EPMC5020616 | biostudies-literature

Mutant p53 cancers reprogram macrophages to tumor supporting macrophages via exosomal miR-1246

Project description:exosomes isolated from: HT29+control shRNA; HT29+p53 shRNA; HCT116 WT p53; HCT116 mutant p53; HCT116 null p53; media used as negative control

2018-02-09 | MSV000082047 | MassIVE

High-dose oncogenic PIK3CA drives constitutive cellular stemness through increased NODAL/TGFb signaling

Project description:Oncogenic PIK3CA mutations activate phosphoinositide 3-kinase (PI3K) and are among the commonest somatic mutations in cancer and mosaic, developmental overgrowth disorders. We recently demonstrated that the ‘hotspot’ variant PIK3CAH1047R exerts striking allele dose-dependent effects on stemness in human induced pluripotent stem cells (iPSCs), and moreover demonstrated multiple oncogenic PIK3CA copies in a substantial subset of human cancers. To identify the molecular mechanism underpinning PIK3CAH1047R allele dose-dependent stemness, we profiled isogenic wild-type, PIK3CAWT/H1047R and PIK3CAH1047R/H1047R iPSCs by high-depth transcriptomics, proteomics and reverse-phase protein arrays (RPPA). PIK3CAH1047R/H1047R iPSCs exhibited altered expression of 5644 genes and 248 proteins, whereas heterozygous hPSCs showed 492 and 54 differentially-expressed genes and proteins, respectively, confirming a nearly deterministic phenotypic effect of homozygosity for PIK3CAH1047R. Pathway and network-based analyses predicted a strong association between self-sustained TGFb/NODAL signaling and the ‘locked’ stemness phenotype induced by homozygosity for PIK3CAH1047R. This stemness gene signature was maintained without exogenous NODAL in PIK3CAH1047R/H1047R iPSCs and was reversed by pharmacological inhibition of TGFb/NODAL signaling but not by PIK3CA-specific inhibition. Analysis of PIK3CA-associated human breast cancers revealed increased expression of the stemness markers NODAL and POU5F1 as a function of disease stage and PIK3CAH1047R allele dosage. Together with emerging realization of the link between NODAL re-expression and aggressive cancer behavior, our data suggest that TGFb/NODAL inhibitors warrant testing in advanced breast tumors with multiple oncogenic PIK3CA copies.

2021-03-03 | PXD014719 | Pride

Probing multiphoton light-induced molecular potentials.

Project description: Not available

| S-EPMC7244592 | biostudies-literature

RNAseq expression of p53-null and p53-null/PLK2-null mammary tumors

Project description:RNAseq expression of p53-null and p53-null/PLK2-null mammary tumors

| PRJNA731110 | ENA