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Links from GEO DataSets

Items: 20

1.

Ablation of Cdh1 and Trp53 in the uterus reveals novel mechanisms controlling tumor microenvironment in endometrial cancer.

(Submitter supplied) Because TP53 mutation and CDH1 inactivation are the most common abnormalities found in human type II endometrial carcinomas, the contribution of dysfunctional TRP53 and CDH1 in the tumor microenvironment to induce type II endometrial cancer was characterized using mouse as a model. The results of our analysis revealed that conditional deletion of Cdh1 and Trp53 in the uterus regulated most of the genes categorized by their involvement in inflammatory responses, immune cell trafficking, cellular movement, cell-to-cell signaling and interaction and cellular growth and proliferation.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
12 Samples
Download data: TXT
Series
Accession:
GSE48131
ID:
200048131
2.

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

(Submitter supplied) 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.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE81441
ID:
200081441
3.

Puberty-specific promotion of mammary tumorigenesis by a high animal fat diet in P53 -/- mice

(Submitter supplied) Gene expression for genes differentially expressed between early vs. late tumor onset and high fat diet (HFD) vs. low fat diet (LFD) in P53 -/- mice.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL11202
41 Samples
Download data: TXT
Series
Accession:
GSE74294
ID:
200074294
4.

Wild Type Tumor Repressor Protein 53 (TRP53) Promotes Ovarian Cancer Cell survival

(Submitter supplied) Loss of Pten in the KrasG12D;Amhr2-Cre mutant mice leads to the transformation of ovarian surface epithelial (OSE) cells and rapid development of low-grade, invasive serous adenocarcinomas. Tumors occur with 100% penetrance and express elevated expression of wild type tumor repressor protein 53 (TRP53). To test the functions of TRP53 in the Pten;Kras (Trp53+) mice, we disrupted the Trp53 gene yielding Pten;Kras(Trp53-) mice. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
3 Samples
Download data: CEL
Series
Accession:
GSE34882
ID:
200034882
5.

Synergistic Tumor Suppressor Activity of E-cadherin and p53 in a Conditional Mouse Model for Diffuse-Type Gastric Cancer

(Submitter supplied) BACKGROUND & AIMS: Gastric cancer is the second most frequent cause of death from cancer in the world, diffuse-type gastric cancer (DGC) exhibiting a poor prognosis. Germline mutations of CDH1, encoding E-cadherin, have been reported in hereditary DGCs, and genetic and/or epigenetic alterations of CDH1 are frequently detected in sporadic DGCs. Genetic alterations of TP53 are also frequently found in DGCs. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL11202
3 Samples
Download data: TXT
Series
Accession:
GSE25302
ID:
200025302
6.

Tumor repressor protein 53 and steroid hormones provide a new paradigm for ovarian cancer metastases

(Submitter supplied) The functional status of the tumor repressor protein (TP53 or TRP53) is a defining feature of ovarian cancer. Mutant or null alleles of TP53 are expressed in greater than 90% of all high-grade serous adenocarcinomas. Wild type TP53 is elevated in low-grade serous adenocarcinomas in women and in our Pten/Kras/Amhr2-Cre mutant mouse model. Disruption of the Trp53 gene in this mouse model did not lead to high-grade ovarian cancer but did increase expression of estrogen receptor alpha (ERalpha; ESR1) and markedly enhanced the responsiveness of these cells to estrogen. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
2 Samples
Download data: CEL
Series
Accession:
GSE51095
ID:
200051095
7.

Mouse gastric adenocarcinoma

(Submitter supplied) We have created mice by performing gastric epithelium-specific knockout of common tumor suppressor genes.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
8 Samples
Download data: CEL, TXT
Series
Accession:
GSE45956
ID:
200045956
8.

Spontaneous SCC induced by the somatic inactivation of Rb1 and Trp53 tumor suppressors in mouse stratified epithelia

(Submitter supplied) The squamous cell carcinomas represent the aggressive type of non melanoma skin cancer, the most frequent malignancy among human population. We have studied here the possible relationship between these two pathways in skin using epidermal-specific mutant mice. Loss of p53, but not pRb, produces spontaneous tumor development, indicating that, contrary to pRb, p53 is the predominant tumor suppressor acting in mouse epidermis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL339
8 Samples
Download data: CEL
Series
Accession:
GSE9144
ID:
200009144
9.

Co-existing TP53 and ARID1A mutations promote aggressive endometrial tumorigenesis

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Other
Platforms:
GPL19057 GPL24247
10 Samples
Download data: BROADPEAK, TAB
Series
Accession:
GSE184499
ID:
200184499
10.

Co-existing TP53 and ARID1A mutations promote aggressive endometrial tumorigenesis [CUT&RUN]

(Submitter supplied) TP53 and ARID1A are frequently mutated across cancer but rarely in the same primary tumor. Endometrial cancer has the highest TP53-ARID1A mutual exclusivity rate. However, the functional relationship between TP53 and ARID1A mutations in the endometrium has not been elucidated. We used genetically engineered mice and in vivo genomic approaches to discern both unique and overlapping roles of TP53 and ARID1A in the endometrium. more...
Organism:
Mus musculus
Type:
Other
Platform:
GPL24247
4 Samples
Download data: BROADPEAK
Series
Accession:
GSE184498
ID:
200184498
11.

Co-existing TP53 and ARID1A mutations promote aggressive endometrial tumorigenesis [RNA-seq]

(Submitter supplied) TP53 and ARID1A are frequently mutated across cancer but rarely in the same primary tumor. Endometrial cancer has the highest TP53-ARID1A mutual exclusivity rate. However, the functional relationship between TP53 and ARID1A mutations in the endometrium has not been elucidated. We used genetically engineered mice and in vivo genomic approaches to discern both unique and overlapping roles of TP53 and ARID1A in the endometrium. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: CSV, TAB
Series
Accession:
GSE167275
ID:
200167275
12.

Apc, Kras, and Trp53 mutations

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17400
27 Samples
Download data: CEL
Series
Accession:
GSE125262
ID:
200125262
13.

Organoids derived from mouse normal colon and tumor samples with Apc, Kras, and Trp53 mutations in several combinations.

(Submitter supplied) For organoid preparation, we first treated the following 4 groups of 8-12 week old mice with tamoxifen: 1) CDX2P-CreERT2, Apc flox/+, Kras LSL-G12D/+, Trp53 flox/flox mice (n=2); 2) CDX2P-CreERT2, Apc flox/+, Kras LSL-G12D/+,Trp53 R270H/flox mice (n=3); 3) CDX2P-CreERT2, Apc flox/flox mice (n=3); 4) Wild-type control mice (n=4). The CDX2P-CreERT2 transgene expresses a tamoxifen (TAM)-regulated Cre protein (CreERT2) under control of human CDX2 regulatory sequences, allowing for TAM-inducible targeting of flox alleles in adult mouse terminal ileum, cecum, and colon epithelium. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17400
12 Samples
Download data: CEL, XLSX
Series
Accession:
GSE125261
ID:
200125261
14.

Mouse colon tumor samples with Apc, Kras, and Trp53 R270H or Tpr53 null mutations, and wild type controls.

(Submitter supplied) We treated the following 3 groups of 8-16 week old mice with tamoxifen: 1) CDX2P-CreERT2, Apc flox/+, Kras LSL-G12D/+, Trp53 flox/flox mice (n=6); 2) CDX2P-CreERT2, Apc flox/+, Kras LSL-G12D/+,Trp53 R270H/flox mice (n=6); 3) Wild-type control mice (n=3). The CDX2P-CreERT2 transgene expresses a tamoxifen (TAM)-regulated Cre protein (CreERT2) under control of human CDX2 regulatory sequences, allowing for TAM-inducible targeting of flox alleles in adult mouse terminal ileum, cecum, and colon epithelium. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL17400
15 Samples
Download data: CEL, XLSX
Series
Accession:
GSE125260
ID:
200125260
15.

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
49 Samples
Download data: TXT
Series
Accession:
GSE117552
ID:
200117552
16.

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [thyroid]

(Submitter supplied) This study assessed tumor suppressor roles of CREBBP in SCLC and other neuroendocrine tumors. Genetically engineered mouse models were used to determine the tumor suppressor role of Crebbp in SCLC and other neuroendocrine tumors. 
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
12 Samples
Download data: TXT
Series
Accession:
GSE117551
ID:
200117551
17.

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [preSC cell line]

(Submitter supplied) This study assessed tumor suppressor roles of CREBBP in SCLC and other neuroendocrine tumors. Genetically engineered mouse models were used to determine the tumor suppressor role of Crebbp in SCLC and other neuroendocrine tumors. 
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
6 Samples
Download data: TXT
Series
Accession:
GSE117550
ID:
200117550
18.

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [pituitary tumor]

(Submitter supplied) This study assessed tumor suppressor roles of CREBBP in SCLC and other neuroendocrine tumors. Genetically engineered mouse models were used to determine the tumor suppressor role of Crebbp in SCLC and other neuroendocrine tumors. 
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
17 Samples
Download data: TXT
Series
Accession:
GSE117549
ID:
200117549
19.

Crebbp loss drives small cell lung cancer and increases sensitivity to HDAC inhibition [SCLC]

(Submitter supplied) This study assessed tumor suppressor roles of CREBBP in SCLC and other neuroendocrine tumors. Genetically engineered mouse models were used to determine the tumor suppressor role of Crebbp in SCLC and other neuroendocrine tumors. 
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
14 Samples
Download data: TXT
Series
Accession:
GSE117547
ID:
200117547
20.

Loss of Fbxw7 triggers mammary tumorigenesis associated with E2F/c-Myc activation and Trp53 mutation

(Submitter supplied) Fbw7 is a tumor suppressor protein that regulates the degradation of a multitude of oncogenic substrates, such as c-Jun, c-Myc, Notch1 intracellular domain, and cyclin E. Loss of FBXW7 expression is relatively common in breast cancer. Despite this, the effect of FBXW7 loss on breast tumorigenesis has not been examined. We demonstrate here that loss of FBXW7 is sufficient for breast tumorigenesis. Many of Fbw7’s substrates are transcription factors or are closely linked to transcription factor pathways. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
13 Samples
Download data: TXT
Series
Accession:
GSE144690
ID:
200144690
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