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Mammary gland tumor immunoinfiltrate analysis

ABSTRACT: The project in which this experiment is included demostrate that the developtment and growth of breast tumors are under immunosurveillance. We perform as screaning of multiple nutritional interventions to observe the impact of each of them in the tumor incidence, tumor growth and overall survival of the animasls. We concluded that safe nutritional measures including nicotinamide (NAM) supplementation efficiently mediates immunotherapeutic effects against established transplantable BC. In particular, the aim of this experiment was to analyse the effect that NAM has in the immune cells that infiltrate the breast tumors, more specifically the TSA mammary gland tumors. Our findings identify NAM as a potential strategy for the prevention and treatment of HR+ BC.

ORGANISM(S): Mus musculus

PROVIDER: GSE150921 | GEO | 2020/06/22

REPOSITORIES: GEO

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Mammary gland tumor immunoinfiltrate analysis

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Tumor-reactive tissue resident memory T cells, regulatory T cells and prognosis in early luminal-like breast cancer

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Novel bio-marker discovery for stratification and prognosis of breast cancer patients

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microRNA-143/145 loss induces Ras-signaling and cooperates with Pten-deficiency to promote basal-like breast cancer [gene expression]

Project description:The tumor suppressor PTEN is frequently inactivated in breast and other cancers; yet, germ-line mutations in this gene induce non-malignant hamartomas, indicating dependency on additional cooperating events. Here we show that most tumors derived from conditional deletion of mouse Pten in mammary epithelium are highly differentiated and lack transplantable tumor initiating cells (TICs) capable of seeding new tumors following orthotopic injection of FACS-sorted or tumorsphere cells. A rare group of poorly differentiated tumors did harbour transplantable TICs. These transplantable tumors exhibited distinct molecular classification, signaling pathways, chromosomal aberrations and mutational landscape, as well as reduced expression of microRNA-143/145. Stable knockdown of miR-143/145 conferred tumorigenic potential upon poorly transplantable Pten-deficient tumor cells through a mechanism involving induction of RAS signaling, leading to increased sensitivity to MEK inhibition. In humans, miR145-deficiency significantly correlated with elevated RAS pathway activity in basal-like breast cancer, and patients with combined PTEN/miR-145 loss or PTEN-loss/RAS pathway activation exhibited poor clinical outcome. These results underscore a selective pressure for combined PTEN loss together with miR-145 loss or high RAS-pathway activity in aggressive forms of breast cancer, and a need to identify and prioritize these tumors for aggressive therapy. Expression data comparing 2 types of Pten-deficient tumors (spindle and poorly differentiated) with other models of mouse mammary tumors

2017-06-02 | GSE99493 | GEO

microRNA-143/145 loss induces Ras-signaling and cooperates with Pten-deficiency to promote basal-like breast cancer [CGH]

Project description:The tumor suppressor PTEN is frequently inactivated in breast and other cancers; yet, germ-line mutations in this gene induce non-malignant hamartomas, indicating dependency on additional cooperating events. Here we show that most tumors derived from conditional deletion of mouse Pten in mammary epithelium are highly differentiated and lack transplantable tumor initiating cells (TICs) capable of seeding new tumors following orthotopic injection of FACS-sorted or tumorsphere cells. A rare group of poorly differentiated tumors did harbour transplantable TICs. These transplantable tumors exhibited distinct molecular classification, signaling pathways, chromosomal aberrations and mutational landscape, as well as reduced expression of microRNA-143/145. Stable knockdown of miR-143/145 conferred tumorigenic potential upon poorly transplantable Pten-deficient tumor cells through a mechanism involving induction of RAS signaling, leading to increased sensitivity to MEK inhibition. In humans, miR145-deficiency significantly correlated with elevated RAS pathway activity in basal-like breast cancer, and patients with combined PTEN/miR-145 loss or PTEN-loss/RAS pathway activation exhibited poor clinical outcome. These results underscore a selective pressure for combined PTEN loss together with miR-145 loss or high RAS-pathway activity in aggressive forms of breast cancer, and a need to identify and prioritize these tumors for aggressive therapy. Array CGH data comparing 2 types of Pten-deficient tumors (well and poorly differentiated) with other modles of mouse mammary tumors

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Expression data transgenic mouse mammary tumors

Project description:Immunosurveillance constitutes the first step of cancer immunoediting in which developing malignant lesions are eliminated by anti-tumorigenic immune cells. However, the mechanisms by which neoplastic cells induce an immunosuppressive state to evade the immune response are still unclear. The transcription factor Stat3 has been implicated in breast carcinogenesis and tumor immunosuppression in advanced disease, but its involvement in early disease development has not been established. Here, we genetically ablated Stat3 in the tumor epithelia of the inducible PyVmT mammary tumor model and found that Stat3-deficient mice recapitulated the three phases of immunoediting: elimination, equilibrium, and escape. Pathological analyses revealed that Stat3-deficient mice initially formed hyperplastic and early adenoma-like lesions that later completely regressed, thereby preventing the emergence of mammary tumors in the majority of animals. Furthermore, tumor regression was correlated with massive immune infiltration into the Stat3-deficient lesions, leading to their elimination. In a minority of animals, focal, non-metastatic Stat3-deficient mammary tumors escaped immunosurveillance after a long latency or equilibrium period. Taken together, our findings suggest that tumor epithelial expression of Stat3 plays a critical role in promoting an immunosuppressive tumor microenvironment during breast tumor initiation and progression, and prompt further investigation of Stat3 inhibitory strategies that may reactivate the immunosurveillance program. We used microarrays to detail determine the transcriptional difference between PyVmT-driven mouse mammary tumors that progressed in the presence or absense of epithelial Stat3. Mammary tumors from transgenic mice were excise and flash frozen. Tumors were analyzed from 8 Stat3-proficient tumors and 6 Stat3-deficient tumors. RNA was extracted and hybridization on Affymetrix microarrays.

2015-11-25 | E-GEOD-75325 | biostudies-arrayexpress

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