Abrogated response to cellular stress identifies DCIS associated with subsequent tumor events and defines basal-like breast tumors - Wikidata - wikimedia - TriplyDB

Abrogated response to cellular stress identifies DCIS associated with subsequent tumor events and defines basal-like breast tumors

Abrogated response to cellular stress identifies DCIS associated with subsequent tumor events and defines basal-like breast tumors

http://www.wikidata.org/entity/Q36707456

about

PD 0332991, a selective cyclin D kinase 4/6 inhibitor, preferentially inhibits proliferation of luminal estrogen receptor-positive human breast cancer cell lines in vitro Activation of host wound responses in breast cancer microenvironment Retinoblastoma tumor suppressor functions shared by stem cell and cancer cell strategies Form and function: how estrogen and progesterone regulate the mammary epithelial hierarchy Twists in views on RB functions in cellular signaling, metabolism and stem cells Retinoblastoma tumor suppressor pathway in breast cancer: prognosis, precision medicine, and therapeutic interventions Rb suppresses collective invasion, circulation and metastasis of breast cancer cells in CD44-dependent manner Expression of p16 and retinoblastoma determines response to CDK4/6 inhibition in ovarian cancer.Breast cancer signatures for invasiveness and prognosis defined by deep sequencing of microRNA Biomarker expression and risk of subsequent tumors after initial ductal carcinoma in situ diagnosis Efficacy of neoadjuvant Cisplatin in triple-negative breast cancer Rb deletion in mouse mammary progenitors induces luminal-B or basal-like/EMT tumor subtypes depending on p53 status.Cyclin D1 kinase activity is required for the self-renewal of mammary stem and progenitor cells that are targets of MMTV-ErbB2 tumorigenesis Ischemia in tumors induces early and sustained phosphorylation changes in stress kinase pathways but does not affect global protein levels.Sparse multitask regression for identifying common mechanism of response to therapeutic targets.αB-crystallin promotes oncogenic transformation and inhibits caspase activation in cells primed for apoptosis by Rb inactivation.Tailoring to RB: tumour suppressor status and therapeutic response.The retinoblastoma tumor suppressor pathway modulates the invasiveness of ErbB2-positive breast cancer.Stage of breast cancer progression influences cellular response to activation of the WNT/planar cell polarity pathway DNA damage drives an activin a-dependent induction of cyclooxygenase-2 in premalignant cells and lesions.The meaning of p16(ink4a) expression in tumors: functional significance, clinical associations and future developments Postpartum mammary gland involution drives progression of ductal carcinoma in situ through collagen and COX-2.The interface between biomarker discovery and clinical validation: The tar pit of the protein biomarker pipeline.Most basal-like breast carcinomas demonstrate the same Rb-/p16+ immunophenotype as the HPV-related poorly differentiated squamous cell carcinomas which they resemble morphologically.Analysis of stromal signatures in the tumor microenvironment of ductal carcinoma in situ.ANCCA/ATAD2 overexpression identifies breast cancer patients with poor prognosis, acting to drive proliferation and survival of triple-negative cells through control of B-Myb and EZH2.Treatment options for patients with triple-negative breast cancer The role of the RB tumour suppressor pathway in oxidative stress responses in the haematopoietic system.Palbociclib (PD 0332991) : targeting the cell cycle machinery in breast cancer.Cooperativity of Rb, Brca1, and p53 in malignant breast cancer evolution.Effects of an Indolocarbazole-Derived CDK4 Inhibitor on Breast Cancer Cells Minireview: Basal-like breast cancer: from molecular profiles to targeted therapies Systems biology and genomics of breast cancer.Genetic predisposition directs breast cancer phenotype by dictating progenitor cell fate.Biological Markers in DCIS and Risk of Breast Recurrence: A Systematic Review.Emerging roles of E2Fs in cancer: an exit from cell cycle control P16 and p53 play distinct roles in different subtypes of breast cancer Gerosuppressant metformin: less is more Carcinoma initiation via RB tumor suppressor inactivation: a versatile approach to epithelial subtype-dependent cancer initiation in diverse tissues.CpG island hypermethylation of BRCA1 and loss of pRb as co-occurring events in basal/triple-negative breast cancer.

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P2860

Abrogated response to cellular stress identifies DCIS associated with subsequent tumor events and defines basal-like breast tumors

http://www.wikidata.org/entity/Q36707456

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Abrogated response to cellular ...... fines basal-like breast tumors

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Abrogated response to cellular ...... fines basal-like breast tumors

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Abrogated response to cellular ...... fines basal-like breast tumors

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Abrogated response to cellular ...... fines basal-like breast tumors

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Caroline Miller

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Dan Moore

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Hal K Berman

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Joseph Rabban

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Thea D Tlsty

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Yunn Yi Chen

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P2860

Growth suppression by p16ink4 requires functional retinoblastoma protein

A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4

Identification of a novel E2F3 product suggests a mechanism for determining specificity of repression by Rb proteins

Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis

p16(INK4a) prevents centrosome dysfunction and genomic instability in primary cells.

Molecular portraits of human breast tumours

Repeated observation of breast tumor subtypes in independent gene expression data sets

Tumor suppression by Ink4a-Arf: progress and puzzles

The regulation of E2F by pRB-family proteins

Histological type and marker expression of the primary tumour compared with its local recurrence after breast-conserving therapy for ductal carcinoma in situ

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