Proliferative suppression by CDK4/6 inhibition: complex function of the retinoblastoma pathway in liver tissue and hepatoma cells. - Wikidata - wikimedia - TriplyDB

Proliferative suppression by CDK4/6 inhibition: complex function of the retinoblastoma pathway in liver tissue and hepatoma cells.

Proliferative suppression by CDK4/6 inhibition: complex function of the retinoblastoma pathway in liver tissue and hepatoma cells.

http://www.wikidata.org/entity/Q33812043

about

Therapeutically activating RB: reestablishing cell cycle control in endocrine therapy-resistant breast cancer.Recent advances of highly selective CDK4/6 inhibitors in breast cancer CDK4/6 Inhibitors in Cancer Therapy: A Novel Treatement Strategy for Bladder Cancer.Tandem E2F binding sites in the promoter of the p107 cell cycle regulator control p107 expression and its cellular functions.Decorin deficiency promotes hepatic carcinogenesis Smad3 signaling in the regenerating liver: implications for the regulation of IL-6 expression Palbociclib (PD-0332991), a selective CDK4/6 inhibitor, restricts tumour growth in preclinical models of hepatocellular carcinoma.The retinoblastoma tumor suppressor pathway modulates the invasiveness of ErbB2-positive breast cancer.The meaning of p16(ink4a) expression in tumors: functional significance, clinical associations and future developments CDK4/6 inhibitors have potent activity in combination with pathway selective therapeutic agents in models of pancreatic cancer.The history and future of targeting cyclin-dependent kinases in cancer therapy.Effects of an Indolocarbazole-Derived CDK4 Inhibitor on Breast Cancer Cells Cyclin-dependent kinase 6 phosphorylates NF-κB P65 at serine 536 and contributes to the regulation of inflammatory gene expression.RB deletion disrupts coordination between DNA replication licensing and mitotic entry in vivo.Translating bioinformatics in oncology: guilt-by-profiling analysis and identification of KIF18B and CDCA3 as novel driver genes in carcinogenesis.Retinoblastoma protein potentiates the innate immune response in hepatocytes: significance for hepatocellular carcinoma.The Evolutionarily Conserved C-terminal Domains in the Mammalian Retinoblastoma Tumor Suppressor Family Serve as Dual Regulators of Protein Stability and Transcriptional Potency.Mir-33 regulates cell proliferation and cell cycle progression.Early G₁ cyclin-dependent kinases as prognostic markers and potential therapeutic targets in esophageal adenocarcinoma.Nuclear translocation of PKM2 modulates astrocyte proliferation via p27 and -catenin pathway after spinal cord injury Downregulation of microRNA‑33a promotes cyclin‑dependent kinase 6, cyclin D1 and PIM1 expression and gastric cancer cell proliferation.miRNA-338-3p/CDK4 signaling pathway suppressed hepatic stellate cell activation and proliferation.An integrative model links multiple inputs and signaling pathways to the onset of DNA synthesis in hepatocytes.Palbociclib inhibits epithelial-mesenchymal transition and metastasis in breast cancer via c-Jun/COX-2 signaling pathway.Targeting cell cycle and hormone receptor pathways in cancer.PCAF acts as a gastric cancer suppressor through a novel PCAF-p16-CDK4 axis CDK4/6-dependent activation of DUB3 regulates cancer metastasis through SNAIL1.Progress with palbociclib in breast cancer: latest evidence and clinical considerations.PRMT5 competitively binds to CDK4 to promote G1-S transition upon glucose induction in hepatocellular carcinoma.Effective combination therapies in preclinical endocrine resistant breast cancer models harboring ER mutations.The Complex Relationship between Liver Cancer and the Cell Cycle: A Story of Multiple Regulations.Cyclin-dependent kinase inhibitors and the treatment of gastrointestinal cancers.Biological specificity of CDK4/6 inhibitors: dose response relationship, in vivo signaling, and composite response signature.The Strange Case of CDK4/6 Inhibitors: Mechanisms, Resistance, and Combination Strategies.Bone morphogenetic protein 4 (BMP4) signaling in retinoblastoma cells.Palbociclib induces activation of AMPK and inhibits hepatocellular carcinoma in a CDK4/6-independent manner.circRNA_100290 plays a role in oral cancer by functioning as a sponge of the miR-29 family.CDK4/6 inhibition is more active against the glioblastoma proneural subtype.CDK4/6 inhibition provides a potent adjunct to Her2-targeted therapies in preclinical breast cancer models.High trefoil factor 1 (TFF1) expression in human retinoblastoma cells correlates with low growth kinetics, increased cyclin-dependent kinase (CDK) inhibitor levels and a selective down-regulation of CDK6.

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P2860

Proliferative suppression by CDK4/6 inhibition: complex function of the retinoblastoma pathway in liver tissue and hepatoma cells.

http://www.wikidata.org/entity/Q33812043

description

2010 nî lūn-bûn

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2010 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2010 թվականի հունվարին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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Proliferative suppression by C ...... ver tissue and hepatoma cells.

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Proliferative suppression by C ...... ver tissue and hepatoma cells.

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J.GASTRO.2010.01.007

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Gastroenterology

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Proliferative suppression by C ...... ver tissue and hepatoma cells.

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Chellappagounder Thangavel

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Christopher A Reed

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Christopher N Mayhew

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Dayana B Rivadeneira

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Elena Sotillo

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Erik S Knudsen

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Xavier Graña

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P2860

Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

Global cancer statistics, 2002

Pocket proteins and cell cycle control

RB-dependent S-phase response to DNA damage

E1A blocks hyperphosphorylation of p130 and p107 without affecting the phosphorylation status of the retinoblastoma protein.

The Rb/E2F pathway: expanding roles and emerging paradigms.

Retinoblastoma tumor suppressor: where cancer meets the cell cycle.

The retinoblastoma tumor suppressor modifies the therapeutic response of breast cancer.

Inhibition of DNA synthesis by RB: effects on G1/S transition and S-phase progression

Targeted disruption of the three Rb-related genes leads to loss of G(1) control and immortalization.

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1920-1930

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5

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41138797

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20100483

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2860048

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