Stem cells, senescence, neosis and self-renewal in cancer. - Test2 - elhamkhani - TriplyDB

Stem cells, senescence, neosis and self-renewal in cancer.

Stem cells, senescence, neosis and self-renewal in cancer.

http://www.wikidata.org/entity/Q27497212

about

Endopolyploidy in irradiated p53-deficient tumour cell lines: persistence of cell division activity in giant cells expressing Aurora-B kinase The Growing Complexity of Cancer Cell Response to DNA-Damaging Agents: Caspase 3 Mediates Cell Death or Survival?The "virgin birth", polyploidy, and the origin of cancer Docetaxel-induced polyploidization may underlie chemoresistance and disease relapse Atypical cell populations associated with acquired resistance to cytostatics and cancer stem cell features: the role of mitochondria in nuclear encapsulation Three steps to the immortality of cancer cells: senescence, polyploidy and self-renewal.Role of senescence and mitotic catastrophe in cancer therapy.CoCl2, a mimic of hypoxia, induces formation of polyploid giant cells with stem characteristics in colon cancer.Invading basement membrane matrix is sufficient for MDA-MB-231 breast cancer cells to develop a stable in vivo metastatic phenotype.Resistance to discodermolide, a microtubule-stabilizing agent and senescence inducer, is 4E-BP1-dependent.Chemical induction of cardiac differentiation in p19 embryonal carcinoma stem cells Biocompatible micro-sized cell culture chamber for the detection of nanoparticle-induced IL8 promoter activity on a small cell population Insights into 4E-BP1 and p53 mediated regulation of accelerated cell senescence Macroautophagy-aided elimination of chromatin: sorting of waste, sorting of fate?A multi-stage process including transient polyploidization and EMT precedes the emergence of chemoresistent ovarian carcinoma cells with a dedifferentiated and pro-inflammatory secretory phenotype Activation of the Wnt pathway through AR79, a GSK3β inhibitor, promotes prostate cancer growth in soft tissue and bone.Cellular senescence induced by aberrant MAD2 levels impacts on paclitaxel responsiveness in vitro Linking genomic reorganization to tumor initiation via the giant cell cycle Bafilomycin A1 triggers proliferative potential of senescent cancer cells in vitro and in NOD/SCID mice.MOS, aneuploidy and the ploidy cycle of cancer cells.Harnessing the complexity of DNA-damage response pathways to improve cancer treatment outcomes.Advances in melanoma senescence and potential clinical application.Targeting aneuploid cancer cells.Ionizing radiation-induced responses in human cells with differing TP53 status.Multinucleated polyploidy drives resistance to Docetaxel chemotherapy in prostate cancer.Nanoscale characterization illustrates the cisplatin-mediated biomechanical changes of B16-F10 melanoma cells.Therapeutic resistance and cancer recurrence mechanisms: Unfolding the story of tumour coming back.The failure in the stabilization of glioblastoma-derived cell lines: spontaneous in vitro senescence as the main culprit.Significance of Wild-Type p53 Signaling in Suppressing Apoptosis in Response to Chemical Genotoxic Agents: Impact on Chemotherapy Outcome.Respiration characteristics of mitochondria in parental and giant transformed cells of the murine Nemeth-Kellner lymphoma.Polyploid tumour cells elicit paradiploid progeny through depolyploidizing divisions and regulated autophagic degradation.Chemoresponse Assay in Head and Neck Cancer Patients: A Three-Year Follow Up.Mitotic Kinases and p53 Signaling.Some chemotherapeutics-treated colon cancer cells display a specific phenotype being a combination of stem-like and senescent cell features.Roles of Polyploid/Multinucleated Giant Cancer Cells in Metastasis and Disease Relapse Following Anticancer Treatment.

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Stem cells, senescence, neosis and self-renewal in cancer.

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description

2006 nî lūn-bûn

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2006 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2006年の論文

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Stem cells, senescence, neosis and self-renewal in cancer

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Stem cells, senescence, neosis and self-renewal in cancer.

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Stem cells, senescence, neosis and self-renewal in cancer.

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Stem cells, senescence, neosis and self-renewal in cancer

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Stem cells, senescence, neosis and self-renewal in cancer.

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Stem cells, senescence, neosis and self-renewal in cancer.

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Stem cells, senescence, neosis and self-renewal in cancer

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Stem cells, senescence, neosis and self-renewal in cancer.

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Stem cells, senescence, neosis and self-renewal in cancer.

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Cancer Cell International

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Stem cells, senescence, neosis and self-renewal in cancer.

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Duane L Guernsey

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Murali M Rajaraman

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Rengaswami Rajaraman

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Selva R Rajaraman

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Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling

Oncogene-Induced Senescence: Putting the Brakes on Tumor Development

The Hallmarks of Cancer

Epigenetic gene silencing in cancer – a mechanism for early oncogenic pathway addiction?

PML regulates p53 stability by sequestering Mdm2 to the nucleolus

Human SIR2 deacetylates p53 and antagonizes PML/p53-induced cellular senescence.

A novel role for high-mobility group a proteins in cellular senescence and heterochromatin formation

Nucleophosmin regulates the stability and transcriptional activity of p53

hEST2, the putative human telomerase catalytic subunit gene, is up-regulated in tumor cells and during immortalization

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

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