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5 results on '"Michel M. Ouellette"'

1. Radiation‐activated prosurvival signaling pathways in cancer cells

Author

Michel M. Ouellette and Ying Yan

Subjects
apoptosis, cell cycle checkpoint, DNA repair, radiation therapy, signaling pathways, Medical physics. Medical radiology. Nuclear medicine, R895-920, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Radiation therapy is a standard treatment for local disease control of solid tumors. Although radiation therapy has significantly improved the overall survival and quality of life of cancer patients, its efficacy has been limited by the development of radiation resistance and the presence of residual disease after therapy, leading to cancer recurrence. Radiation induces cytotoxicity in cancer cells, mainly by causing DNA damage. However, concurrently radiation can also activate multiple protective signaling pathways, such as ataxia telangiectasia mutated/ataxia telangiectasia mutated and Rad3‐related protein, phosphoinositide‐3‐kinase/protein kinase B, extracellular signal‐regulated kinase, and nuclear factor‐κB, which promote cell cycle checkpoint activation, leading to cell cycle arrest/DNA repair and inhibition of apoptosis. Conjointly, these signaling pathways protect cancer cells by reducing the magnitude of radiation‐induced cytotoxicity and promoting radioresistance of cancer cells. Thus, targeting these prosurvival pathways could have great potential for sensitizing cancer cells to radiation therapy. In the present review, we summarize the current literature on the radiation‐activated prosurvival signaling pathways that promote radioresistance.

Published
2019
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2. Telomeres and Telomerase in Ageing and Cancer

Author

Michel M. Ouellette

Subjects
Genetics, Senescence, Telomerase, Ageing, Somatic cell, Cancer cell, medicine, Cancer research, Cancer, Biology, medicine.disease, Telomere
Abstract

Telomeres protect the ends of chromosomes and shorten each time somatic human cells divide. As a consequence, cells enter senescence after a limited number of divisions. The enzyme telomerase expressed in cancer cells and renewal tissues can prevent the shortening of telomeres and extend cellular lifespan. Keywords: telomere; telomerase; cancer; ageing

Published
2018

3. Expression of oncogenic K-ras and loss of Smad4 cooperate to induce the expression of EGFR and to promote invasion of immortalized human pancreas ductal cells

Author

James W. Freeman, Shujie Zhao, Yubao Wang, Lin Cao, and Michel M. Ouellette

Subjects
Cancer Research, Cell signaling, medicine.medical_specialty, Receptor, ErbB-2, Ductal cells, Cellular differentiation, medicine.disease_cause, Article, Cell Line, Downregulation and upregulation, Internal medicine, medicine, Humans, Neoplasm Invasiveness, Smad4 Protein, Gene knockdown, biology, Pancreatic Ducts, Transforming growth factor beta, Up-Regulation, ErbB Receptors, Cell Transformation, Neoplastic, Genes, ras, Endocrinology, Gene Expression Regulation, Oncology, Gene Knockdown Techniques, Mutation, biology.protein, Cancer research, Signal transduction, Carcinogenesis, Signal Transduction
Abstract

Activating mutation of K-ras and inactivation of DPC4 are two common genetic alterations that occur in the development and progression of pancreatic ductal adenocarcinomas (PDAC). A separate common event in PDAC progression is increased expression of phosphotyrosine kinase receptors (PTKRs). In this study, we examined whether activating mutations of K-ras and loss of Smad4 play a role in causing the aberrant expression of PTKRs. Immortalized human pancreas ductal cells (HPNE) were genetically modified by expressing oncogenic K-ras and /or by shRNA knock down of Smad4. EGFR and erbB2 protein levels but not Ron or IGF-1R were substantially up regulated in HPNE cells that express K-ras (GD12). The increased expression of EGFR in HPNE cells that expressed K-ras (GD12) was mediated by both stabilizing EGFR protein and by increasing EGFR transcription. TGF-β signaling partially suppressed K-ras (GD12) induced EGFR transcription in Smad4 intact HPNE cells; whereas, knockdown of Smad4 in cells expressing K-ras (GD12) further enhanced expression of EGFR and erbB2. The up regulation of EGFR and erbB2 was associated with an increase of invasion, which was blocked by a kinase inhibitor of EGFR. This study indicates for the first time, that oncogenic ras and loss of Smad signaling cooperate to up regulate EGFR and erbB2, which plays a role in promoting invasion.

Published
2010

5. Telomeres and Telomerase in Aging and Cancer

Author

Michel M. Ouellette

Subjects
Genetics, Senescence, Telomerase, Somatic cell, media_common.quotation_subject, medicine, Cancer, Immortality, Biology, medicine.disease, Cell biology, Telomere, media_common
Abstract

Telomeres protect the ends of chromosomes and shorten each time somatic human cells divide. As a consequence, cells enter senescence after a limited number of divisions. The enzyme telomerase expressed in rare cells of the skin, blood and intestine can prevent the shortening of telomeres and extend cellular lifespan. Keywords: cancer; aging; senescence; immortality; telomerase; telomeres

Published
2006

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