Autophagy and Senescence in Cancer Therapy

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Release : 2021-04-13
Genre : Medical
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Book Rating : 594/5 ( reviews)

Autophagy and Senescence in Cancer Therapy - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Autophagy and Senescence in Cancer Therapy write by . This book was released on 2021-04-13. Autophagy and Senescence in Cancer Therapy available in PDF, EPUB and Kindle. Advances in Cancer Research, Volume 150, the latest release in this ongoing series, covers the relationship(s) between autophagy and senescence, how they are defined, and the influence of these cellular responses on tumor dormancy and disease recurrence. Specific sections in this new release include Autophagy and senescence, converging roles in pathophysiology, Cellular senescence and tumor promotion: role of the unfolded protein response, autophagy and senescence in cancer stem cells, Targeting the stress support network regulated by autophagy and senescence for cancer treatment, Autophagy and PTEN in DNA damage-induced senescence, mTOR as a senescence manipulation target: A forked road, and more. Addresses the relationship between autophagy and senescence in cancer therapy Covers autophagy and senescence in tumor dormancy Explores autophagy and senescence in disease recurrence

Self-Eating on Demand: Autophagy in Cancer and Cancer Therapy

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Release : 2018-02-19
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Book Rating : 223/5 ( reviews)

Self-Eating on Demand: Autophagy in Cancer and Cancer Therapy - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Self-Eating on Demand: Autophagy in Cancer and Cancer Therapy write by Patrizia Agostinis. This book was released on 2018-02-19. Self-Eating on Demand: Autophagy in Cancer and Cancer Therapy available in PDF, EPUB and Kindle. Macroautophagy, the major lysosomal pathway for recycling intracellular components including whole organelles, has emerged as a key process modulating tumorigenesis, tumor–stroma interactions, and cancer therapy. An impressive number of studies over the past decade have unraveled the plastic role of autophagy during tumor development and dissemination. The discoveries that autophagy may either support or repress neoplastic growth and contextually favor or weaken resistance and impact antitumor immunity have spurred efforts from many laboratories trying to conceptualize the complex role of autophagy in cancer using cellular and preclinical models. This complexity is further accentuated by recent findings highlighting that various autophagy-related genes have roles beyond this catabolic mechanism and interface with oncogenic pathways, other trafficking and degradation mechanisms and the cell death machinery. From a therapeutic perspective, knowledge of how autophagy modulates the tumor microenvironment is crucial to devise autophagy-targeting strategies using smart combination of drugs or anticancer modalities. This eBook contains a collection of reviews by autophagy researchers and provides a background to the state-of-the-art in the field of autophagy in cancer, focusing on various aspects of autophagy regulation ranging from its molecular components to its cell autonomous role, e.g. in cell division and oncogenesis, miRNAs regulation, cross-talk with cell death pathways as well as cell non-autonomous role, e.g. in secretion, interface with tumor stroma and clinical prospects of autophagy-based biomarkers and autophagy modulators in anticancer therapy. This eBook is part of the TransAutophagy initiative to better understand the clinical implications of autophagy in cancer.

Modulation of Autophagy and Senescence to Enhance the Response to Therapy in Triple Negative Breast Cancer

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Release : 2019
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Modulation of Autophagy and Senescence to Enhance the Response to Therapy in Triple Negative Breast Cancer - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Modulation of Autophagy and Senescence to Enhance the Response to Therapy in Triple Negative Breast Cancer write by Liliya Tyutyunyk-Massey. This book was released on 2019. Modulation of Autophagy and Senescence to Enhance the Response to Therapy in Triple Negative Breast Cancer available in PDF, EPUB and Kindle. Abstract Although great strides have been made over the decades in development and optimization of anti-cancer therapies, even highly effective drugs often fail to completely eliminate tumors. Residual tumor cells can enter into a state of dormancy for prolonged periods of time but eventually are able to regain proliferative capacity and reemerge as chemotherapy-resistant disease. Because recurrent disease is a leading contributor to patient's mortality, it is paramount to identify strategies for effectively destroying residual tumor cells. Cytotoxic drugs and ionizing radiation are used as standard therapies in a variety of cancers. These modalities induce apoptosis, autophagy and senescence. Senescence is a state of prolonged growth arrest, which cells are able to eventually escape regaining proliferative capacity. Autophagy is generally considered to be a protective mechanism; however, it can take non-protective or even cytotoxic form in response to anti-cancer treatments. Furthermore, chemotherapy or radiation induced autophagy was shown to be a contributor to the immune response against tumor cells. Using a model of Triple Negative Breast Cancer, we were able to show increased immunosurveillance of tumor cells after enhanced autophagy was achieved by combining epigenetic remodeling with chemotherapy. Alternatively, we were able to achieved effective clearance of tumor cells induced into senescence by chemotherapy or radiation by the senolytic drug ABT-263 (Navitoclax). In summary, autophagy and senescence alone or in concert, can be induced by conventional anti-tumor modalities. Those processes can be modulated independently to achieve clearance of residual tumor cells following anti-cancer therapies.

Apoptosis, Senescence and Cancer

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Release : 2007-10-23
Genre : Medical
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Book Rating : 211/5 ( reviews)

Apoptosis, Senescence and Cancer - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook Apoptosis, Senescence and Cancer write by David A. Gewirtz. This book was released on 2007-10-23. Apoptosis, Senescence and Cancer available in PDF, EPUB and Kindle. This book provides insight into established practices and research into apoptosis and senescence. The volume thoroughly examines novel and emerging techniques and research in the fields of cell death pathways, senescence growth arrest, drugs and resistance, DNA damage response, and other topics that still hold mysteries for researchers. In total, this volume provides basic scientists and clinicians with a deeper and more complete understanding of the cellular responses of malignancies which may determine the effectiveness of treatment, both in the initial stages of the disease as well as in disease recurrence.

The Effects of Autophagy and Senescence on Sensitivity to Cisplatin in Head and Neck Cancer

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Release : 2020
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The Effects of Autophagy and Senescence on Sensitivity to Cisplatin in Head and Neck Cancer - read free eBook in online reader or directly download on the web page. Select files or add your book in reader. Download and read online ebook The Effects of Autophagy and Senescence on Sensitivity to Cisplatin in Head and Neck Cancer write by Zara Hafeez Siddiqui. This book was released on 2020. The Effects of Autophagy and Senescence on Sensitivity to Cisplatin in Head and Neck Cancer available in PDF, EPUB and Kindle. While current treatments in cancer, such as chemotherapy and radiation, can generally be effective in eliminating disease in patients, there also exists the possibility of recurrence of cancer cells over time. In patients diagnosed with locally advanced head and neck carcinoma, about 50-60% develop a loco-regional recurrence within two years, and 20-30% of patients develop metastatic disease at distant sites in the body [5]. On a cellular level, one mechanism for this survival may be that natural mechanisms such as autophagy and senescence play a role in allowing cells to survive after undergoing treatment. One standard of care chemotherapy for head and neck cancer is cisplatin, which was used as the primary treatment in this project. HN12 cells (head and neck tumor cells; p53-null) showed significant growth arrest and decreased viability in response to 5 [mu]M cisplatin treatment, but proliferative recovery over time. It was found that apoptosis did not play a significant role in this growth arrest, as assessed by annexin V/propidium iodide assays to measure apoptotic cell death. Additionally, cisplatin was shown to induce significant levels of autophagy in head and neck tumor cells with acridine orange staining and western blot analysis; however, pharmacological inhibition of autophagy with either chloroquine (5 [mu]M), bafilomycin (5 nM), or 3-methyladenine (1 mM) did not sensitize cells to treatment with cisplatin, indicating a nonprotective role of autophagy. Additionally, HN12 cells showed significant levels of senescence, a form of cellular growth arrest, as indicated by beta-galactosidase upregulation, flattened morphology, and cell cycle arrest. Targeting of senescent cells with the senolytic ABT-263, a Bcl-2/Bcl-xl inhibitor, was effective in sensitizing cells to treatment with cisplatin, but cellular proliferation still occurred over time. Additionally, the HN30 cell line (p53 wild type) was compared to the HN12 line and experiments suggested that p53 status did not play a significant role in induction of autophagy or the sensitization to the senolytic, although more work needs to be done. Overall, these studies provide evidence that autophagy is nonprotective in the HN12 cell line in response to cisplatin treatment, and that senescence plays a role in allowing cells to survive over time. Further, ABT-263 is effective in targeting the remaining population of senescent cells after cisplatin treatment and may be a potential therapeutic mechanism in preventing the recurrence of head and neck cancers.