Apoptosis in Hormone-Dependent Cancers PDF Download
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Author: Martin Tenniswood
Publisher: Springer Science & Business Media
ISBN: 3662031221
Category : Medical
Languages : en
Pages : 296
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Book Description
It is now widely accepted that cells have the ability to initiate a program of gene-directed death, a process called "apoptosis" which may also be used as an innovative strategy for therapeutic intervention in cancer therapy. Experts in this area report on the regulation and control of apoptosis in hormone dependent (neoplastic) tissue and the possibility to exploit active cell death for therapeutic application.
Author: Martin Tenniswood
Publisher: Springer Science & Business Media
ISBN: 3662031221
Category : Medical
Languages : en
Pages : 296
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Book Description
It is now widely accepted that cells have the ability to initiate a program of gene-directed death, a process called "apoptosis" which may also be used as an innovative strategy for therapeutic intervention in cancer therapy. Experts in this area report on the regulation and control of apoptosis in hormone dependent (neoplastic) tissue and the possibility to exploit active cell death for therapeutic application.
Author: Martin Tenniswood
Publisher: Springer
ISBN: 9783540588405
Category : Medical
Languages : en
Pages : 250
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Book Description
It is now widely accepted that cells have the ability to initiate a program of gene-directed death, a process called "apoptosis" which may also be used as an innovative strategy for therapeutic intervention in cancer therapy. Experts in this area report on the regulation and control of apoptosis in hormone dependent (neoplastic) tissue and the possibility to exploit active cell death for therapeutic application.
Author: M Sluyser
Publisher: CRC Press
ISBN: 148229527X
Category : Medical
Languages : en
Pages : 275
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Book Description
In apoptosis in the mammalian system, cells have a finite life - they develop, are used and then die. Cancer cells escape this programmed routine but, from an understanding of apoptosis, they can be programmed to die. This book addresses the
Author: Danyetta Denise Davis
Publisher:
ISBN:
Category : Apoptosis
Languages : en
Pages : 157
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Book Description
Abstract: Genistein, the predominant isoflavone, has several interesting properties including and not limited to cell cycle arrest, induction of apoptosis, tyrosine kinase inhibition, and effecting cell signaling transduction pathways. To enhance the anti-cancer activity of genistein, a series of novel isoflavone analogs were synthesized based on the isoflavone skeleton backbone and the side chain of raloxifene. The synthetic isoflavone analogs were shown to be effective antiproliferative, cytotoxic, and apoptosis agents in both hormone-dependent and hormone-independent breast cancer cell lines. We also determined that the MDA-MB-231 cell line was more sensitive to the cytotoxic and apoptosis inducing ability of the isoflavone analogs. Flow cytometry analysis revealed that selected isoflavone analogs arrested breast cancer cells at the G1 to S transition with concomitant increase in the endogenous cdk inhibitors (p21 and p27). Of this series, compound 5 showed selectivity in its mechanism of action for the MDA-MB-231 cell line, suggesting that its activity was not strictly mediated through estrogen-dependent pathways. Potential cell death mediated targets in the apoptosis pathway were further explored. A 48 hour treatment with 5 and 10 mM of compound 5 resulted in a significant increase in Bax expression in both breast cancer cell lines. Additionally, the Bax/Bcl-2 ratio was significantly increased in the MDA-MB-231 breast cancer cell line. Also, treatment with compound 5 in the MDA-MB-231 breast cancer cell line resulted in decreased expression of activated Akt at Serine-473. High-throughput analysis revealed an increase in gene expression of the caspase-dependent, TNF/FAS-mediated, and death domain related families following treatment with compound 5 in the MDA-MB-231 breast cancer cell line. Gene expression was validated by real time PCR, western blotting of relevant caspase proteins, and decrease in apoptosis in the presence of the general caspase inhibitor, z-VAD-fmk. A series of nimesulide analogs were also examined and not found to induce apoptosis in SK-BR-3 cells, which supports their further exploration as novel aromatase suppression modulators in breast cancer cells. These findings provide important insights into the potential molecular targets of a novel series of synthetic isoflavone analogs, with valuable implications that can impact the overall etiology and treatment of breast cancer.
Author: Jonathan J. Li
Publisher: Springer Science & Business Media
ISBN: 0387237615
Category : Medical
Languages : en
Pages : 562
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Book Description
It has been over a decade since the First International Symposium on Hormonal Carcinogenesis convened in 199 1. Since then, the field has rapidly expanded with considerable progress in both breast and prostate cancers; while ovarian and endometrial cancer have been hampered, in part, due to the absence of suitable hormone-mediated animal models. While knock-out, transgenic, and cell-culture systems have been extremely useful in identifying specific genelprotein alterations and the ensuing pathways affected, the precise molecular mechanisms whereby sex hormones elicit their oncogenic effects still remain elusive. Moreover, despite the considerable progress made in breast cancer research, the exact role of progestins in the presence or absence of estrogen in breast growth, differentiation, and malignant transformation is lacking. Elucidating the incipient molecular alterations in earlylpre-invasive lesions elicited by these hormones is a growing important focus of this field. The main purpose of these Symposia has been to address vital questions that impact our understanding of the causation, dependency, progression, resistance, and prevention of hormonally-associated cancers. We are indebted to the Scientific Advisory Board members who worked with us reviewing and offering suggestions to finalize the scientific program. We offer special thanks for the guidance and support of Dr. Gerald Mueller. His wisdom played an indispensable role in maintaining the excellence of these Symposia. We also acknowledge the numerous external reviewers that worked diligently to revise and improve the quality of the manuscripts. We are very grateful to Ms. Tandria Price.
Author: Russo Jose
Publisher: World Scientific
ISBN: 9813271213
Category : Medical
Languages : en
Pages : 688
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Book Description
This narrative of a cancer researcher spans a period in which biomedicine research has been so revolutionary. The educational background and socioeconomic circumstances of the author make the story unique, shedding light on many important intellectual achievements. The author also provides an insightful view on how decisions at the upper echelon of scientific institutions affect cancer researchers. The vivid account of scientific discovery and intellectual evolution provides a fine example for the next generation of cancer researchers.
Author: Janet K. Hess-Wilson
Publisher:
ISBN:
Category :
Languages : en
Pages : 116
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Book Description
Due to its pivotal role in prostatic growth and survival, the androgen receptor (AR) is the primary target of disseminated prostate cancer (CaP), as achieved via androgen deprivation therapy (ADT). Unfortunately, ADT is circumvented by restoration of AR activity, resulting in ADT resistant tumors for which there is no alternate treatment option. Through multiple mechanisms, reactivation of the AR specifically underlies the progression to therapy resistant tumors. The environmentally prevalent endocrine disrupting compound (EDC), bisphenol A (BPA) is able to activate specific somatically mutated ARs commonly found in CaP, resulting in androgen-independent proliferation of CaP cells. To directly assess the effect of BPA on ADT, we used an in vivo xenograft model of CaP that expresses a BPA-sensitive mutant AR, and mimics standard human cytotoxic response to ADT, followed by subsequent tumor re-growth. When tumor-bearing animals were exposed to environmentally relevant levels of BPA during ADT, the tumors failed therapy more rapidly (compared to placebo controls), with AR reactivation and concomitant increased tumor cell proliferation. These data suggest that environmentally relevant exposure to EDCs may reduce the efficacy of mainline ADT for CaP. We next determined that the environmentally persistent pesticide, DDE, was able to activate select AR mutants, and in in vitro models of CaP, DDE induces cellular proliferation in the absence of androgen, demonstrating that this observed response was not unique to BPA. Strikingly, the mechanism of DDE impact on CaP cells was distinct from BPA, in that at low doses this agent also activated the MAPK pathway, and requires this activation for mitogenesis. Given the context specific impact of AR activation by EDCs, and the deleterious effect of exposure to BPA on ADT in vivo, we next addressed the impact of AR action on taxane-based therapy. These cytotoxic agents have recently been shown to improve survival outcome for patients with advanced CaP, and are potentially new second line therapies, however the impact of AR action on this cytotoxic modality had yet to be assessed. Contrary to the stigma of AR as a survival factor, we found that AR activation by both endogenous and exogenous agonists (i.e. DHT and BPA), synergized with taxanes to decrease cell survival, through p53-mediated, caspase dependent apoptosis. This synergistic action was attributed directly to the AR-dependent mitogenic capacity of these agents. Importantly, these data further support the conclusion that the environmental impact on AR action and CaP therapeutic outcome is context specific. We further evaluated the complexity of EDC affects by assessing the impact of these agents under clinically relevant conditions in another hormone-dependent tissue, breast cancer. BPA and the phytoestrogen, coumestrol (COU), were able to activate the estrogen receptor (ERalpha), but this activation was restricted to estrogen-depleted conditions, and could be blocked by the standard ER antagonist, tamoxifen. Additionally, BPA and COU have disparate affects in multiple analyses including mutant ERalpha activation, and specific coactivator deregulation. In conclusion, the environmental impact on nuclear receptor signaling and hormone dependent cancer progression and treatment is highly molecular context specific. Therefore, the impact of EDCs on hormone dependent cancer treatment needs to be identified under specific and well defined, clinically relevant, molecular contexts.
Author: William L. McGuire
Publisher:
ISBN:
Category : Medical
Languages : en
Pages : 320
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Book Description
Author: Anne Le
Publisher: Springer
ISBN: 331977736X
Category : Medical
Languages : en
Pages : 186
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Book Description
Genetic alterations in cancer, in addition to being the fundamental drivers of tumorigenesis, can give rise to a variety of metabolic adaptations that allow cancer cells to survive and proliferate in diverse tumor microenvironments. This metabolic flexibility is different from normal cellular metabolic processes and leads to heterogeneity in cancer metabolism within the same cancer type or even within the same tumor. In this book, we delve into the complexity and diversity of cancer metabolism, and highlight how understanding the heterogeneity of cancer metabolism is fundamental to the development of effective metabolism-based therapeutic strategies. Deciphering how cancer cells utilize various nutrient resources will enable clinicians and researchers to pair specific chemotherapeutic agents with patients who are most likely to respond with positive outcomes, allowing for more cost-effective and personalized cancer therapeutic strategies.
Author: L. Castagnetta
Publisher:
ISBN:
Category : Medical
Languages : en
Pages : 360
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Book Description
The papers in this volume cover the biology and biochemistry of normal and cancer cell growth exhibited in a range of cancers including liver cancer, colorectal cancer, breast cancer, prostate cancer and leukaemia. Studies include the epidermilogy, risk factors and the natural histories of these cancers. Additional chapters examine different treatment modalities for various cancers.
