Mitochondrial Dysfunction

Mitochondrial Dysfunction
Author: Lawrence H. Lash
Publisher: Elsevier
Total Pages: 527
Release: 2013-10-22
Genre: Science
ISBN: 1483218619

Methods in Toxicology, Volume 2: Mitochondrial Dysfunction provides a source of methods, techniques, and experimental approaches for studying the role of abnormal mitochondrial function in cell injury. The book discusses the methods for the preparation and basic functional assessment of mitochondria from liver, kidney, muscle, and brain; the methods for assessing mitochondrial dysfunction in vivo and in intact organs; and the structural aspects of mitochondrial dysfunction are addressed. The text also describes chemical detoxification and metabolism as well as specific metabolic reactions that are especially important targets or indicators of damage. The methods for measurement of alterations in fatty acid and phospholipid metabolism and for the analysis and manipulation of oxidative injury and antioxidant systems are also considered. The book further tackles additional methods on mitochondrial energetics and transport processes; approaches for assessing impaired function of mitochondria; and genetic and developmental aspects of mitochondrial disease and toxicology. The text also looks into mitochondrial DNA synthesis, covalent binding to mitochondrial DNA, DNA repair, and mitochondrial dysfunction in the context of developing individuals and cellular differentiation. Microbiologists, toxicologists, biochemists, and molecular pharmacologists will find the book invaluable.

The Heterogeneity of Cancer Metabolism

The Heterogeneity of Cancer Metabolism
Author: Anne Le
Publisher: Springer
Total Pages: 186
Release: 2018-06-26
Genre: Medical
ISBN: 331977736X

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.

Cross-Talk and Interaction between Endocrinology and Urology: Challenges and Opportunities

Cross-Talk and Interaction between Endocrinology and Urology: Challenges and Opportunities
Author: Xiao-qiang Liu
Publisher: Frontiers Media SA
Total Pages: 237
Release: 2023-11-22
Genre: Medical
ISBN: 2832536840

The genitourinary system is closely related to the endocrine system. Some genitourinary organs are endocrine organs themselves. Over the past decades, the diagnosis and treatment on both endocrine and urological diseases have developed rapidly. Concerns regarding the normal growth, development, and physiological functions of the genitourinary system, as well as the pathogenesis and treatment of urinary diseases have been raised. The diseases from these two different systems belong to the specialties of internal medicine and surgery respectively. For example, prostate is regulated by androgen originates from testis, adrenal and even malignancies. Androgen deprivation therapy has definite effect on prostatic adenocarcinoma but may also develop castration resistance. The disorders of gonad and reproductive health are also implicated in hormone regulation, such as delayed hypogonadism. Many diseases such as Cushing's syndrome and aldosteronism are transdisciplinary. However, the research on the normal physiological function, and the comprehensive diagnosis and treatment of both systems are short of cross-integration, resulting in a lack of close cooperation between physicians and surgeons. We are calling for more attention on the joint participation in multidisciplinary diagnosis and treatment, as well as collaboration on basic research in the field of genitourinary and endocrine diseases.

Autophagy and Senescence in Cancer Therapy

Autophagy and Senescence in Cancer Therapy
Author:
Publisher: Academic Press
Total Pages: 384
Release: 2021-04-13
Genre: Medical
ISBN: 0128241594

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

Cell Death Signaling in Cancer Biology and Treatment

Cell Death Signaling in Cancer Biology and Treatment
Author: Daniel Johnson
Publisher: Springer Science & Business Media
Total Pages: 412
Release: 2012-11-19
Genre: Science
ISBN: 1461458471

A key goal in the treatment of cancer is to achieve selective and efficient killing of tumor cells. The aim of Cell Death Signaling in Cancer Biology and Treatment is to describe state-of-the-art approaches and future opportunities for achieving this goal by targeting mechanisms and pathways that regulate cancer cell death. In this book, molecular defects in cell death signaling that characterize cancer cells, including dysregulation of cell death due to overexpression/hyperactivation of oncoproteins, as well as the loss of tumor suppressor proteins will be described. The potential for targeting microRNAs will be discussed. Multiple chapters will describe preclinical and clinical approaches that are currently being used to target epigenetic modifications, DNA repair pathways, and protein chaperones, as a means of provoking tumor cell death. Finally, the development and application of novel agents and approaches for targeting specific components of cell death signaling pathways and machinery will be reviewed.

Crosstalk between Cell Death, Oxidative Stress, and Immune Regulation

Crosstalk between Cell Death, Oxidative Stress, and Immune Regulation
Author: Chao Yang
Publisher: Frontiers Media SA
Total Pages: 182
Release: 2024-11-11
Genre: Medical
ISBN: 2832556647

Cell death, a biological event important for maintaining the growth, development, and life processes of organisms, mainly includes programmed death (apoptosis, pyroptosis, autophagy, mitochondrial apoptosis, ferroptosis, cuproptosis, and disulfidptosis, etc.) and non-programmed death (cell necrosis). Many diseases, including cancers, exhibit dysregulated immune activities as key features due to the increase in oxidative stress, which eventually leads to cell death. Understanding the intricate relationships between cell death, oxidative stress, and immune regulation could be critical in elucidating the key molecular mechanisms of these diseases, possibly uncovering novel therapeutics/diagnostics for disease management. For example, ferroptosis, a form of iron-dependent cell death that is triggered by the toxic accumulation of oxidative stress, can induce immunosuppression in tumor neutrophils, whereas inhibition of ferroptosis can slow tumor progression. For another example, pyroptosis, a form of lytic cell death which can be triggered by oxidative stress, when occurs in tumor cells, can induce a strong inflammatory response and significant tumor regression.