p53 in Breast Cancer

Know about the book -

p53 in Breast Cancer is written by Manzoor Ahmad Mir and published by CRC Press. It's available with International Standard Book Number or ISBN identification 1040261981 (ISBN 10) and 9781040261989 (ISBN 13).

p53 in Breast Cancer: Molecular Mechanisms, Clinical Implications, and Therapeutic Targets comprehensively reviews the role of p53 in breast cancer development, progression, and treatment. It explores the multifaceted functions of p53, from its fundamental connection to breast cancer and pathway mechanisms to its influence on cancer metabolism and the impact of mutational alterations. The initial chapters discuss the complex landscape of p53's involvement in cancer metabolism, the ramifications of its mutations, and its crucial role as a tumor suppressor. The subsequent chapters review the regulatory functions of p53 in cell death, DNA repair, genomic stability, and cell cycle dynamics, highlighting its interactions with transcription factors, DNA repair enzymes, and family members p63 and p73. It further reviews the regulation of mutant p53 via post-translational modifications and delves into the approaches to combat mutated p53, highlighting targeted therapies and efforts to overcome chemoresistance. The chapters also address the role of p53 biomarkers in diagnosis and prognosis, the optimization of treatment responses, and the impact of nutrition on p53 activity. This book is an important resource for oncology and molecular biology researchers. Key Features Provides a thorough examination of the p53 gene and its crucial involvement in breast cancer. Explores the critical implications of mutational alterations in p53 on the development and progression of breast cancer. Examines the role of p53 in managing apoptosis and contributing to DNA repair and genomic stability. Discusses the complex interactions of p53 with transcription factors, DNA repair enzymes, p63, and p73. Highlights the role of p53 as a biomarker in diagnosing and predicting breast cancer prognosis.