2 edition of Apoptosis and cell cycle control in cancer found in the catalog.
Apoptosis and cell cycle control in cancer
Includes bibliographical references and index
|Statement||[edited by] N. Shaun B. Thomas|
|Series||UCL molecular pathology series -- v. 3|
|Contributions||Thomas, N. Shaun B|
|The Physical Object|
|Pagination||xiv, 238 p. :|
|Number of Pages||238|
|LC Control Number||95097459|
Cancer is a collective name for many different diseases caused by a common mechanism: uncontrolled cell division. Despite the redundancy and overlapping levels of cell-cycle control, errors occur. One of the critical processes monitored by the cell-cycle checkpoint surveillance mechanism is the proper replication of DNA during the S phase. Cancer cells, however, may be relatively more dependent on apoptosis suppression than normal cells, due to aberrations in protooncogene activity and cell cycle checkpoint control, wandering of cancer cells from their normal sites of trophic support, and hypoxic .
Loss of cell cycle and senescene control, dysregulation of apoptosis, and liver inflammation triggered by cytokines and NF-κB pathway are important mechanisms associated with the HCC. Many risk factors and different mechanisms increase the difficulty on the therapy of HCC. Thus the main reason for cancer is the failure to induce apoptosis in an unwanted cell and as a result of this, the unwanted cell perpetuates without any control. Learn more: Cell Cycle Checkpoints and Regulation of Cancer (short notes).
E2F transcription factors regulate the expression of a number of genes important in cell proliferation, particularly those involved in progression through G1 and into the S-phase of the cell cycle. The activity of E2F factors is regulated through association with the retinoblastoma tumor suppressor . The only book to comprehensively cover both the foundations and cutting-edge advances in understanding cell cycle and growth control, this text also contains an expert perspective on innovative strategies for cancer treatment, making it a vital companion for researcher and clinician alike.
Legends of the West
Plasma reactions and their applications.
Jorge Luis Borges
short history of the opposition during the last session of Parliament.
Handbook of national parks, sanctuaries, and biosphere reserves in India
More next week!
Evergreen review reader, 1957-1967
Oedipus, king of Thebes
Massachusetts Housing Finance Agency, Massachusetts Home Mortgage Finance Agency
Effects of temperature, thermal exposure, and fatigue on an alumina/aluminum composite
production, dissemination and consumption of knowledge
Over the past few years, there have been major breakthroughs in our understanding of the molecular mechanisms which control cell division and apoptosis (programmed cell death). This book adopts a multi-disciplinary approach to explore how the deregulation of basic molecular controls can lead to malignancy in a variety of cell types.
The authors are leading international experts whose chapters. W.S. El-Deiry, The retinoblastoma family of proteins. Whyte, Interactions of HPV E6 and E7 with regulators of cell cycle and proliferation. N.J. Marston and K.H.
Vousden, Integrated control of cell proliferation and apoptosis by oncogenes. G.I. Evan et al, Overview: The nature of malignancy. M.J. Cline, Cancer therapy, cell cycle control and. These substrates control key cellular processes such as apoptosis, cell cycle progression, transcription, and translation, all of which are critical events in Akt signal transduction pathway is probably the best survival pathway by: 5.
Cancer Metastasis Rev. Mar;14(1) P53, cell cycle control and apoptosis: implications for cancer. Kastan MB(1), Canman CE, Leonard CJ. Author information: (1)Johns Hopkins Oncology Center, Baltimore, Maryland, USA. Cellular proliferation depends on the rates of both cell division and cell by: Genetic changes resulting in loss of programmed cell death (apoptosis) are likely to be critical components of tumorigenesis.
Many of the gene products which appear to control apoptotic tendencies are regulators of cell cycle progression; thus, cell cycle control and cell death appear to be tightly linked by: It is involved in several different aspects of cell cycle arrest, apoptosis, control of genome integrity, and DNA repair (Figure 3).
It regulates a variety of processes by transactivating genes that are involved in different cellular functions (e.g.
p21, Gadd45, Mdm2, Egfr, PCNA, cyclin D1, cyclin G, TGF α, σ, Bax, Bcl-XL, Fas1, FasL. Proliferation, cell cycle and apoptosis in cancer. Nature ; – Liu J-j Lin M, Yu J-y, Liu B, Bao J-k.
Targeting apoptotic and autophagic pathways for cancer therapeutics. Cancer Lett ; – Apoptosis is a normal part of the life cycle of a cell, and it helps your body work efficiently and stay healthy.
Scientists are learning more about how apoptosis occurs and is regulated. Cancer comprises many different diseases caused by a common mechanism: uncontrolled cell growth. Despite the redundancy and overlapping levels of cell cycle control, errors do occur.
One of the critical processes monitored by the cell cycle checkpoint surveillance mechanism is the proper replication of DNA during the S phase. Apoptosis (Programmed Cell Death 1): Apoptosis is a tightly regulated, multi-step pathway responsible for cell death during development and tissue homeostasis.
Enzyme action is required for this (unlike necrosis) - Genetic control is maintained right to the end. Apoptosis is a genetically controlled response by which eukaryotic cells undergo programmed cell death.
This phenomenon plays a major role in developmental pathways (1), provides a homeostatic balance of cell populations, and is deregulated in many diseases including cancer. Altering gene expression and the signaling pathways that control the cell cycle and apoptosis can contribute to the tumorigenic process and cell transformation from a normal to a malignant phenotype.
This paper serves to review what is currently known about the effects of aberrant methylation and other epigenetic mechanisms on the regulation of cell cycle and apoptosis in osteosarcoma. Hints & Tips on how to study cell cycle and apoptosis.
The study of cell cycle can be rather daunting for students, as it appears to involve many genes implicated in its regulation. The key to the cell cycle is to understand the role of cyclins, cyclin-dependent kinases (CDKs) and the different ‘checkpoints’.
Summary. Alternative splicing is a vast source of biological regulation and diversity that is misregulated in cancer and other diseases. To investigate global control of alternative splicing in human cells, we analyzed splicing of mRNAs encoding Bcl2 family apoptosis factors in a genome-wide siRNA screen.
The screen identified many regulators of Bcl-x and Mcl1 splicing, notably an extensive. Apoptosis is one of the checks and balances built into the cell cycle. Normally when something goes wrong in a cell, it is quickly destroyed via apoptosis.
3 This safeguard helps prevent the development of cancer. For example, when skin cells are damaged by ultraviolet radiation (i.e. sun, tanning beds) apoptosis is normally triggered. Therefore, the aim of this study was to dissect the role of transcription targets of p53, p21 CIP/WAF-1 (cell cycle regulation) and Bax (pro-apoptotic multidomain Bcl-2 family member), in cell death induced by the individual components of the multimodal neoadjuvant therapy applied in treatment of rectal cancer, i.e.
5-fluoruracil (5-FU. Apoptosis and cancer: an overview --Apoptosis: an introduction --Apoptosis and necrosis in tumors --Apoptosis and the cell cycle --Bcl-2 family proteins: role in dysregulation of apoptosis and chemoresistance in cancer --Abl tyrosine kinase and the control of apoptosis --Roles of p53 in apoptosis and cancer --Retinoblastoma gene and the control.
The cell cycle assay revealed that the combination induced apoptosis by increasing the pre-G 1: % compared to % of control. pAKT and Cyclin D1 protein expressions were significantly more downregulated by the combination treatment compared to the single drug treatment.
Cancer is the result of unchecked cell division caused by a breakdown of the mechanisms that regulate the cell cycle. The loss of control begins with a change in the DNA sequence of a gene that codes for one of the regulatory molecules.
Shane O’Grady, Matthew W. Lawless, in Epigenetic Cancer Therapy, Cell Cycle Arrest. Cell cycle arrest was the first identified effect of HDAC inhibitors on cancer cells. HDAC inhibitors are capable of causing a cell cycle arrest in a broad range of cells, including numerous forms of cancer and both cancerous and noncancerous cells .The type of arrest seems to be dependent on.
The cell cycle assay revealed that the combination induced apoptosis by increasing the pre-G1: % compared to % of control. pAKT and Cyclin D1 protein expressions were signiﬁcantly more downregulated by the combination treatment compared to the single drug treatment.
Centaurea bruguierana inhibits cell proliferation, causes cell cycle arrest, and induces apoptosis in human MCF-7 breast carcinoma cells Fahd A. Nasr, Abdelaaty A. Shahat.Tissue microarray analysis (TMA) indicated that low PTBP1 expression predicted a favorable overall survival for colon cancer patients.
Using small interfering RNA technology, we found that down-regulation of PTBP1 significantly inhibited colon cancer cell growth/proliferation, and induced cell cycle arrest as well as apoptosis in vitro.