Tumor suppressor genes (TSGs) and their signaling networks are fast growing areas in current biomedical science. These groups of genes, which are not limited to tumor suppression, play critical roles in many cellular activities. This book, "Future Aspects of Tumor Suppressor Genes", contains some fascinating fields, from basic to translational researches, in recent TSG studies. For example, several TSG signaling pathways are addressed in this book, and both mouse and Drosophila models used for the exploration of these genes are described based on the experimental evidence....
Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Retraction: The candidate tumor suppressor gene ECRG4 inhibits cancer cells migration and invasion in esophageal carcinoma
Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Down-regulation of UHRF1, associated with re-expression of tumor suppressor genes, is a common feature of natural compounds exhibiting anti-cancer properties
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: p53 tumor suppressor gene mutations in fibroblast-like synoviocytes from erosion synovium and non-erosion synovium in rheumatoid arthritis...
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Isolation of suppressor genes that restore retrovirus susceptibility to a virus-resistant cell line
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Systematic detection of putative tumor suppressor genes through the combined use of exome and transcriptome sequencing...
Over the last three decades, knowledge on the molecular biology of human cancers has vastly expanded. A host of genes and proteins involved in cancer development and progression have been defined and many mechanisms at the molecular, cellular and even tissue level have been, at least partly, elucidated. Insights have also been gained into the molecular mechanisms underlying carcinogenesis by chemical, physical, and biological agents and into inherited susceptibility to cancer. Accordingly, Part I of the book presents many of the molecules and mechanisms generally important in human cancers.
Another local approach uses adenoviral-mediated expression of the tumor suppressor p53, which is mutated in a wide variety of cancers. This strategy has shown complete and partial responses in squamous cell carcinoma of the head and neck, esophageal cancer, and non-small cell lung cancer after direct intratumoral injection of the vector. Response rates (~15%) are comparable to those of other single agents.
HIC1(hypermethylated in cancer) is a tumour suppressor gene located in
17p13.3, a region frequently hypermethylated or deleted in many types of
prevalent human tumour.HIC1is also a candidate for a contiguous-gene
syndrome, the Miller–Dieker syndrome, a severe form of lissencephaly
accompanied by developmental anomalies.
(BQ) Part 2 book "High-Yield cell and molecular biology - Cell and molecular biology" presents the following contents: Proto-Oncogenes, oncogenes and tumor-suppressor genes, the cell cycle, molecular biology of cancer, cell biology of the immune system, cell biology of the immune system, molecular biology techniques, identification of human disease genes, gene therapy.
Ung thưcó phải bệnh di truyền? Các dạng biểu hiện của bệnh ung thư Ung thư và sự điều khiển chu trình tế bào Khái niệm về các gen gây KHốI U (oncogene) Khái niệm về các gen ức chế khối u (tumor suppressor genes) Các cơ chế di truyền liên quan đến sự phát sinh ung thư
In addition, although more rare, some patients might not present until weeks, if
not longer, after their infarction with symptoms that prompt the discovery of a chronic PI-
VSD. Early PI-VSDs tend to be catastrophic and typically result in early death.
This book describes a course of cancer growth starting from normal cells to cancerous form and the genomic instability, the cancer treatment as well as its prevention in form of the invention of a vaccine. Some diseases are also discussed in detail, such as breast cancer, leucaemia, cervical cancer, and glioma. Understanding cancer through its molecular mechanism is needed to reduce the cancer incidence.
General Classes of Cancer Genes There are two major classes of cancer genes. The first class comprises genes that directly affect cell growth either positively (oncogenes) or negatively (tumor-suppressor genes). These genes exert their effects on tumor growth through their ability to control cell division (cell birth) or cell death (apoptosis). Oncogenes are tightly regulated in normal cells. In cancer cells, oncogenes acquire mutations that relieve this control and lead to increased activity of the gene product.
Familial adenomatous polyposis (FAP) is a dominantly inherited colon cancer syndrome due to germline mutations in the adenomatous polyposis coli (APC) tumor-suppressor gene on chromosome 5. Patients with this syndrome develop hundreds to thousands of adenomas in the colon. Each of these adenomas has lost the normal remaining allele of APC but has not yet accumulated the required additional mutations to generate fully malignant cells (Fig. 79-2).
While most autosomal dominant inherited cancer syndromes are due to mutations in tumor-suppressor genes (Table 79-1), there are a few interesting exceptions. Multiple endocrine neoplasia type II, a dominant disorder characterized by pituitary adenomas, medullary carcinoma of the thyroid, and (in some pedigrees) pheochromocytoma, is due to gain-of-function mutations in the protooncogene RET on chromosome 10. Similarly, gain-of-function mutations in the tyrosine kinase domain of the MET oncogene lead to hereditary papillary renal carcinoma.
Familial Cancer Syndromes A small fraction of cancers occur in patients with a genetic predisposition. In these families, the affected individuals have a predisposing loss-of-function mutation in one allele of a tumor-suppressor gene or caretaker gene. The tumors in these patients show a loss of the remaining normal allele as a result of somatic events (point mutations or deletions), in agreement with the Knudson hypothesis (Fig. 79-3).