scholarly journals BTG3 tumor suppressor gene promoter demethylation, histone modification and cell cycle arrest by genistein in renal cancer

2009 ◽  
Vol 30 (4) ◽  
pp. 662-670 ◽  
Author(s):  
S. Majid ◽  
A. A. Dar ◽  
A. E. Ahmad ◽  
H. Hirata ◽  
K. Kawakami ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Histone Modification ◽  
Cell Cycle Arrest ◽  
Tumor Suppressor Gene ◽  
Renal Cancer ◽  
Gene Promoter ◽  
Suppressor Gene ◽  
Cycle Arrest

scholarly journals DC-SCRIPT is a novel regulator of the tumor suppressor gene CDKN2B and induces cell cycle arrest in ERα-positive breast cancer cells

2015 ◽  
Vol 149 (3) ◽  
pp. 693-703 ◽  
Author(s):  
Marleen Ansems ◽  
Jonas Nørskov Søndergaard ◽  
Anieta M. Sieuwerts ◽  
Maaike W. G. Looman ◽  
Marcel Smid ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
Breast Cancer Cells ◽  
Suppressor Gene ◽  
Cycle Arrest ◽  
Positive Breast Cancer

scholarly journals 3p21.3 Tumor Suppressor Gene H37/Luca15/RBM5 Inhibits Growth of Human Lung Cancer Cells through Cell Cycle Arrest and Apoptosis

2006 ◽  
Vol 66 (7) ◽  
pp. 3419-3427 ◽  
Author(s):  
Juliana J. Oh ◽  
Ali Razfar ◽  
Idolina Delgado ◽  
Rebecca A. Reed ◽  
Anna Malkina ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Lung ◽  
Suppressor Gene ◽  
Human Lung Cancer ◽  
Cycle Arrest ◽  
Human Lung Cancer Cells

scholarly journals p53 connects tumorigenesis and reprogramming to pluripotency

2010 ◽  
Vol 207 (10) ◽  
pp. 2045-2048 ◽  
Author(s):  
Natalia Tapia ◽  
Hans R. Schöler
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Suppressor Gene ◽  
Tumor Formation ◽  
Nuclear Reprogramming ◽  
Differentiation Process ◽  
Cycle Arrest ◽  
Tumor Suppressor Gene P53

The tumor suppressor gene p53 prevents the initiation of tumor formation by inducing cell cycle arrest, senescence, DNA repair, and apoptosis. Recently, the absence or mutation of p53 was described to facilitate nuclear reprogramming. These findings suggest an influence of p53 on the de-differentiation process, and highlight the similarities between induction of pluripotency and tumor formation.

Neuroradiology Manifestations of Li-Fraumeni Syndrome: Epidemiology, Genetics, Imaging Findings, and Management

Neurographics ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 228-235
Author(s):  
S. Naganawa ◽  
T. Donohue ◽  
A. Capizzano ◽  
Y. Ota ◽  
J. Kim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Soft Tissue Sarcomas ◽  
Suppressor Gene ◽  
Imaging Findings ◽  
Li Fraumeni Syndrome ◽  
Increased Risk ◽  
Li Fraumeni ◽  
Risk Of Cancer

Li-Fraumeni syndrome is a familial cancer predisposition syndrome associated with germline mutation of the tumor suppressor gene 53, which encodes the tumor suppressor p53 protein. Affected patients are predisposed to an increased risk of cancer development, including soft-tissue sarcomas, breast cancer, brain tumors, and adrenocortical carcinoma, among other malignancies. The tumor suppressor gene TP53 plays an important, complex role in regulating the cell cycle, collaborating with transcription factors and other proteins. The disruption of appropriate cell cycle regulation by mutated TP53 is considered to be the cause of tumorigenesis in Li-Fraumeni syndrome. Appropriate surveillance, predominantly by using MR imaging, is used for early malignancy screening in an effort to improve the survival rate among individuals who are affected. Patients with Li-Fraumeni syndrome are also at increased risk for neoplasm development after radiation exposure, and, therefore, avoiding unnecessary radiation in both the diagnostic and therapeutic settings is paramount. Here, we review the epidemiology, genetics, imaging findings, and the current standard surveillance protocol for Li-Fraumeni syndrome from the National Comprehensive Cancer Network as well as potential treatment options.Learning Objective: Describe the cause of second primary malignancy among patients with Li-Fraumeni syndrome.

The Tumor Suppressor Role of the Ras Association Domain Family 10

2020 ◽  
Vol 20 (18) ◽  
pp. 2207-2215
Author(s):  
Yulong Hou ◽  
Shuofeng Li ◽  
Wei Du ◽  
Hailong Li ◽  
Rumin Wen
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Gene Promoter ◽  
Disease Free Survival ◽  
Suppressor Gene ◽  
Detection Methods ◽  
Tumor Type ◽  
Domain Family ◽  
Invasion And Migration ◽  
Cancer Breast

The Ras association domain family 10(RASSF10), a tumor suppressor gene, is located on human chromosome 11p15.2, which is one of the members homologous to other N-terminal RASSF families obtained through structural prediction. RASSF10 plays an important role in inhibiting proliferation, invasion, and migration, inducing apoptosis, making cancer cells sensitive to docetaxel, and capturing G2/M phase. Some studies have found that RASSF10 may inhibit the occurrence and development of tumors by regulating Wnt/β-catenin, P53, and MMP2. Methylation of tumor suppressor gene promoter is a key factor in the development and progression of many tumors. Various methylation detection methods confirmed that the methylation and downregulation of RASSF10 often occur in various tumors, such as gastric cancer, lung cancer, colon cancer, breast cancer, and leukemia. The status of RASSF10 methylation is positively correlated with tumor size, tumor type, and TNM stage. RASSF10 methylation can be used as a prognostic factor for overall survival and disease-free survival, and is also a sign of tumor diagnosis and sensitivity to docetaxel chemotherapy. In this review, we mainly elucidate the acknowledged structure and progress in the verified functions of RASSF10 and the probably relevant signaling pathways.

scholarly journals Tumor Suppressor Inactivation in the Pathogenesis of Adult T-Cell Leukemia

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Christophe Nicot
Keyword(s):  
Cell Cycle ◽  
T Cell ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Tumor Suppressors ◽  
Epigenetic Mechanisms ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia ◽  
Cycle Arrest

Tumor suppressor functions are essential to control cellular proliferation, to activate the apoptosis or senescence pathway to eliminate unwanted cells, to link DNA damage signals to cell cycle arrest checkpoints, to activate appropriate DNA repair pathways, and to prevent the loss of adhesion to inhibit initiation of metastases. Therefore, tumor suppressor genes are indispensable to maintaining genetic and genomic integrity. Consequently, inactivation of tumor suppressors by somatic mutations or epigenetic mechanisms is frequently associated with tumor initiation and development. In contrast, reactivation of tumor suppressor functions can effectively reverse the transformed phenotype and lead to cell cycle arrest or death of cancerous cells and be used as a therapeutic strategy. Adult T-cell leukemia/lymphoma (ATLL) is an aggressive lymphoproliferative disease associated with infection of CD4 T cells by the Human T-cell Leukemia Virus Type 1 (HTLV-I). HTLV-I-associated T-cell transformation is the result of a multistep oncogenic process in which the virus initially induces chronic T-cell proliferation and alters cellular pathways resulting in the accumulation of genetic defects and the deregulated growth of virally infected cells. This review will focus on the current knowledge of the genetic and epigenetic mechanisms regulating the inactivation of tumor suppressors in the pathogenesis of HTLV-I.

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