scholarly journals The role of PGP9.5 as a tumor suppressor gene in human cancer

2008 ◽  
Vol 123 (4) ◽  
pp. 753-759 ◽  
Author(s):  
Yutaka Tokumaru ◽  
Keishi Yamashita ◽  
Myoung Sook Kim ◽  
Hannah L. Park ◽  
Motonobu Osada ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Human Cancer ◽  
Suppressor Gene

Role of the p16 tumor suppressor gene in cancer.

1998 ◽  
Vol 16 (3) ◽  
pp. 1197-1206 ◽  
Author(s):  
W H Liggett ◽  
D Sidransky
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Human Cancer ◽  
Suppressor Gene ◽  
Premalignant Lesions ◽  
Early Event ◽  
Cyclin Dependent Kinase ◽  
Primary Tumors

Since its discovery as a CDKI (cyclin-dependent kinase inhibitor) in 1993, the tumor suppressor p16 (INK4A/MTS-1/CDKN2A) has gained widespread importance in cancer. The frequent mutations and deletions of p16 in human cancer cell lines first suggested an important role for p16 in carcinogenesis. This genetic evidence for a causal role was significantly strengthened by the observation that p16 was frequently inactivated in familial melanoma kindreds. Since then, a high frequency of p16 gene alterations were observed in many primary tumors. In human neoplasms, p16 is silenced in at least three ways: homozygous deletion, methylation of the promoter, and point mutation. The first two mechanisms comprise the majority of inactivation events in most primary tumors. Additionally, the loss of p16 may be an early event in cancer progression, because deletion of at least one copy is quite high in some premalignant lesions. p16 is a major target in carcinogenesis, rivaled in frequency only by the p53 tumor-suppressor gene. Its mechanism of action as a CDKI has been elegantly elucidated and involves binding to and inactivating the cyclin D-cyclin-dependent kinase 4 (or 6) complex, and thus renders the retinoblastoma protein inactive. This effect blocks the transcription of important cell-cycle regulatory proteins and results in cell-cycle arrest. Although p16 may be involved in cell senescence, the physiologic role of p16 is still unclear. Future work will focus on studies of the upstream events that lead to p16 expression and its mechanism of regulation, and perhaps lead to better therapeutic strategies that can improve the clinical course of many lethal cancers.

Abstract B18: Role of the tumor suppressor gene DLC-2 in ERBB2 induced mouse mammary tumorigenesis and metastasis

2016 ◽  
Author(s):  
Pratima Basak ◽  
Pratima Basak ◽  
Heather Leslie ◽  
Heather Leslie ◽  
Afshin Raouf ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Mammary Tumorigenesis ◽  
Suppressor Gene

scholarly journals A High-Throughput Screen with Isogenic PTEN+/+ and PTEN−/− Cells Identifies CID1340132 as a Novel Compound That Induces Apoptosis in PTEN and PIK3CA Mutant Human Cancer Cells

2011 ◽  
Vol 16 (4) ◽  
pp. 383-393 ◽  
Author(s):  
Hui-Fang Li ◽  
Adam Keeton ◽  
Michele Vitolo ◽  
Clinton Maddox ◽  
Lynn Rasmussen ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
High Throughput ◽  
Human Cancer ◽  
Genetic Difference ◽  
Suppressor Gene ◽  
Pten Gene ◽  
Target Cells ◽  
Mutant Cells

The PTEN tumor suppressor gene is one of the most commonly mutated genes in human cancer. Because inactivation of PTEN is a somatic event, PTEN mutations represent an important genetic difference between cancer cells and normal cells and therefore a potential anticancer drug target. However, it remains a substantial challenge to identify compounds that target loss-of-function events such as mutations of tumor suppressors. In an effort to identify small molecules that preferentially kill cells with mutations of PTEN, the authors developed and implemented a high-throughput, paired cell-based screen composed of parental HCT116 cells and their PTEN gene-targeted derivatives. From 138 758 compounds tested, two hits were identified, and one, N′-[(1-benzyl-1H-indol-3-yl)methylene]benzenesulfonohydrazide (CID1340132), was further studied using a variety of cell-based models, including HCT116, MCF10A, and HEC1A cells with targeted deletion of either their PTEN or PIK3CA genes. Preferential killing of PTEN and PIK3CA mutant cells was accompanied by DNA damage, inhibition of DNA synthesis, and apoptosis. Taken together, these data validate a cell-based screening approach for identifying lead compounds that target cells with specific tumor suppressor gene mutations and describe a novel compound with preferential killing activity toward PTEN and PIK3CA mutant cells.

Role of the class II tumor suppressor gene maspin in thyroids

2004 ◽  
Vol 200 (4) ◽  
pp. 326
Author(s):  
C. Boltze ◽  
C. Hoang-Vu ◽  
R. Schneider-Stock ◽  
H. Lehnert ◽  
A. Roessner
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Class Ii ◽  
Suppressor Gene

scholarly journals Possible Role of Semaphorin 3F, a Candidate Tumor Suppressor Gene at 3p21.3, in p53-Regulated Tumor Angiogenesis Suppression

2007 ◽  
Vol 67 (4) ◽  
pp. 1451-1460 ◽  
Author(s):  
Manabu Futamura ◽  
Hiroki Kamino ◽  
Yuji Miyamoto ◽  
Noriaki Kitamura ◽  
Yasuyuki Nakamura ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Tumor Angiogenesis ◽  
Suppressor Gene ◽  
Candidate Tumor Suppressor ◽  
Candidate Tumor Suppressor Gene ◽  
Semaphorin 3F
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