نتایج جستجو برای: fragile histidine triad

تعداد نتایج: 35876  

2014
Sung-Suk Suh Ji Young Yoo Ri Cui Balveen Kaur Kay Huebner Taek-Kyun Lee Rami I. Aqeilan Carlo M. Croce Marshall S. Horwitz

Metastasis is the principal cause of cancer death and occurs through multiple, complex processes that involve the concerted action of many genes. A number of studies have indicated that the Fragile Histidine Triad (FHIT) gene product, FHIT, functions as a tumor suppressor in a variety of common human cancers. Although there are suggestions of a role for FHIT loss in progression of various cance...

Journal: :Cancer research 1997
S Hayashi K Tanimoto K Hajiro-Nakanishi E Tsuchiya M Kurosumi Y Higashi K Imai K Suga K Nakachi

Deletions in the short arm of chromosome 3 have been found in various human cancers, including breast cancer. Recently, the FHIT (fragile histidine triad) gene was identified at 3p14.2 as a candidate tumor suppressor gene. We examined the abnormal transcripts of the FHIT gene in 61 Japanese primary breast cancer specimens and found that 23 (38%) of them exhibited abnormalities, about half of wh...

Journal: :Molecular cancer research : MCR 2014
Audrey Joannes Simon Grelet Laurent Duca Christine Gilles Claire Kileztky Véronique Dalstein Philippe Birembaut Myriam Polette Béatrice Nawrocki-Raby

UNLABELLED In many cancers, including lung carcinomas, Fragile histidine triad (Fhit) is frequently decreased or lost. Fhit status has recently been shown to be associated with elevated in vitro and in vivo invasiveness in lung cancer. Tumor cell invasion is facilitated by epithelial-mesenchymal transition (EMT), a process by which tumor cells lose their epithelial features to acquire a mesench...

Journal: :Cancer research 2005
Baocheng Hu Hongyan Wang Xiang Wang Hua-Rui Lu Cuifen Huang Simon N Powell Kay Huebner Ya Wang

Fragile histidine triad (FHIT) gene deletion or promoter methylation and reduced Fhit protein expression occur in approximately 70% of human epithelial tumors and, in some cancers, are clearly associated with tumor progression. Specific Fhit signal pathways have not been identified. We previously reported that compared with Fhit+/+ cells, Fhit-/- cells with an overactivated ATR/CHK1 pathway sho...

2008
Li Mao

S A N D I E G O — Smokingrelated cell damage may leave molecular footprints in saliva and oral epithelial cells, offering the potential for noninvasive early diagnosis of lung cancer and of head and neck cancers, researchers reported in separate studies at the annual meeting of the American Association for Cancer Research. “When people smoke cigarettes, the whole field is exposed to carcinogens...

2014
Ameneh Eslamparast Mohammad Hossein Ghahremani Soroush Sardari

BACKGROUND Fragile Histidine Triad protein (FHIT), as a known tumor suppressor protein, has been proposed to play crucial role in inhibiting p53 degradation by MDM2. Studies have confirmed FHIT interaction with p53 or MDM2, although functional interacting domains of FHIT with MDM2 and/or p53 are not completely defined. Thus, through determining the significant structural interacting domains of ...

2016
Antonio Agostini Marta Brunetti Ben Davidson Claes G. Trope Sverre Heim Ioannis Panagopoulos Francesca Micci

Malignant tumors of the vulva, most of them squamous cell carcinomas, account for only 5% of cancers of the female genital tract. Though little is known about the genetic features of these tumors, the Fragile Histidine Triad (FHIT) and High Mobility Group AT-hook 2 (HMGA2) genes were found deregulated. We wanted to gain more knowledge about the expression of HMGA2-related miRNAs such as miR-30c...

2011
Heba M. S. Ismail Amina M. Medhat Amr M. Karim Nadia I. Zakhary

Fragile histidine triad (FHIT) gene encodes a putative tumour suppressor protein. Loss of Fhit protein in cancer is attributed to different genetic alterations that affect the FHIT gene structure. In this study, we investigated the pattern of homozygous deletion that target the FHIT gene exons 3 to 9 genomic structure in Egyptian breast cancer patients. We have found that 65% (40 out of 62) of ...

Journal: :Cancer research 1997
D T Hendricks R Taylor M Reed M J Birrer

The fragile histidine triad (FHIT) gene, located at 3p14.2, has been shown to be altered in numerous epithelial cancers. Because previous studies have shown a loss of heterozygosity and cytogenetic abnormalities at the 3p region in ovarian, endometrial, and cervical carcinomas, we examined the status of the FHIT gene in 14 ovarian, 8 cervical, and 4 endometrial human cancer cell lines. RNA was ...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1998
R M Gemmill J D West F Boldog N Tanaka L J Robinson D I Smith F Li H A Drabkin

The 3;8 chromosomal translocation, t(3;8)(p14.2;q24.1), was described in a family with classical features of hereditary renal cell carcinoma. Previous studies demonstrated that the 3p14.2 breakpoint interrupts the fragile histidine triad gene (FHIT) in its 5' noncoding region. However, evidence that FHIT is causally related to renal or other malignancies is controversial. We now show that the 8...

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