allelic loss of the FHIT gene may be involved in carcinogenesis in the peripheral lung of patients with IPF.

reduced Fhit protein expression and loss of heterozygosity at FHIT gene in tumours from smoking and asbestos-exposed lung cancer patients

Restoration of fragile histidine triad (FHIT) expression induces apoptosis and suppresses tumorigenicity in lung and cervical cancer cell lines

The result of this study suggests that FHIT gene may be a tumor suppressor gene in human lung cancer cells.

MYCL1, FHIT, SPARC, p16(INK4) and TP53 genes associated to lung cancer in idiopathic pulmoary fibrosis

FHIT may cooperate with p16 gene for the development of squamous cell carcinoma of lung in individuals exposed to tobacco smoke.

FHIT hypermethylation analys9s could enrich a panel of DNA methylation markers in breast, lung and bladder cancer.

Frequent FHIT gene loss of heterozygosity is associated with human papillomavirus-infected non-smoking female lung cancer

Reintroduction of exogeneous FHIT can obviously suppress the proliferation and tumorigenicity in human lung cancer cell line A549 and induce apoptosis.

paclitaxel-induced apoptosis enhanced by FHIT expression in lung cancer cells might be associated with modulation of Bcl-2-caspase signaling

Loss of FHIT expression and methylation of the FHIT gene promoter is associated with advanced lung cancer

FHIT induces apoptosis through a sequential activation of death receptor-mediated pro-apoptotic signaling pathways in human non-small-cell lung cancer cells

Deletion and abnormal expression of FHIT gene are common in Yunnan tin miners and non-miners with lung cancer.

The polymorphisms and haplotypes in the FHIT gene are not associated with lung cancer in the Korean population.

Microsatellite instability and loss of heterozygosity in FHIT gene could be detected in sputum of lung cancer patients.

FHIT-/p53+ status might be a biological variable influencing the efficacy of carboplatin/gemcitabine treatment in non-small cell lung cancer.

mutation of the FHIT gene is assopciated with lung cancer.

Data show that FHIT expression in lung cancer cells is protective from TRAIL-induced apoptosis, and that FHIT exerts this protective effect downstream of TRAIL-receptors and likely requires its dinucleoside-triphosphate hydrolase activity.

5'-CpG island hypermethylation of the FHIT gene is associated with lung cancer.

In 22 lung cancer patients with negative histology and cytology at initial bronchoscopy, FHIT and p16 mRNA loss was detected in 40.9% (9/22) and 36.4% (8/22) cases, respectively.

FHIT loss was observed in 64% of non-small-cell lung carcinoma patients and was significantly associated with squamous cell carcinoma and poor tumor grade.

Fhit delocalizes annexin A4 from plasma membrane to cytosol and sensitizes lung cancer cells to paclitaxel.

the decrease in the expression of miR-29b by c-Myc may be responsible for FHIT loss-mediated tumor aggressiveness and for poor outcome in non-small cell lung cancer.

methylation of FHIT is a useful biomarker of biologically aggressive disease in patients with non-small cell lung carcinomas

the induction of Slug expression by AKT/NF-kappaB signaling pathway due to FHIT loss not only promotes tumor invasion, but also confers cisplatin resistance due to Slug-mediated PUMA reduction in lung cancer cells.

The total frequency of FHIT, RASSF1A and RARbeta gene methylation was significantly higher in lung cancer.

we demonstrate that the expression pattern of FHIT and miR-30c is inversely correlated with that of MTDH and HMGA2 in normal tissue, non-metastatic and metastatic tumors, serving as a potential biomarker for metastasis in lung cancer.

FHIT hypermethylation, which induces the inactivation of FHIT gene, plays an important role in the carcinogenesis and clinical outcome and may serve as a potential drug target of non-small cell lung cancer.

FHIT hypermethylation, which induces the inactivation of FHIT gene, plays an important role in the carcinogenesis and clinical outcome and may serve as a potential diagnostic marker and drug target of non-small-cell lung carcinoma

Study indicate that the observed level of FHIT promoter methylation was not enough to suppress gene expression in non-small cell lung cancer (NSCLC). Lack of negative correlation between FHIT expression and methylation, or positive correlation between gene expression and immunoexpression suggest the role of another molecular mechanisms regulating FHIT expression on mRNA and protein levels in NSCLC patients.

High methylation in the FHIT promoter region is associated with lung cancer.

Review/Meta-analysis: significant difference in FHIT gene promoter methylation status in non-small cell lung carcinoma patients was found in Asians but not in Caucasian population.

This literature review aims to clarify the involvement of the FHIT gene in carcinogenesis, tumor progression and clinical outcome in prevalent solid malignancies, such as breast, lung, cervical, esophageal, gastric and colorectal cancers