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Previously, we evaluated the effect of trichostatin A (TSA) on the expression of DNA methyltransferase 1 (DNMT1) in Hepatocellular Carcinoma (HCC). Fragile histidine triad (FHIT) and WW domain-containing oxidoreductase (WWOX) are two of the most common down-regulated genes in many cancers located on chromosome 3p14.2 and 16q23.3-24.1 respectively. The aim of the current study was to assess the effect of TSA on these genes expression, cell growth, and apoptosis in HCC WCH 17 cell. The cells were seeded and treated with TSA at different times. Then, MTT assay, flow cytometry, and qRT-PCR were achieved to determine viability, apoptosis and gene expression respectively. Cell growth was significantly inhibited, 92 to 36% after 24 h, 86 to 28% after 48 h, and 78 to 24% after 72 h. The results of flow cytometry confirmed that TSA increased apoptosis compared to the control group, the apoptosis percentage increased to 12%, 16%, and 18% in comparison to control groups (2%). Significant up-regulation of the genes was observed in all treated groups. We concluded that re-expression of silenced WWOX and FHIT genes could be achieved by TSA resulting in cell growth inhibition and apoptosis induction in WCH 17 cell.
Subject(s)
Apoptosis/physiology , Carcinoma, Hepatocellular/pathology , WW Domain-Containing Oxidoreductase , Growth/physiology , Chromosomes/classification , Flow Cytometry/instrumentation , Neoplasms/classificationABSTRACT
Objective To investigate the expression of FHIT,WWOX and MDR1 gene in nasopharyngeal carcinoma and FHIT and WWOX mechanism of inactivation.Methods Real-time PCR was used to test FHIT,WWOX and MDR1 gene′s mRNA expression in 89 nasopharyngeal carcinoma patients (experimental group) and 61 inflammatory patients (control group).Q-MSP was used to test the FHIT and WWOX promoter methylation status.Denatured polyacrylamide gel electrophoresis was used to test the LOH of FHIT and WWOX gene.Results (1)The three genes′ mRNA expression were different between experimental group and control group (P<0.05).After grouped according to the histological type and clinical stages,the expression of FHIT and WWOX mRNA between the patients with serious illness or poorly differentiated squamous cell carcinoma and mild cases or highly differentiated squamous cell carcinoma were significantly different in the experimental group,the difference is statistically significant (P<0.05)Meanwhile,the FHIT and WWOX mRNA expression had statistical association with the clinical stage and histological type(r=-0.731,P=0.000;r=-0.816,P=0.000;r=-0.626,P=0.000;r=-0.536,P=0.001).The MDR1 mRNA expression was different between poorly and highly differentiated squamous cell carcinoma (P=0.021),which was statistical associated with the histological type (r=-0.697,P<0.001).(2)The degrees of FHIT and WWOX promoter methylation in the experimental group was higher than those in the control group,the difference was statistically significant (P<0.05);Also,the expression of FHIT and WWOX mRNA were closely related to the degree of promoter methylation(r=-0.689,P=0.000;r=-0.594,P=0.000).(3) In the experimental group,there were 39 cases (43.8%) of LOH in the FHIT gene,and 42 cases (47.2%)of the WWOX genes were significantly higher than those in the control group (4.9% and 3.3%),the difference was statistically significant (P<0.05).The FHIT and WWOX gene mRNA were negatively correlated with the loss of heterozygosity(r=-0.239,P=0.049;r=-0.364,P=0.013).Conclusion Promoter methylation is the main reason for the down-regulation of FHIT gene and WWOX gene expression in nasopharyngeal carcinoma patients,which may be the main reason for the occurrence and development of nasopharyngeal carcinoma.The higher expression of MDR 1 mRNA is statistical association with the histological type.
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En Chile, el cáncer es la segunda causa de muerte después de las enfermedades cardiovasculares. Los principales cánceres asociados a muerte en mujeres fueron mama, estómago, vesícula biliar, broncopulmonar y cérvico uterino. Alteraciones de las E-cadherinas han sido relacionadas con varios tipos de cáncer, ya que uno de los principales eventos involucrados con su disfunción es el gatillar la invasión y metástasis del tumor. La inactivación del gen CDH1 ha sido demostrada en el cáncer gástrico difuso y el cáncer de mama lobulillar. Asimismo, la inactivación del gen FHIT parece estar asociado con la progresión a neoplasias más agresivas. Se realizaron determinaciones inmunohistoquímicas (IHQ) en fibroadenomas mamarios y cánceres previamente diagnosticados por RE, RPg y Her2, mostrando positividad en todos los casos. La detección (IHQ) de la expresión de FHIT y E-cadherina en tejidos con patologías benignas y malignizados, puede aportar una importante información diagnóstica y pronóstica en el cáncer de mama.
In Chile, cancer is the second leading cause of death after cardiovascular diseases. The major death-related cancers in women were breast, stomach, gallbladder, lung and cervical cancer. Alterations of E-cadherin have been linked to various cancers, as one of the main events involved in its dysfunction is the trigger of tumor invasion and metastasis. CDH1 gene inactivation has been demonstrated in diffuse gastric cancer and lobular breast cancer. Furthermore, inactivation of the FHIT gene to be associated with progression to more aggressive tumors. Immunohistochemistry (IHC) determinations were performed in fibroadenomas and breast cancers previously diagnosed by ER, PgR and Her2, showing positivity in all cases. Immunohistochemical detection of FHIT and E-cadherin expression in tissues with benign disease and malignant, may provide an important diagnostic and prognostic information in breast cancer.
Subject(s)
Humans , Female , Acid Anhydride Hydrolases/metabolism , Cadherins/metabolism , Breast Neoplasms/diagnosis , Breast Neoplasms/metabolism , Neoplasm Proteins/metabolism , Carcinoma, Ductal, Breast/diagnosis , Carcinoma, Ductal, Breast/metabolism , Carcinoma, Lobular/diagnosis , Carcinoma, Lobular/metabolism , Fibroadenoma/diagnosis , Fibroadenoma/metabolism , ImmunohistochemistryABSTRACT
Objective To study the expression of pl6, FHIT genes in cervical carcinoma and its clinical significance. Methods By immunohistochemistry SP method, the expression of pl6, FHIT in different 118 cases of cervical lesions were detected and the results were analyzed in combination with clinical pathological features. Results Of 118 patients, 15 cases suffered cervicitis;38 cases took place cervical tumor-like changes;65 cases caught cervical cancer. p16 expression rates were 0, 33.3 %, 70.0 %, 87.5 %,and 92.3 % respectively;while FHIT expression rates were 73.3 %, 75.5 %, 60.0 %, 37.5%, and 30.8 % respectively. Compared with cervicitis, pl6 and FHIT expression rates in the cervix tumor-like changes,cervical carcinoma had significant difference (P <0.05). There was positive correlation in protein expression between p16 and FHIT (x2 =33.33, P <0.001). Conclusion Combination of p16, FHIT detection can be used as early diagnostic tool of cervical lesions and cervical cancer markers;meanwhile, the method can serve as a clinical evaluation of tumor biological behavior and prognosis of auxiliary indexes.
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The expressions of Ki67 and FHIT were detected by immunohistochemical staining in 15 cases of adrenocortical carcinoma, 42 cases with adrenocortical adenoma,6 cases of adrenocortical hyperplasia, and 10 cases of normal adrenocortical tissue. The results showed that the highest expression of Ki67 and the lowest expression of FHIT were found in adrenocortical carcinoma. There were significant differences in the Ki67 and FHIT between adrenocortical adenoma and adrenocortical carcinoma ( both P < 0. 05 ). There existed negative correlation between the expressions of Ki67 and FHIT( r=-0. 712, P<0.05 ). Ki67 over-expression and loss of FHIT expression may be involved in the occurrence and development of adrenocortical carcinoma. It is suggested that combined detections of Ki67 and FHIT may have reference significance in the differentiation of adrenocortical adenoma from adrenocortical carcinoma.
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Objective:To explore the effect of radiotherapy on the FHIT protein expression and cell apoptosis of cervical squamous carcinoma and discuss the relationship between FHIT protein expression and cell apoptosis. Methods:Expression of FHIT protein was measured by immunohistochemical method and cell apoptosis was detected by TdT-mediated dUTP terminal nick end labeling (TUNEL) staining in 50 cases of squamous cell cervical carcinoma at ⅡB-ⅢB stages before, during (Dt 10 Gy and Dt 30 Gy), and after radiotherapy. Results:Of the 50 patients, the positive rates of the expression of FHIT protein was 56% at Dt 10 Gy, 68% at Dt 30 Gy, and 84% after radiotherapy, which were significantly increased compared with that before radiotherapy (36%, P<0.05). The positive rates of cell apoptosis was 52% at Dt 10 Gy, 64% at Dt 30 Gy and 78% after radiotherapy, which were significantly elevated compared with that before radiotherapy (28%, P<0.05). In the process of radiotherapy, cell apoptosis was positively related to the expression of FHIT protein (P<0.05). Conclusion:Radiotherapy reinforces the expression of FHIT protein and induces apoptosis cocurrently. FHIT protein has regulatory effects in cell apoptosis induced by radiotherapy.
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Fragile histidine triad (FHIT) gene is an important tumor suppressor gene,in non-small-cell lung cancer and precancerous lesions its protein deficiency is common,reflecting the FHIT gene is changing in lung cancer occurred in the early molecular events.Ferredoxin in the participation of Fhit protein promotes the electron transport function,and promotes the apoptosis of tumour cells in oxidative stress environment.Fhit protein expression combined platinum enhanced the apoptosis of tumor cell response.With early occuring,high-frequency and facilitate detection,the abnormal changes of FHIT/FRA3B,which take great significance to explain the factors,such as race,genetic polymorphism,geography,environment,respiratory diseases in the pathogenesis of lung cancer.
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Objective: To investigate the interaction between fragile histamine triad (FHIT) and protein kinase C alpha (PKCα) in human non-small cell lung cancer tissues. Methods: FHIT and PKCα double positive samples were screened by immunohistochemical staining from 13 human non-small cell lung cancer tissues. Co-immunoprecipitation was performed by using anti-FHIT and anti-PKCα. The immune precipitate was analyzed by SDS-PAGE and Western blot. Results: Immune precipitate staining detection showed that 3 samples out of the 13 cases were double positive for FHIT and PKCα. FHIT protein was present in the immune precipitate of anti-PKCα while there was PKCα in the immune precipitate of anti-FHITmAb. Conclusion: FHIT and PKCα exist as a complex in human non-small cell lung cancer tissues, which will provide a new route for studying the pathogenesis and immunotherapy of human non-small cell lung cancer.
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Objective To investigate the expression of FHIT gene in the 60Co gamma-ray irradiated human lymphocytoblast(AHH-1) cell and the bystander effect cell,and to explore the function of FHIT gene in the bystander effect of ionizing radiation.Method Preparation of bystander effect cell model:after irradiated with different dose of 60Co gamma-ray(0,2,5 Gy),the directly irradiated AHH-1 ceils were collected immediately by centfifugation and co-cultivated with non-irradiated cells in Transwell.forming the bystander effect group P1.In addition,some culture media supernatant of direcfly irradiated cells were transfefred to the non- irradiated cells culture medium,forming the group P2.Then cells were collected at 0,6,12,and 24 h after irradiation and the total RNA and protein were extracted.RT-PcR and Western blot were performed to determine the FHIT mRNA and protein level.respectively.Flow cytometry assay and cell counting were conducted to detect the alteration of cell cycle and cell proliferation,respectively at 0,24 h after irradiation.Results The mRNA level of FHIT gene among control cells,directly irradiated cells and bystander cells showed no obvious difference. while the FHIT protein level of the directly irradiated ceils and bystander cells was siguificandy down-regulated compared with the control cells(F=102.45,P<0.001).Moreover,the directly irradiated cells and bystander cells showed significant G2 phase arrest and obviously inhibited the proliferation ability.Conclusions 2 and 5 Gy of 60Co γ-ray irradiated AHH-1 cells can result in down regulation of the FHIT protein expression,which suggests that FHIT gene is involved in the process of bvstander effect induced by irradiation.
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BACKGROUND: The goal of this study was to investigate the expression of p16, retinoblastoma (Rb) and fragile histidine triad (FHIT) proteins in urothelial carcinomas of the urinary bladder, and to evaluate the relationship between clinicopathlogic parameters and each protein expression level. METHODS: The expression of p16, Rb, and FHIT proteins were studied in 176 patients with urothelial carcinoma of the urinary bladder by immunohistochemistry. RESULTS: The diffuse positive expression of the p16 protein was significantly associated with high grade and advanced tumor depth (p=0.007 and p=0.020). The loss of the Rb protein was significantly associated with old age and disease recurrence (p=0.020 and 0.037). The loss of the FHIT protein was significantly associated with advanced tumor depth (p=0.002). CONCLUSION: Our data suggest that p16 and FHIT proteins may be involved in the progression of urothelial carcinoma. In addition, p16 may be a useful prognostic marker for individual urothelial carcinoma patients.
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OBJECTIVE: The abnormal expression of fragile histidine triad (FHIT) gene has been frequently reported in a variety of epithelial malignancies including cervical carcinoma. Furthermore, in a recent study it was proposed that transcriptional inactivation of FHIT, as a consequence of aberrant 5'-CpG island methylation, plays an important role in the carcinogenesis of human cervical carcinoma. The authors sought to determine whether abnormal FHIT transcription occurs in human cervical carcinoma, and if so, whether this abnormal expression is associated with aberrant 5'-CpG island methylation. In addition, the clinical significance of FHIT inactivation was investigated in Korean women with cervical cancer. METHODS: To examine for abnormal transcripts of the FHIT gene, quantitative RT-PCR, genomic DNA-PCR and nonisotopic RT-PCR-SSCP analysis were performed using the standard method. The methylation status was determined by methylation specific PCR and bisulfite DNA sequencing. RESULTS: The FHIT gene was down-regulated in 15 of 58 (25.9%) cervical carcinomas. FHIT promoter hypermethylation was detected in 15 of 15 (100%) abnormally expression in cervical carcinomas. Bisulfite DNA sequencing confirmed these findings and a significant correlation was found between CpG site hypermethylation and low FHIT expression. However, no significant correlation was found between reduced FHIT expression and clinicopathological characteristics. CONCLUSION: In this study, FHIT inactivation in cervical cancer was found to be strongly correlated with 5'-CpG island hypermethylation rather than a genetic alteration. Furthermore, no significant relation was found between a lack of FHIT expression and the prognostic factors of cervical cancer in our Korean cohort.
Subject(s)
Female , Humans , Cohort Studies , Histidine , Methylation , Polymerase Chain Reaction , Sequence Analysis, DNA , Sulfites , Uterine Cervical NeoplasmsABSTRACT
Objective: To study the effect of the c-myc antisense oligodeoxynucleotide (ASODN) on the proliferation and apoptosis of colon cancer cells with FHIT gene expression. Methods: PRC/CMV vector expressing FHIT gene and empty vector were transfected into human colon cancer SW480 cells by liposome mediation, respectively. Then, c-myc ASODN was transfected into SW480 cells. The FHIT and c-myc proteins were detected by western blotting. The proliferation of SW480 cells was assessed by MTT assay. The apoptosis was determined by AO/EB staining and flow cytometry analysis. Results: Marked expression of FHIT protein was detected in SW480 cells after transfection with PRC/CMV vector. But it was not observed in SW480 cells after transfection with empty vector. The expression of c-myc protein was significantly inhibited in SW480 cells after transfection with c-myc ASODN ( P < 0.01 ). ASODN of c-myc inhibited the proliferation and induced the apoptosis of SW480 cells. However the growth-inhibiting and apoptosis-inducing effect of c-myc ASODN were stronger on FHIT + SW480 cells compared with FHIT - SW480 cells (P < 0.05). Conclusions: The expression of tumor suppressor gene FHIT and down-regulation of oncogene c-myc have stronger anti-tumor efficiency and provides the basis for multiple gene interference therapy.
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OBJECTIVE: This study was to investigate the status of hypermethylation and loss of heterozygosity (LOH) in chromosome 3p tumor-suppressor gene for cervical carcinoma. METHODS: We examined the promoter methylation status of the chromosome 3p gene, fragile histidine triad (FHIT), in 37 samples of cervical squamous cell carcinoma and corresponding noncancerous tissues using a methylation-specific polymerase chain reaction. We also analyzed the 37 paired samples for LOH at two loci on chromosome 3p. RESULTS: Promoter hypermethylation in FHIT was detected in 24% of tumors, whereas no hypermethylation was detected in the corresponding noncancerous tissues. LOH in the regions of FHIT was observed in 10% of informative cases. There were no correlations between LOH and promoter hypermethylation for the gene. FHIT hypermethylation was associated with small tumors and, when adjusted for tumor size, correlated significantly with more frequent lymph node metastasis. CONCLUSION: Promoter hypermethylation and LOH of FHIT gene may play a role in cervical carcinogenesis. In addition, hypermethylation of FHIT may be associated with the status (aggressiveness) of cervical carcinoma.
Subject(s)
Female , Carcinogenesis , Carcinoma, Squamous Cell , Cervix Uteri , Histidine , Loss of Heterozygosity , Lymph Nodes , Methylation , Neoplasm Metastasis , Polymerase Chain ReactionABSTRACT
Objective To investigate the expression and significance of Survivin and Fhit protein in colorectal benign and malignant disease.Methods Test the expression of Survivin and Fhit proteins in 20 cases normal colorectal mucosa,30 cases low grade colorectal intraepithelial lesion,30 cases high grade colorectal intraepithelial lesion and 68 cases colorectal adenocarcinoma by immunohistochemical staining S-P method.Results The unexpression of Survivin in normal colorectal mucosa,postive expression rates of Survivin in low grade colorectal intraepithelial lesion,high grade colorectal intraepithelial lision and colorectal adenocarcinoma were 43.3%,76.7% and 91.2%(P
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Objective To investigate the role of FHIT,cyclinD1,CDK4 in NSCLC.Methods Immunochemical(S-P) was used to determined 81 cases of NSCLC.Results The postive expression rates of FHIT,cyclinD1,CDK4 were significantly different between in NSCLC and in nomal lung tisses(P
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AIM:To construct a recombinant adenovirus carrying Fhit gene,a tumor suppressor in many types of cancer,and to observe its biological function on the proliferation of colon cancer cells.METHODS:Fhit gene was cloned from the fetal liver cDNA library using the PCR method.The PCR product was inserted into the T vector to construct the plasmid pMD18T-Fhit.The Fhit fragment from the pMD18T-Fhit was inserted into the vector ptrack-CMV to construct a shuttle plasmid ptrack-CMV-Fhit.After PmeI digested and linearized process,ptrack-CMV-Fhit was co-transformed into Escherichia coli strain BJ5183 together with the adenovirus backbone vector pAdEasy-1 to generate a recombinant adenovirus plasmid by homologous recombination.The adenovirus plasmid was identified by PacI digestion and transfected into 293A cells to package a recombinant adenovirus which expressed the Fhit protein.Furthermore,the adenovirus rAd-Fhit was infected into colon cancer cells,and the expression of the ectogenic protein was detected by Western blotting.Finally,the proliferation of colon cancer cells was observed in adenovirus-infected cells by the MTT assay.RESULTS:Constructed the recombinant adenovirus encoding Fhit gene and expressed it in colon cancer cells successfully.Detected that the proliferation of colon cancer cells was inhibited obviously in rAd-Fhit-infected cells with comparison to the control groups.CONCLUSION:Fhit may function as a tumor suppressor in colon cancer cells,and the adenovirus-mediated Fhit can be a novel strategy for the colon cancer therapeutics.
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OBJECTIVE: To investigate the expression of fragile histidine triad (FHIT) protein and the possible relationship between FHIT expression and clinicopathological indices in cervical adenocarcinoma. METHODS: FHIT protein expression was examined in 40 cases of cervical adenocarcinoma stage Ia to IIa and 28 cases of corresponding normal endocervical tissue by immunohistochemical method. We analyzed the relationship between the reduction of FHIT protein expression and several prognostic factors such as histological grade, lymph node metastasis, tumor size, cervical invasion depth and parametrial invasion. We used Fisher's exact test for statistical analysis. RESULTS: The FHIT protein expression was positive in 77.5% (31/40) of cervical adenocarcinoma tissue, and reduced its expression in 22.5% (9/40) whereas positive in 100% (28/28) cases of adjacent normal endocervical gland. The FHIT expression was decreased in 14.3% (4/28) of cancers without lymph node metastasis but 55.5% (5/9) of those with metastasis (p=0.023). And the reduction of FHIT expression was found in 34.8% (8/23) of grade II and III cancers and only 6.3% (1/16) of grade I (p=0.056). CONCLUSION: Loss of FHIT protein expression may be associated with metastasis and poor prognosis of cervical adenocarcinoma.
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Adenocarcinoma , Histidine , Immunohistochemistry , Lymph Nodes , Neoplasm Metastasis , PrognosisABSTRACT
Objective To investigate the effect of the exogenous fragile hisdidine triad(FHIT) gene on the proliferation and the apoptosis of cutaneous carcinoma cell line A431,and to explore the mechanism of tumor suppression by the FHIT gene.Methods The plasmids pcDNA3-FHIT and pcDNA3-vector were transfected into the cutaneous carcinoma cell line A431 without FHIT gene expression,and then the transfected cells were screened by G418 and the expression of FHIT was determined by the immunocytochemical staining technique.The effect of FHIT on the growth characteristics of cutaneous carcinoma cell line A431 was observed by MTT,colony forming test and flow cytometry.Results Stable FHIT gene expressing A431 cells were produced,the proliferation activity and colony forming capability of A431FHIT were suppressed,whereas the apoptosis was increased.All these differences between A431-FHIT cells and the two control groups of cutaneous carcinoma cells had statistical significance.Conclusion Transfecting the exogenous FHIT gene into cutaneous carcinoma cells line A431can suppress the proliferation of tumor cells,and can also induce apoptosis and cell cycle arrest.
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OBJECTIVE: This study was performed to determine the exact pattern of FHIT expression of the cervical carcinoma cell per se by microdissection and to investigate the clinical significance of the FHIT alteration in cervical cancer. METHODS: RT-PCR for FHIT transcript was performed in 18 cervical cancer tissues. Microdissection was performed using laser capture microdissection device and RNA was extracted by RT-nested PCR. PCR products were compared with known aberrant FHIT transcripts. Immunohistochemical analysis was performed to evaluate correlation between the altered expression of FHIT protein and clinical parameters. RESULTS: Six different size of aberrant FHIT transcripts were observed in cervical cancer tissues. Six of 18 (33.3%) cervical cancer sections exhibited full-length normal FHIT transcript only. Aberrant FHIT transcripts with normal one were observed in 9 (50%) and only aberrant transcripts in 3 (16.7%) frozen sections. Five normal cervical tissues expressed only a normal FHIT transcript. The sequences of the 6 different sizes of aberrant FHIT transcripts showed (1) deletion of exons 4-8, (2) deletion of exons 4-7, (3) deletion of exons 5-8, (4) deletion of exons 5-7, (5) deletion of exons 5-7 and insertion of intronic sequences, 153 bp, (6) deletion of exons 5-7 and insertion of intronic sequences, 84 bp. Microdissection of paired cervical tumor and normal stroma showed expression of aberrant FHIT transcripts only in tumor tissues. CONCLUSION: Aberrant FHIT expression was observed frequently in cervical carcinoma and they were observed mainly in cervical cancer cells by microdissection, but not in normal stromal cells. However, absence of FHIT expression did not correlate with clinical prognostic factors in cervical carcinoma.
Subject(s)
Exons , Frozen Sections , Introns , Laser Capture Microdissection , Microdissection , Polymerase Chain Reaction , RNA , Stromal Cells , Uterine Cervical NeoplasmsABSTRACT
BACKGROUND: BCAR1/p130Cas protein is the human homologue of rat p130Cas protein, and it is a docking protein involved in the intracellular signaling pathways. This protein also causes the proliferating human breast cancer cells to be resistant to antiestrogen drugs. The fragile histidine triad (FHIT) protein is presumed to have a tumor suppressor function in a number of human tumors. The aim of this study was to investigate expressions of p130Cas and FHIT in breast carcinomas and to evaluate their relationship with the clinicopathological prognostic factors. METHODS: A total of 93 cases of invasive breast carcinomas was retrospectively reviewed. The expressions of p130Cas and FHIT were examined by immunohistochemical methods. RESULTS: p130Cas expression was observed in all breast carcinomas: p130Cas immunoreactivity was strongly positive in 39 cases (41.9%), moderately positive in 49 cases (52.7%) and weakly positive in 5 cases (5.4%) of 93 cases. It was statistically correlated with the p53 (p=0.035) and c-erbB-2 (p=0.024) expressions. The FHIT protein expression was markedly reduced or completely negative in 59 cases (63.4%), but it was not correlated with the clinicopathological prognostic factors. There was no significant correlation between p130Cas and FHIT expressions. CONCLUSIONS: This study seems to provide meager information on whether these proteins may be useful prognostic factors, and so this topic needs further study.