Loss of heterozygosity and loss of expression of the DCC gene in gastric cancer.

نویسندگان

  • D C Fang
  • J R Jass
  • D X Wang
چکیده

AIM To investigate the role of DCC gene inactivation in the development and progression of gastric cancer. METHODS Loss of heterozygosity and loss of expression of the DCC gene was studied in 51 surgical specimens of gastric cancer using detection based on polymerase chain reaction. RESULTS Loss of heterozygosity was found in 35.3% (18 of 51) of specimens and was detected more often in stage III and IV (50%) than in stage I and II cancers (14.3%) (p < 0.05). Occurrence of loss of heterozygosity was not correlated with histological type, tumour size, depth of invasion, or lymph node metastasis. Loss of expression was found in 49% of cases (25 of 51). Loss of expression was not significantly correlated with any clinicopathological variable. CONCLUSIONS Loss of heterozygosity and loss of expression of the DCC gene are often encountered in gastric cancer. Loss of heterozygosity of the DCC gene is a late event and associated with malignant progression.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Putative Tumor Suppressor Gene Frequent Loss of Expression and Loss of Heterozygosity of the Updated Version

The putative tumor suppressor gene DCC has been shown to be fre quently lost or expressed at low levels in coloréela!,gastric, pancreatic, and esophageal carcinomas. In the present study, the DCC gene and its mRNA expression in human and rat prostatic carcinoma cells as well as in prostatic carcinoma tissues were examined by reverse transcriptase-polymerase chain reaction and polymerase chain ...

متن کامل

Infrequent loss of heterozygosity of APC/MCC and DCC genes in gastric cancer showing DNA microsatellite instability.

AIM To investigate the role of DNA microsatellite instability (MSI) in gastric carcinogenesis by studying associations between MSI status, clinicopathological features, and loss of genetic loci. METHODS Six microsatellite loci and loss of heterozygosity at APC, DCC, and MCC were analysed by polymerase chain reaction based methods in 53 cases of advanced gastric cancer. RESULTS MSI was obser...

متن کامل

P53 and Rb tumor suppressor gene alterations in gastric cancer.

UNLABELLED Inactivation of tumor suppressor genes has been frequently observed in gastric carcinogenesis. Our purpose was to study the involvement of p53, APC, DCC, and Rb genes in gastric carcinoma. METHOD Loss of heterozygosity of the p53, APC, DCC and Rb genes was studied in 22 gastric cancer tissues using polymerase chain reaction; single-strand conformation polymorphism of the p53 gene e...

متن کامل

Evaluation of the Prognostic Value and TRIP13 gene Expression in Gastric Cancer

Introduction: Gastric cancer is a major public health issue worldwide. The factors that initiate cancer are not well understood, however aberrant expression of genes is associated with this cancer. TRIP13 plays pivotal roles in meiotic recombination, DNA repair, and cell cycle progression. An increasing body of evidence suggests that TRIP13 may possess functions other than meiosis and mitosis, ...

متن کامل

Increased Expression of CYP2E1 Gene in Gastric Cancer May be a Molecular Marker for Mazandaran Province Population

Cytochrome P450 2E1 (CYP2E1) enzyme metabolically activates a large number of low molecular mass xenobiotics probably involved in gastric cancer incidence through activation of procarcinogens. North of Iran is amongst high incidence rate areas of gastric carcinoma where environmental carcinogenic compounds, including agricultural pesticides, are massively used. In this report, we quantitatively...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Journal of clinical pathology

دوره 51 8  شماره 

صفحات  -

تاریخ انتشار 1998