Comparison of C-Myc Oncogene Expression in Benign and Malignant Odontogenic Tumors.

Aims: The aim of this study was to comparatively investigate the expression of cMyc oncoprotein in benign and malignant odontogenic tumors and also to assess its potential prognostic role in these conditions. Study Design: The cMyc protein is a nuclear transcription factor which centrally regulates cell proliferation, arrest, cell differentiation and cell death. Ameloblastomas are benign uncommon tumors. They are the most frequently encountered odontogenic tumors arising from the epithelium of the odontogenic apparatus. They rarely have the potentiality to turn malignant in the form of either malignant ameloblastoma or ameloblastic carcinoma. The expression of cMyc oncogene products were detected in normal tissue and cancer cells. It is related to the proliferation of odontogenic epithelial cells and its degree of differentiation. Materials and Methods: Eleven cases of amelobastomas were included in this study. Six cases were benign and five cases were malignant ameloblastomas. All the specimens were retrieved from Alexandria University, Maxillofacial and Oral Pathology department. Biopsy specimens were prepared, fixed in paraffin wax and processed for immunohistochemical staining using the standard streptavidin Biotin peroxidase complex method, and the primary monoclonal antibody specific for cMyc. Results: Results revealed strong staining reaction of the nucleus and cytoplasm of the peripheral columnar cells and to a lesser extent in the polyhedral cells. The intensity of the reaction was stronger in malignant cases and mild in the benign cases. Conclusion: Immunoreactivity of the cMyc oncogene was directly proportional with the degree of malignancy and was a valuable marker for elucidating the mode of growth and development of odontogenic epithelial cells from the pathological point of view.

The Expression of c-met, c-Ha-ras and c-myc Oncogene in Thyroid Papillary Cancer and Prognostic Factor

BACKGROUND: Many oncogenes have been recently identified in human thyroid carcinomas, but the molecular mechanisms that lead to thyroid neoplasia are not well understood. To assess whether oncogene- encoded proteins can be regarded as useful prognostic indicators, we have evaluated the expressions of c-met, c-Ha-ras, c-myc oncogenes in patients with papillary thyroid cancer (PTC) in relation to the prog nostic factors. METHODS: We used immunohistochemistry to examine the expressions of c-met, c-Ha-ras, and c-myc oncogenes in 54 paraffin-embedded PTC specimens. We measured both the proportion (scale of 0-3) and the intensity (scale of 0-3) of the stained cells and then calculated the staining index (scale of 0-9) by multiplying the proportion and the intensity scores. The staining index was thus categorized as negative/low (staining index 5). The considered prognostic factors were age (over 45), tumor size (over 1.5 cm), lymph node metastasis, capsular invasion, vascular invasion, and distant metastasis. RESULTS: 1) The rates of expression of c-met, c-Ha-ras, c-myc oncogenes were 100%, 81.5%, and 70.3% in papillary thyroid cancer and 100%, 30%, and 10% in benign tumors and 60%, 10%, and 0% in normal thyroid tissue, respectively. The expression of c-met oncogene was restricted to the membrane the expression of c-Ha-ras was stromal in 95.5% of the specimens, and that of c-myc was stromal in 94.7%. 2) High expression (staining index >5) of c-met, c-Ha-ras and c-myc were not associated with the prognostic factors such as age, tumor size, lymph node metastasis, capsular invasion, vascular invasion and distant metastasis. CONCLUSION: Although the rates of expression of c-met, c-Ha-ras, and c-myc oncogenes were high in papillary carcinomas (100%, 81.5%, and 70.3%, respectively), there was no relationship between the high expression rates of the oncogenes and prognostic factors.

Correlation between Amplification of c-myc Oncogene and Histophthologic Prognostic Factors in Endomentrial Cancer / 대한부인종양콜포스코피학회잡지

The c-myc oncogene encodes a 62,000 daltons nuclear transcriptional factor and is believed to regulate cellular proliferation. Although its mechanism of action is incompletely understood, oncogene amplification followed by increased expression and ultimately the production of large amounts of specific protein seem to play a central role in the oncogene mediated progression of certain solid tumor, including breast and uterine cervical cancer. We used an Southern blot hybridization to explore the relationship between c-myc onco-gene and prognostic factors of endometrial cancer and analysed the tissues from the 21 patients with endometrial cancer and 4 control cases. Six of 21 patients (29%) with endometrial cancer had at least two fold gene amplification and none of the four normal controls revealed amplified sequences. Three of the four poorly differentiated specimens (75%) demonstrated c-myc gene amplification, whereas only three of 17 low and moderately differentiated specimens (17.6%) showed c-myc oncogene amplification. Thus tumor grade was significantly associated with c-myc oncogene amplification (p=0.002). The other known prognostic factors including stage, histologic cell type, myometrial invasion and lymph node metastases showed no statistically significant association with c-myc oncogene amplification, although they were correlated with increased amplification rate of c-myc oncogene. A much larger number of patients must be studied to determine the prognostic significance of c-myc oncogene amplification in endometrial carcinoma, although these preliminary data suggest that it may predict biologically aggressive behavior of endometrial carcinoma.

Oncogene expressions detected by in situ hybridization of squamous metaplasia, dysplasia and primary lung cancer in human

In order to elucidate the dynamic changes of oncogene expression in the sequential cascade of squamous metaplasia, dysplasia, and squamous cell carcinoma of the bronchial epithelium, hybridization in situ was employed with a biotinylated oncogene probe. The expression of c-myc was localized exclusively in nuclei. While normal bronchial epithelium revealed no discernible clumps of c-myc grains, except occasional grains less than 3 per cell, squamous metaplasia showed increased number of grains and a few clusters of c-myc grains. In dysplasia, c-myc expression was more intensive than in squamous metaplasia. Approximately, 1/3 to 2/3 of tumor cell populations of squamous cell carcinomas of the lung revealed tremendously increased c-myc expression. In addition clumpy grains of c-myc in squamous cell carcinoma appeared more frequently than in squamous metaplasia or dysplasia. The c-myc expression was found to vary between different samples and within each cancer, and not all cancer cells expressed c-myc. These data indicate that c-myc oncogene plays it's role on reprogramming for growth control of cell populations particularly in multistage carcinogenesis and progression of lung cancer. These dynamic alterations of c-myc expression suggest that neoplastic transformation may occur conceivably at the dysplastic phase eventually resulting in carcinoma in situ. This means, in turn, squamous dysplasia is a putative precancerous lesion of the human lung.