Apoptosis in multiple primary cancers of oral cavity, pharynx and larynx

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Background : Head and neck cancers are vulnerable to stimulation by various toxic substances because anatomically, their initiation sites are the pathways of food or respiration. It is considered that genetic alteration by such stimulation may cause cancer, and that when multiple cancers, such as cases of multiple primary cancer, occur in the living body, gene mutation may be accumulated by frequent exposure to carcinogenic substance. The leading cause of death in cases with head and neck cancer is the underlying disease, and the second is multiple primary cancer. This means that early discovery and control of the multiple primary cancer, as well as control of the underlying disease, is important. We therefore considered that discovery of clinical factors and molecular biological factors characteristic to cases with multiple primary cancer could lead to prognostic improvement in cases with head and neck cancer. Methods; 62 cases of multiple primary cancer among the 403 cases of oral, pharyngeal and laryngeal cancer who had undergone primary treatment at the department of otolaryngology, Kinki University from 1990 to 2002 were targeted. First, it was examined whether or not smoking or drinking may induce development of multiple primary cancer, by comparison of the Brinkman index and Sake index. We examined the expressions of p53, bcl-2, EGFR protein in relation to apoptosis by immunohistochemical staining, the p53 gene mutation by PCR-SSCP, and the degree of apoptosis by TUNEL staining. Results : The Brinkman index of cases with multiple primary cancer was significantly higher than that of cases with single cancer in oral and oropharyngeal cancer. The Sake index of cases with multiple primary cancer was significantly higher than that of cases with single cancer in oral cancer.Single cancer showed many p53 positive cases and bcl-2 negative cases but was not significant for multiple primary cancer. Excessive exposure to smoking and drinking tended to increase the rate of p53 gene mutation. Five-year disease free survival rate of bcl-2 positive cases showed a significantly bad prognosis (p<0.005). The mean TUNEL labeling index (below to TLI) of multiple primary cancer and single cancer were 1.8±1.6, 2.3±2.5. The mean TLI between multiple primary cancer and single cancer was not significant.The mean TLI of EGFR positive cases and negative cases were 1.1±0.7%, 2.4±1.7%. The mean TLI of EGFR positive cases was significantly lower (p<0.05).Conclusions : Many patients with multiple primary cancer had excessive exposure to smoking or drinking, and thus tended to be exposed to stimulation by various toxic substances. Heavy smoker and drinker often showed p53 gene mutation. In the cases with multiple primary cancer it was assumed that greater gene mutation might be accumulated. Therefore, it was assumed that decreased apoptosis in the multiple primary cancer might be caused by the strong proliferative potential of cancer cells in the multiple primary cancer resulting in a low ratio of cells dying by apoptosis.
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Apoptosis in multiple primary cancers of oral cavity, pharynx and larynx

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