The AA carried out a immunohistochemical and genetic research on the tumor suppressor protein p53 and H-RAS oncogene in oromaxillofacial neoplasms. The purpose was to verify, by genetic control, the possibility of find the eventual correlations between histopathological overexpression degree (per cent) of the oncogenes and chemoresistance. The study was carried out on 15 cases of squamous cell carcinomas of the oromaxillofacial region, in advanced stage, with equal histopathological grading (G2), underwent neoadjuvant chemotherapy according to the following protocol: Cis-diamonodichloroplatinum (CDDP, 20 mg/mq i.v. days 1,2,3,4,5) and 5Fluorouracil (5-FU 1000mg/mq continous infusion, volumetric pump 2 ml/hour, for five days). The restaging was carried out after three cycles of chemotherapy to value the clinical response. The p53 immunohistochemical study (clone DO-7) showed a pathological overexpression in 9/15 cases; whwreas, the genetic control (PCR method, wild DNA) showed mutations in 5/15 cases, corresponding to, respectively, 95%, 80%, 70% and 95%. The H-RAS immunohistochemical study (AB-1) (clone 235-1.7.1) showed a pathological overexpression in 12/15 cases; the genetic control showed mutations in 9/15 cases, corresponding to, respectively, 90%, 35%, 10%, 20%, 77%, 90%, 85%, 25%, 75%. The response to the neoadjuvant chemotherapic treatment was as follows: 2 partial response (PR) (90%) in 1 K of the cheek (p53 and H-RAS: imm -, gen -) and in 1 K of the soft palate (p53 and H-RAS: imm -, gen -), with global survival (GS) at diagnosis of, respectively, 18 and 15 months. 1 PR (75%) (p53: imm - , gen -; H-Ras: imm 10%, gen -) and 4 PR (55%) (1 – p53: imm 25%, gen -; H-RAS: imm 20%, gen MUT. 2- p53: imm 45%, gen -; H-RAS: imm 90%, gen MUT. 3- p53: imm -, gen -; H-RAS: imm -, gen -. 4- p53: imm -, gen -, H-RAS: imm 30%, gen -) in 5 K of the gum, with GS of, respectively, 10,6,8,9 and 8 months. 2 objective improvements (OI) in, respectively, 1 K of the floor of the mouth (p53: imm 15%, gen -; H-RAS: imm 37%, gen -) and 1 K of the gum (p53: imm -, gen -; H-RAS: imm 10%, gen MUT), with GS of, respectively, 5 and 6 months. 3 Stability of disease (S) in 2 K of the tongue (1- p53: imm 70%, gen MUT; H-RAS: imm 35%, gen MUT. 2- p53: imm 25%, gen -; H-RAS: imm 25%, gen MUT) and 1 K of the gum (p53: imm 45%, gen MUT; H-RAS: imm 85%, gen MUT), with GS of, respectively, 10,7 and 7 months. 3 Progressione (P) in 2 K of the floor of the mouth (1- p53: imm 95%, gen MUT; H-RAS: imm 90%, gen MUT. 2- p53: imm 80%, gen MUT; H-RAS: imm 75%, gen MUT) and in 1 K of the cheek (p53: imm 95%, gen MUT; H-RAS: imm 77%, gen MUT), with GS of, respectively, 8,8 and 6 months. The study showed a degree of correlation between genetic analysis and immunohistochemical investigation of, respectively, 73.3% of cases for the p53 and of 80% of cases for the H-RAS (Chi-Square Test: p = 0.3089).

P53 and H-RAS immunohistochemical and genetic investigation in maxillofacial tumours

CUTILLI, Tommaso;
1997

Abstract

The AA carried out a immunohistochemical and genetic research on the tumor suppressor protein p53 and H-RAS oncogene in oromaxillofacial neoplasms. The purpose was to verify, by genetic control, the possibility of find the eventual correlations between histopathological overexpression degree (per cent) of the oncogenes and chemoresistance. The study was carried out on 15 cases of squamous cell carcinomas of the oromaxillofacial region, in advanced stage, with equal histopathological grading (G2), underwent neoadjuvant chemotherapy according to the following protocol: Cis-diamonodichloroplatinum (CDDP, 20 mg/mq i.v. days 1,2,3,4,5) and 5Fluorouracil (5-FU 1000mg/mq continous infusion, volumetric pump 2 ml/hour, for five days). The restaging was carried out after three cycles of chemotherapy to value the clinical response. The p53 immunohistochemical study (clone DO-7) showed a pathological overexpression in 9/15 cases; whwreas, the genetic control (PCR method, wild DNA) showed mutations in 5/15 cases, corresponding to, respectively, 95%, 80%, 70% and 95%. The H-RAS immunohistochemical study (AB-1) (clone 235-1.7.1) showed a pathological overexpression in 12/15 cases; the genetic control showed mutations in 9/15 cases, corresponding to, respectively, 90%, 35%, 10%, 20%, 77%, 90%, 85%, 25%, 75%. The response to the neoadjuvant chemotherapic treatment was as follows: 2 partial response (PR) (90%) in 1 K of the cheek (p53 and H-RAS: imm -, gen -) and in 1 K of the soft palate (p53 and H-RAS: imm -, gen -), with global survival (GS) at diagnosis of, respectively, 18 and 15 months. 1 PR (75%) (p53: imm - , gen -; H-Ras: imm 10%, gen -) and 4 PR (55%) (1 – p53: imm 25%, gen -; H-RAS: imm 20%, gen MUT. 2- p53: imm 45%, gen -; H-RAS: imm 90%, gen MUT. 3- p53: imm -, gen -; H-RAS: imm -, gen -. 4- p53: imm -, gen -, H-RAS: imm 30%, gen -) in 5 K of the gum, with GS of, respectively, 10,6,8,9 and 8 months. 2 objective improvements (OI) in, respectively, 1 K of the floor of the mouth (p53: imm 15%, gen -; H-RAS: imm 37%, gen -) and 1 K of the gum (p53: imm -, gen -; H-RAS: imm 10%, gen MUT), with GS of, respectively, 5 and 6 months. 3 Stability of disease (S) in 2 K of the tongue (1- p53: imm 70%, gen MUT; H-RAS: imm 35%, gen MUT. 2- p53: imm 25%, gen -; H-RAS: imm 25%, gen MUT) and 1 K of the gum (p53: imm 45%, gen MUT; H-RAS: imm 85%, gen MUT), with GS of, respectively, 10,7 and 7 months. 3 Progressione (P) in 2 K of the floor of the mouth (1- p53: imm 95%, gen MUT; H-RAS: imm 90%, gen MUT. 2- p53: imm 80%, gen MUT; H-RAS: imm 75%, gen MUT) and in 1 K of the cheek (p53: imm 95%, gen MUT; H-RAS: imm 77%, gen MUT), with GS of, respectively, 8,8 and 6 months. The study showed a degree of correlation between genetic analysis and immunohistochemical investigation of, respectively, 73.3% of cases for the p53 and of 80% of cases for the H-RAS (Chi-Square Test: p = 0.3089).
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11697/12256
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