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Ann Thorac Surg 1996;61:1476
© 1996 The Society of Thoracic Surgeons
DR DANIEL L. MILLER (Louisville, KY): That was an excellent presentation. The data presented will be very important for years to come.
The question I have is in regard to the 58 patients who had greater than three markers present. I would like to know, was there any correlation between the number of markers present in these patients and the mode of cancer death such as local recurrent disease versus distant recurrent disease, and if so, are there any future plans to institute specific adjuvant therapy in regard to the markers and number of markers found?
DR HARPOLE: Thank you, Dr Miller. The minimal follow-up period on each patient was more than 5 years. For patients who had cancer recurrence, 85% of the recurrences were located at a distant site. The local recurrence rate was insignificant. There was no association between recurrence and type of lung resection. These data are consistent with previously reported retrospective series, and make one wonder if some sort of adjuvant therapy may be useful. This project concerns the initial four markers out of a series of 12 that we are analyzing in these 275 patients. The molecular biologic substaging is irrespective of routine histopathologic factors, and is being used to categorize patients with respect to risk of recurrence. The present information on four distinct markers demonstrates a survival disadvantage of patients who expressed two or more of the four markers compared with those who expressed none or one marker. If this large difference in survival continues once the entire data set has been finished, we would probably treat patients who had two or more markers expressed. Most importantly, these data need to be reproduced in a prospective, multiinstitutional setting.
DR HARVEY I. PASS (Bethesda, MD): Is the p53 antibody that you used a mutant p53 antibody or normal?
DR HARPOLE: The antibody used for p53 stains mutant p53 and is a monoclonal antibody PAB 1801.
DR PASS: You mentioned histology briefly, but as you well know, many of these markers, including ras p53, reflect certain histologies. Have you stratified your data with regard to histology?
DR HARPOLE: We found no difference in survival by the histologic subtypes of non--small cell lung cancer for the entire population. However, there were differences in the expression of the molecular biologic markers with respect to histology. HER-2/neu was expressed more commonly in squamous cell carcinoma, and in fact, we had only 17 HER-2/neu positive adenocarcinomas out of more than 100 specimens. p53 was equally expressed among the histologic groups at approximately 38%. KI-67 proliferative index was higher in large cell undifferentiated tumors. Although we examined intercorrelations between molecular biologic factors and routine histopathologic factors, only three were obvious. Angiogenesis and vascular invasion were highly correlated, and high KI-67 proliferative index and high mitotic index were significantly associated as well as high KI-67 index with poorly differentiated tumors.
DR PASS: 1980 to 1988 covers a long period of time in which there are different staging systems. Is the stage I definition that you are using here only patients who had no N1 disease?
DR HARPOLE: The 275 patients were staged by the new international staging system. They were all T1 or T2 N0 patients, having undergone mediastinal and hilar lymph node sampling.
DR PASS: What is the correlation between in situ T1 and T2 with regard to these markers, specifically angiogenesis?
DR HARPOLE: We were quite interested in the angiogenesis scores from these patients. Data from breast cancer demonstrate that high angiogenesis scores can be seen in the earliest stage cancer, (ie, in situ lesions). One would expect the same findings in lung cancer. We had no in situ lesions from this data set, the smallest being slightly larger than 1 cm in diameter. As you know, the recurrence for T1 N0 non--small cell lung cancers approaches 20% in most retrospective series. This supports the presence of angiogenesis in all sizes of tumors.
Related Article
Ann. Thorac. Surg. 1996 61: 1470-1476.
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