392 Abstracts/Lung Gmcer I4 (1996) 377-408

Relations between chest CT and pathologic tindings in pulmonary infarction associated with lung cancer YoshidaN, SugitaH, Nakajima Y, Nakano H, KawabataY. Department of Inrernal Medicine, Japan Anti-Tuberculosis Association, Fukujuji Hospital, 3-I-24, Mofsuyama, Kiyose, Tokyo 204. Jpn J ‘&xac Dis 1995;33: 1064 72.

Cheat radiographic (mainly CT), and pathological findings in puho~fy infarction associated with lung cancer were studied to obtain information usetiil for the interpretation of CT Endings, and to help determine the cause of infarction. Sixteen cases of lung infarction were chosen from among 518 cases of lung cancer. All patients were operated oo heiweeo January 1980 and December 1990. Sixteen surgical cases and one autopsy case all with evidence of lung cancer and infarction were chosen. There were 13 men and 4 women with a mean age of 56 years. Adenocarcinoma was found in 8 cases, squamous cell carcinoma in 6, adenosquamous carcinoma io 2, and small cell carcinoma in 1. Chest radiographs and CT revealed infarction shadows in 8 of the 16 cases. Typical CT Endings for pulmonary infarction wenzshadows located in the same lobe and periphery as the cancer; illdefined, lo-25 nun nodular shadows; and lesions located both in the subpleural zone and apart from the pleura. Lesion counts in each area were about the same. Observation of ooe patient for 2 months revealed a decrease in the size of the nodular shadows and clarification of their margins. In most cases, centrally extended cancer resulted in vascular stenosis and infarction.

Genetic analysis by fluorescence in situ hybridization of lung cancer cells obtained by bronchial brushing Uemura Y, Kobayashi M, Muneishi H, Urata T, Hakoda E, Tanaka Y et al, l?drd Dept. of Internal Medicine, Kochi Medical School, Kochi 783. Jpo J Tborac Dis 1995;33: 1052-7.

Fluorescence in situ hybridization was done with specimens obtained by bronchial brushing From 25 patients with abnormal lung shadows. A satellite DNA prohe, specific for chromosome 11, was used to detect numerical chromosomeaberrations in tumor cell nuclei. Normal diploid human lymphocytenuclei, which servedascootrol, had twosignal spots in 99.6 96 of the nuclei in response to the chromosome 11 probe. The most frequent signal spots in class V cells (Case 1-7) ranged from 3 to 5, followed by 6 to 8, regardless of histopathological findings of lung cancer. In class I cells (cases E-11) the signal appearance was similar to that in class V cells. The disease in patients from whom class I cells were obtained was found to be malignant by other diagnostic procedures performed afterward. The abnormalities in cases 13 25 were diagnosed as non-malignant by brush cytology, and clinical course showed a little more than 3 spots. These data indicate that fluorescence in situ hybridization with specimens obtained by broochial brushing can be useful for detecting numerical chromosome abnormalities and can aid in the rapid diagnosis of lung cancer.

Enhanced apoptosis predicts shortened survival in non-small cell lung carcinoma Tormanen U, Eerola A-K, Ramio P, Vahakangas K, Soini Y, Sormunen R et al. Dqarrmenr of Pathology. University of Oulu, Kajaanintie 520. FIN-90220 Oulu. Cancer Res 1995;55:5595-602.

This study was undertake0 to determine the extent of apoptosis in lung carcinoma and to evaluate it as a prognostic marker. A series of 75 lung carcinomas (47 squamouscell carcinomas, 24 adenocarcinomas, 3 small cell carcinomas, and 1 large cell carcinoma) was analyzed for the extent ofapoptosis by using the 3’ end-labeling method of DNA in tissue sections. Apoptosis was correlated with the rate of cell proliferation, the immunohistochemically detectable p53 and bcl-2, the extent of tumor necrosis, and the survival data. The end-labeling method allowed a preciseevaluationoftheextent ofapoptosis. In tumor tissue, thenumber

of apoptotic bodies was roughly 2-fold greater than the number of apoptotic cells, whereas in oonneoplastic control tissues, the ratio was 1: 1. The apoptotic indexes (percentages of apoptotic cells and bodies among tumor cells) were slightly higher in adeoocarciooma than in squamous cell carcinoma. There was no associatioo between the extent of apoptosis and the expression of proliferating cell nuclear antigen or ~53. On the other hand, tumor necrosis correlated significantly with proliferating cell nuclear antigen and p53 positivity (P = O.ooo25 and 0.00087, respectively). Surprisingly, the extent of apoptosis was also found to be independent of the expression of bcl-2. Patients with apoptotic indexes greater than 1.5 96 had significantly shorter survival time than patients with apoptotic indexes equal to 1.50% or less (P < 0.01 by log rank). Aberrant p53 positivity also predicted a poor prognosis (p < 0.002 by log rank). By multivariateanalysis, enhanced apoptosis showed a 1.9-fold risk (P = 0.04), and p53 positivity showed a 2.3-fold risk (P = 0.005) for a shortened survival. We conclude that both enhanced apoptosis and p53 positivity are independeot prognostic markers in OOO-small cell lung carcinoma, predicting shortened survival time of the patients.

Disease monitoring by the tumour maskers Cyfra 21.1 and TPA in patients with non-small cell lung cancer Van Der Gaast A, Kok TC, Kho GS, Bhjenberg BG, Splinter TAW. Department of Medical Oncology, Univ. Hospital Rotter&am-Dijkzigr, Dr. Molewatetplein 40,301S ED Rotterdam. EurJ Cancer Part A Geo Top 1995;31:1790-3.

We evaluated the use of two tumour markers Cyfra’21.1 and tissue polypeptide antigen (TPA) for disease monitoring. Assessment of response to WHO criteria was compared to respoose assessmeot according to changes in the tumour marker levels. The criteria defined for marker response were a 65 46 decrease for a partial response and a 40% increase for progressive disease. When response evaluations with a positive lead time were included, 72 I of 115 evaluations for Cyfra 2 1.1 and 59 46 of 107 evaluations for TPA yielded the same result. Most discordant evaluations were caused by those evaluations whereby the patient achieved a partial response according to the WHO criteria and had oorrnalisation of the marker. Less cases with a positive lead time, more negative lead times, and more patients with progressive disease without an increase of the marker were seen with TPA compared to Cyfra 2 1.1. IO conclusion, Cyfra 21.1 follows the changes in the tumour load better than TPA. Rising levels of both markers nearly always indicate disease progression, and such knowledge easily obtained may prevent the continuation of ineffective treatment.

Metastatic lung cancer initially presenting as Gushing’s syndrome of pituitary origin. 25 year follow-up De Gennes JL, Kiortsis DN, Dairou F, Bertagna X, Mahnsky M. Service Endocrinologie-Metabolisme. Groupe Hospitalier Pitie- Salpetriere. 83. Boulevard de l’Hopita1, F-75651 Paris Ceder 13. Prease Med 1995;24:1605-7.

It is often difficult to differentiate between Gushing’s syndrome and ectopic ACTH hypersecretion which, in rare casea, may result from a carcinoid tumour. Several years may be required before development of patent Gushing’s syndrome. We report the 25-year clinical course in a patient with a pulmonary carciooid tumour. Initially, the hormone results led to the diagnosis of Gushing’s syndrome and tbe patient was treated accordingly. Bilateral adrenectomy was performed in 1969 followed by radiotherapy of the pituitary gland in 1975 for suspected Nelson’s syndrome. Actually, the carcinoid tumour, located retrocardially, had gone unnoticed until 1989. Diagnosis was suspected during a hospitalization in our unit and the patient underwent tumor exeresis and left inferior lobectomy. Despite tumour removal and