Oat Cell Carcinoma Of Lung Research Articles

Pontine metastases as a cause of dysphagia in lung carcinoma

Dysphagia is an unusual symptom in the clinical course of lung carcinoma. When it appears, it is necessary to differentiate between regional dissemination, drug toxicity, opportunistic infection and, most rarely, metastatic dissemination to the brain stem. Magnetic resonance imaging (MRI) is the best diagnostic option to exclude this last possibility. We present a male patient with progressive dysphagia 15 months after the diagnosis of an oat-cell lung carcinoma. Cerebral MRI revealed a pontine lesion, probably of metastatic origin.

Diabète insipide dans le cadre d’un carcinome pulmonaire à petites cellules : un paradoxe ?

We observed oat-cell lung carcinoma in a man who presented with diabetes insipidus. The chest radiograph showed a suspect nodule within a context of major nicotine addiction. Histopathological examination of the transbronchial biopsy confirmed the diagnosis of oat-cell carcinoma. Brain CT revealed metastasis to the pituitary gland and the pituitary stalk. Vasopressin was undetectable. This case illustrates an uncommon clinical presentation of small-cell lung carcinoma. Oat-cell carcinoma can modify osmoregulation in two different ways. Only sporadic cases of neurogenic diabetes insipidus due to the primary involvement of small-cell lung carcinoma have been reported. More often, this type of lung tumor is associated with inappropriate antidiuretic hormone secretion.

Síndrome opsoclonus-mioclonus en paciente con cáncer de ovario

The opsoclonus-myoclonus syndrome is a rare entity as a paraneoplastic disorder usually associated to neuroblastoma in children and breast cancer or oat-cell lung carcinoma in adults. The association of opsoclonus-myoclonus syndrome and ovarian carcinoma is very unusual, to our knowledge there is only two cases reported in the literature. In both of them the opsoclonus-myoclonus syndrome preceded the neoplasy, improving with its treatment. In our patient opsoclonus began after ovarian cancer diagnosis, after chemotherapy and radiotherapy, improving with corticoid and clonazepan therapy.

Limbic encephalopathy-case report and review of the literature

A 60 year old male with a long history of low -grade depression and a 12 month history of dysarthria, dysphasia, weakness and altered cognitive function was admitted to Bethlehem Hospital for terminal care. A preadmission diagnosis of Motor Neuron Disease had been made by a private neurologist. He was treated with due care but died of clinical bronchopneumonia 1 month after admission. At autopsy the brain was heavy (1400 gm) and macroscoplcally unremarkable. The lungs showed evidence of congestive cardiac failure but no bronchopneumonia. The left kidney was of small size, showed reduced cortical thickness, dilated pelvicalyceal system and had three cortical masses between 5 and 35 mm in diameter. A fourth Intra-cortical area of yellowish discolouration 3 mm in length was also present. These areas represent renal cortical neoplasms of the proximal tubules which are histologically and macroscopically at the boundary between benign and malignant neoplasms of the renal cortex. No evidence of metatstatic disease was noted. The brain showed sponginess and gliosis of the medial temporal cortex bllaterally. There was also some mild loss of motor neurons in the spinal cord. Only two other cases of renal carcinomas and limbic encephalopathy were found in the last 16 years, one of which was also associated with an oat cell carcinoma of lung. Limbic encephalopathy is a para-neoplastic syndrome, which in its pure form as seen In this case, is exceedingly uncommon. It Is usually in association with bulbar, cord and posterior root ganglia lesions and Is most commonly seen in cases of primary lung carcinomafoat cell carcinoma).

Secretion of chromogranin A by peptide-producing endocrine neoplasms.

Chromogranin A, the protein that is co-stored and co-released with catecholamines from the adrenal medulla, has recently been identified in a variety of human endocrine tissues, both normal and neoplastic. We investigated the secretion of chromogranin A by peptide hormone-producing human tumors in studies of patients with the following neoplastic disorders: pheochromocytoma, parathyroid adenoma, primary parathyroid hyperplasia, medullary thyroid carcinoma, thyroidal C-cell hyperplasia, carcinoid tumor, oat-cell lung carcinoma, pancreatic islet-cell tumor, and aortic-body tumor. All these patient groups had elevated concentrations of plasma chromogranin A. We distinguished different forms of immunoreactive plasma chromogranin A by size with the use of gel filtration. Plasma chromogranin A levels were not elevated in patients with diverse "control" conditions--both benign and malignant and both endocrine and nonendocrine--in which peptide hormones are not produced. The sensitivity and specificity of plasma chromogranin A elevations in the diagnosis of peptide-producing endocrine neoplasms were 81 and 100 percent, respectively. The elevation of plasma chromogranin A in our subjects suggests that their neoplasms co-release chromogranin A along with the usual resident hormone of the tumor, that these neoplasms could be characterized as "chromograninomas," and that measurement of plasma chromogranin A may be a useful diagnostic procedure in subjects with endocrine tumors, especially multiple endocrine neoplasia.

Clinical trials with cyclophosphamide and misonidazole combination for maintaining treatment after radiation therapy of lung carcinoma

Fifteen patients with inoperable non oat cell lung carcinoma, who had already been treated with telecobalt therapy in the mediastinum-hilar region, were treated with continuing therapy with misonidazole (MISO) and cyclophosphamide (Cy). MISO was administered in single doses of 1000 mg/m 2 and 500 mg/m 2, orally. Cy was administered in single doses of 500 mg/m 2 and 250 mg/m 2, i.v. This treatment was given every 4 weeks. All patients ( 15 15 suffered from hyporexia, nausea and vomiting within 48 hours from administration; furthermore, 2 patients had hemoragic cystitis, 2 had peripheral neurotoxicity, 3 had fever, and 2 had serious nervous depression. Leukopenia occurred in all patients immediately after drug administration, although it was not present in any patient by the time of the next administration. This clinical trial was concluded in December 1981. The follow-up at 18 months shows 7 15 cases of relapse (3 patients dead and 1 patient alive with recurrence, 2 patients dead and 1 patient alive with metastasis without recurrence). Eight of 15 patients are alive with progression of disease from 8 to 18 months.

Phase II evaluation of chlorozotocin (NSC-178248) in advanced human cancer

A phase II evaluation of chlorozoticin (CZT), a water soluble nitrosourea, was undertaken to determine its effectiveness and toxicity in a variety of human metastatic neoplasms. The dosage regimen chosen was either 90 or 120 mg/m 2 given by i.v. bolus every six weeks. Dosage escalation or de-escalation was dependent on toxicity. There have been 152 patients evaluable for response. The only significant response rates observed were in non-Hodgkin's lymphoma ( 5/11) and sarcoma ( 4/27). Single responses were observed in breast and oat cell carcinoma of lung. No responses were observed in melanoma, colorectal, kidney, non-oat cell lung, pancreas, stomach and other carcinomas. Hematological toxicity has been minimal as predicted, but does appear to be cumulative. The major G.I. toxicity has been nausea and vomiting—usually controllable. Occasional hepatic enzyme elevations were observed, and azotemia was observed in 6 patients. Both were reversible. Rare skin and occasional CNS reactions were also seen.

Clinical trials in cancer research.

This is a review paper which gives a discussion of various aspects of clinical trials in cancer research. Since the conduct of the first randomized controlled clinical trial in cancer patients in the mid-1950's, substantial progress has been made in the utilization of the clinical trial technique for the evaluation of therapeutic efficiacy. The important elements of a protocol are given with some discussion of items to be considered in designing a protocol. The types of clinical trial (phase I, II, III) are defined, and the place of each phase of study in the context of the search for new treatments is delineated. A comprehensive discussion is given of the elements in the comparative clinical trial (phase III), including objectives, consierations in planning (comparability of treatment groups stratification of patients, feasibility and size of study, and prospective versus retrospective studies). Brief descriptions are given of designs for comparative clinical trials and a trial in oat cell lung carcinoma is discussed in some detail. Finally, some comments and references are given concerning the analysis of clinical trials.

Hormones produced by tumours

There are 2 broad areas of tumour-related endocrinology: (1) Appropriate hormones secreted in inappropriate quantities by recognizable endocrine tumours, and (2) Inappropriate hormones secreted in any quantity by overtly non-endocrine tumours (the so-called ‘ectopic hormones’). In either case, the hormones secreted, and the clinical syndrome resulting from such secretion may serve as a tumour marker for early detection of the tumour and for follow-up reassessment of adequacy of treatment. Recognition of ectopic hormone production is limited only by the interests and intuition of the clinician and the technical facilities available to him for measuring hormones. Underdiagnosis is the rule, although at least 8 syndromes secondary to ectopic hormone production are fairly readily recognized: Cushing's Syndrome due to ectopic ACTH secretion; hyponatraemia due to ectopic antidiuretic hormone; hypercalcaemia due to ectopic parathormone; gynaecomastia in older men and precocious puberty in boys due to ectopic gonadotrophin; galactorrhoea due to ectopic prolactin; erythrocytosis due to ectopic erythropoietin; and hypoglycaemia possibly due to ectopic secretion of insulin-like activity. Ectopic thyrotrophin, calcitonin, growth hormone and human placental lactogen (HPL) rarely lead to clinical manifestations. Ectopic hormones are invariably polypeptides, never steroids. This fact underlies several explanations for the possible mechanism of ectopic hormone production. The concept of derepression within tumours of genetic material for polypeptide synthesis which is inherent in the genetic complement of all cells is now being questioned in favour of the theory that tumours secreting ectopic hormones either themselves arise from, or contain endocrinologically competent cells of neuroectodermal origin. Some go so far as to identify the oat cell carcinoma of lung as an endocrine tumour ‘per se’ This tumour is of particular interest because, like few others, it is capable of secreting multiple ectopic hormones. Taken from a different viewpoint, intensive study of hormone-secreting non-endocrine tumours may lead to an understanding of the mechanisms leading to neoplastic transformation.

Small cell anaplastic (oat cell) carcinoma of the larynx: Report of a case and review of the literature

AbstractThe fifth reported patient with primary laryngeal oat cell carcinoma is described. Electron microscopy of tumor cells revealed typical neurosecretory‐type granules similar to those described for pulmonary oat cell carcinoma. Analysis of clinical data from all five reported patients revealed that this neoplasm is a virulent one which spreads early and rapidly and kills quickly. Combination chemotherapy and/or radiotherapy, which has significantly prolonged life in patients with oat cell carcinoma of lung, may be indicated as an adjunct to surgery for this rare malignant tumor of the larynx.

Comparative Histopathologic, Histochemical, Electron Microscopic and Tissue Culture Studies of Bronchial Carcinoids and Oat Cell Carcinomas of Lung

Although there is compelling evidence to indicate that bronchial carcinoids and oat cell carcinomas of lung have similar histogeneses, their prognoses are divergent, making their pathologic distinction imperative. Although this is not generally difficult, instances do occur, particularly with biopsy material, in which their absolute identification may be tenuous. The results of a systematic, statistical examination of a number, of histopathologic features of 13 bronchial carcinoids and 47 oat cell carcinomas in cases in which follow-up information for 2 to 6 years was available revealed that a ribbon-like architectural arrangement of the monomorphous tumor cells of high (most favorable) nuclear grade represents a presumptive feature of bronchial carcinoids. On the other hand, mitoses, low nuclear grade, necrosis, hematoxylinophilic vascular deposits, pericellular argyrophilic pattern, and perineural space invasion were encountered only in oat cell carcinomas. Argyrophilic granules were more frequent in cells comprising bronchial carcinoids. An argentaffin reaction and other tinctorial methods for enterochromaffin, as well as glycoprotein, were found to be positive only in bronchial carcinoids, and in the latter they were focal. Neurosecretory-type granules observed by electron microscopy were obviously more frequent in cells of bronchial carcinoids, whereas the nuclei and the cytoplasm of cells of oat cell carcinomas appeared more complex. Chromosomal analysis of cells comprising a few samples of each tumor type in which this feature was evaluated revealed aneuploid karyotypes and marker chromosomes in both. The results do not minimize the common histogenesis of bronchial carcinoids and oat cell carcinomas. However, they do provide criteria for their differentiation, as well as evidence to support the view that the bronchial carcinoid is indeed a more benign form of oat cell carcinoma of the lung.

Analysis of human tumors and human malignant cell lines for BK virus-specific DNA sequences

Most humans in the United States have been infected with BK virus (BKV), a human papovavirus. Because BKV has oncogenic properties, we have investigated whether it may be a cause of human cancer. Basic principles of tumor virology imply that BKV-induced tumors should contain BKV DNA sequences. Therefore, we assayed (by molecular hybridization) DNA from human tumors and malignant cell lines for BKV DNA, using BKV [(32)P]DNA as probe. The BKV [(32)P]DNA was labeled in vitro (nick translation) to specific activities of 1 to 2 x 10(8) cpm/mug. The BKV DNA used to prepare our probes had the properties expected of authentic BKV genomes, including density of superhelical DNA, sedimentation velocity in alkaline and neutral sucrose gradients, production of one fragment by endonuclease EcoRI cleavage and four fragments by endonuclease Hin II + III cleavage and reassociation properties. From these studies we conclude that our BKV probes hybridized well, and represented bona fide BKV DNA. Using three different BKV [(32)P]DNA probes, i.e., from three distinct plaque isolates, we have analyzed DNA from BKV-transformed cells, normal human tissues, and a large number of human tumors. All human DNAs (cell lines, normal tissues, tumors) hybridized 5% with BKV DNA. Hybridization analysis of BKV-transformed hamster cell DNA indicated 5-6 copies of at least 88% of the BKV genome per cell. No BKV DNA sequences were detected (above the normal 5% hybridization to all human DNAs) in the following normal human tissues: 10 kidney (BKV is usually isolated from urine), 3 spleen, 13 lung, 23 colon, 2 rectum, 1 ileum, and 1 skin. No BKV-specific DNA was found in 166 tumors, including 5 carcinomas (Ca) of stomach, 3 Ca small intestine, 26 Ca colon, 9 Ca rectum, 31 Ca lung, 9 adenocarcinomas and 5 oat cell carcinomas of lung, 17 melanomas, 5 Ca prostate, 4 Ca bladder, 6 Wilms tumors, 4 hypernephromas, 15 Ca kidney, 7 brain tumors, 5 Hodgkin lymphomas, 10 lymphomas (immunosuppressed patients have a high incidence of lymphomas), 2 reticulum cell sarcomas (spleen), and 3 skin tumors. We have also analyzed 7 human malignant cell lines (melanoma, lung, rhabdomyosarcoma, and glioblastomas), including several clones of a lung melanoma line; no BKV DNA sequences were detected. Because our probes could detect one copy of BKV DNA if only 10% of the cells were tumor cells, our results are very strong evidence that the tumors we analyzed did not have a BKV etiology. The tumors we tested represent about 50% of all cancers in the United States; there is no evidence that BKV is involved in the etiology of these types of tumors.

Bilateral Breast Metastases from Oat-Cell Lung Carcinoma in a Man Treated with Diethylstilbestrol for Prostatic Adenocarcinoma

: A case report is presented of bilateral breast metastases originating from oat-cell carcinoma of the lung in a man treated with diethylstilbestrol for carcinoma of the prostate. The metastatic spread to both breasts apparently was related to the estrogen therapy.

Letter: Management of metastatic oat cell carcinoma of lung.

To the Editor.— The discussion regarding the Management of Oat Cell Carcinoma of Lung With Metastases to the Bones (225:422, 1973), though excellent as far as it went, did not go far enough. The two consultants seem to be concerned only with the systemic chemotherapy for the disease and largely overlook the fact that the radiation therapy was inadequate. Radiation therapy is an extremely useful method of treating incurable carcinoma. In cases where weight-bearing bones are involved with metastatic disease, the purpose of radiation therapy should be, not only to relieve the pain, but also, to prevent pathologic fracture with its resultant complications. In the case mentioned, single session treatments did suffice to relieve the patient's pain; however, he subsequently suffered a spontaneous fracture of the right femoral shaft. Whether or not the patient with widespread metastatic disease receives systemic chemotherapy, I believe strongly that destructive lesions in weight-bearing bones

Asbestosis and carcinoma of the lung.

Asbestosis and carcinoma of the lung.