Alveolar cell carcinoma (bronchiolar carcinoma).
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Bronchiolar carcinoma is a malignant tumour which apparently arises in a terminal bronchiole from which it spreads either by bronchial embolization or by lymphogenous and/or hematogenous dissemination. It is not a common neoplasm.Histologically, the tumour bears a striking resemblance to the disease of sheep, jagziekte, which is of virus etiology. A very common finding in reported cases is preexisting pulmonary fibrosis. At the Nova Scotia Sanatorium, Kentville, 80 cases of primary lung cancer have been encountered within the past 25 years. Six of these were bronchiolar carcinomas. Five patients had co-existing chronic pulmonary disease, bronchiectasis in one and tuberculosis in four. One patient died of a rapidly progressive bilateral lesion and five were explored. Lobectomy was done in all five, but in one for palliation only. Three patients are alive and well three, six and 14 years, respectively, after their operations.
A rare tumour-the diffuse form of mucinous bronchiolar carcinoma involving the entire left lung was seen in a 23 month old female rat that had been given 2,2-dinitrobiphenyl orally. The neoplastic lesion was characterized by many honey-combed spaces lined by tall, mucus-secreting columnar cells and filled with abundant mucus.
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Eleven cases of bronchiolar carcinoma seen between 1970 and 1975 are reviewed. Roentgenographic manifestations at the time of initial examination included single peripheral nodules, multiple nodules, irregular cavities and a persistent infiltrative form. Microscopic tissue examinations showed two patterns of tumor growth: a papillary form resembling tall columnar cells extending along but not invading the alveolar septal walls and a cribriform pattern represented by inflammatory thickening of the alveolar septal walls and pleomorphic cellular proliferation within luminal spaces. The papillary form was associated with the cavitary lesions. Long term survival is dependent on early recognition of the single peripheral nodule, cavity or small persistent infiltrative form managed by a thoracotomy and lobectomy.
Incomplete programmed cell death is one explanation for the escape of cancer cells from therapy. Inhibitors of the enzyme 5-lipoxygenase reduce proliferation and initiate programmed cell death in many different types of malignantly transformed cells. The 5-lipoxygenase inhibitor, MK 886. induces an atypical form of programmed cell death in H-358 bronchiolar lung cancer cells. A genomic response of H-358 cells after 24 hr of culture at a 40 uM concentration that inhibited proliferation was analyzed with a Clontech human cDNA array containing 588 cDNAs corresponding to identified genes. The data grouped into 3 major categories and initial conclusions regarding countervailing, cellular stress, programmed cell death, DNA damage and repair mRNA-responses as possible reasons for escape from the antiproliferative response are discussed. The use of cDNA arrays to estimate the extent to which malignantly transformed cells respond to therapy or why they do not and so infer prognosis and identify possible therapeutic modifications is indicated.
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