Bronchopulmonary kulchitzky cell carcinomas. A new classification scheme for typical and atypical carcinoids

Abstract

Typical and atypical carcinoids constitute less than 5% of lung tumors. They and small cell undifferentiated lung cancers (SCLC) belong to the same family of apudomas arising from bronchopul‐monary Kulchitzky cells. To reflect the overlap among these cancers, the authors suggest calling them Kulchitzky cell carcinomas (KCC); to indicate their spectrum of aggressiveness, the authors suggest calling typical carcinoids KCC‐I, atypical carcinoids KCC‐II, and small cell cancers KCC‐III. One hundred fifty‐six KCCs were reviewed: 115 were KCC‐I and 41 were KCC‐II. The ratio of women to men equals 2:1. At time of initial diagnosis, all patients with KCC‐I, except one patient, were in Stage I. Among patients with KCC‐II, 16 (39%) were in Stages II or III at time of presentation. The incidence of carcinoid syndrome was 1.9%. Treatment was lobectomy in 112 (72%) of patients, the remainder having lesser resections or pneumonectomy in approximately equal distribution. Our data cannot support the use of radical resection in the treatment of KCC because none of the patients died of local recurrence. The mean diameters of KCC‐I and ‐II tumors were 1.5 and 2.8 cm, respectively. Increased mitotic activity and tumor necrosis were reliable criteria for diagnosing KCC‐II. Electron microscopic examination did not help in differentiating KCC‐I and KCC‐II. Thorough sampling of the entire tumor was found to be mandatory for precise diagnosis and for differentiation from KCC‐III (SCLC). Measurement of nuclear DNA was done using integrated optical density (IOD) by image analysis. The IODs of KCC‐I, ‐II and ‐III were 1.36, 1.55 and 1.94, respectively. These significant differences (P < 0.001) correlated with the aggressiveness of the cancers. Of patients with KCC‐I, 1.7% succumbed to KCC; this included one patient reported to have died of KCC‐III (SCLC). Of 41 patients with KCC‐II, 11 (27%) died of KCC; this includes at least 3 deaths from KCC‐III. Cancer 55:1303‐1311, 1985.

What clinicians are asking pathologists when dealing with lung neuroendocrine neoplasms?

“…Many other classifications and terminologies have been proposed over time on lung NET, whose detailed examination is beyond the scope of the current paper, by either introducing a concept of tumor grading 11,13,[46][47][48][49] , applying different thresholds to current defining criteria 50,51 or extending to these tumors the same defining criteria as those used in the gastroenteropancreatic tract 21,[52][53][54] . These different proposals, however, have not gained…”

Calcitonin driven v-Ha-ras induces multilineage pulmonary epithelial hyperplasias and neoplasms

“…Whereas carcinoids arise from well-di erentiated PNECs (Bensch et al, 1965), few SCLCs express markers of mature PNECs (Bensch et al, 1968;Sunday et al, 1991;Tsutsumi et al, 1983;Gould et al, 1983;Chejfec et al, 1985;Stahlman et al, 1985Stahlman et al, , 1987Hamid et al, 1987;Said et al, 1985;Gazdar et al, 1988;Bostwick et al, 1984), suggesting that SCLCs could be derived from an epithelial stem cell. In the WHO classi®cation, only SCLC and carcinoids are considered to be NE (de Bruine and Bosman, 1990;Paladugu et al, 1985), but many NSCLCs can express NE markers. Although this observation suggests an inherent plasticity of airway epithelium (Basbaum and Jany, 1990), it is also consistent with a common lineage for the major forms of lung cancer (Berendsen et al, 1989;Warren et al, 1984;Hammond and Sause, 1985).…”

Pulmonary carcinoid tumours: A clinico-pathological study of 35 cases

“…In another series 16/17 patients with atypical pulmonary carcinoids were smokers (Mills et al, 1982). Thirty-seven of 156 patients in a third paper were smokers (Paladugu et al, 1985).…”