Oat-cell carcinoma of the lung. Its origin and relationship to bronchial carcinoid

Bensch, Klaus G.; Corrin, B.; Pariente, Roberto; Spencer, Herbert R.

doi:10.1002/1097-0142(196811)22:6<1163::aid-cncr2820220612>3.0.co;2-l

Cited by 471 publications

(93 citation statements)

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“…Humans are the only species with naturally occurring SCLCs. 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.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 1999

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We initiated a transgenic model for primary pulmonary neuroendocrine cell (PNEC) hyperplasia/neoplasia using v-Ha-ras driven by the neural/neuroendocrine (NE)-speci®c calcitonin promoter (rascal). Previously, we showed that nitrosamine treated rodents develop PNEC hyperplasia but non-NE lung tumors, with variable outcomes presumably re¯ecting ras activation in multiple cell lineages. Interestingly, all rascal transgenic mouse lineages develop hyperplasias of NE and non-NE cells but mostly non-NE lung carcinomas, with rascal mRNA in di erentiated PNECs and tumor cells. Analyses of embryonic lung demonstrate rascal mRNA in undi erentiated epithelium, consistent with expression in a common pluripotent precursor cell. These unexpected observations indicate that v-Ha-ras can lead to both NE and non-NE hyperplasia/neoplasia in vivo, opening new avenues for studies of lung carcinogenesis.

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Section: Introductionmentioning

confidence: 99%

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

et al. 1999

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“…SCLC and bronchial carcinoids are characterized by neuroendocrine features and are thought to be derived from the Kultschitzky cells of the bronchial tree (2). These tumors have distinct histological morphologies and very different clinical behaviors (1,3).…”

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confidence: 99%

Array comparative genomic hybridization-based characterization of genetic alterations in pulmonary neuroendocrine tumors

Voortman

Lee

Killian

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

120

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The goal of this study was to characterize and classify pulmonary neuroendocrine tumors based on array comparative genomic hybridization (aCGH). Using aCGH, we performed karyotype analysis of 33 small cell lung cancer (SCLC) tumors, 13 SCLC cell lines, 19 bronchial carcinoids, and 9 gastrointestinal carcinoids. In contrast to the relatively conserved karyotypes of carcinoid tumors, the karyotypes of SCLC tumors and cell lines were highly aberrant. High copy number (CN) gains were detected in SCLC tumors and cell lines in cytogenetic bands encoding JAK2, FGFR1, and MYC family members. In some of those samples, the CN of these genes exceeded 100, suggesting that they could represent driver alterations and potential drug targets in subgroups of SCLC patients. In SCLC tumors, as well as bronchial carcinoids and carcinoids of gastrointestinal origin, recurrent CN alterations were observed in 203 genes, including the RB1 gene and 59 microRNAs of which 51 locate in the DLK1-DIO3 domain. These findings suggest the existence of partially shared CN alterations in these tumor types. In contrast, CN alterations of the TP53 gene and the MYC family members were predominantly observed in SCLC. Furthermore, we demonstrated that the aCGH profile of SCLC cell lines highly resembles that of clinical SCLC specimens. Finally, by analyzing potential drug targets, we provide a genomics-based rationale for targeting the AKT-mTOR and apoptosis pathways in SCLC.carcinoid | cell line | gene dosage | small cell lung carcinoma | therapy

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“…8 Bronchial carcinoid tumour constitutes 80-90 per cent of bronchial adenomas; 4,~ this tumour is thought to arise from argentaffln (Kultchitsky) cells in the bronchial mucosa. 6 Patients usually present with signs and symptoms of bronchial obstruction, such as cough, recurrent pneumonia, atelectasis, wheezing, or haemoptysis. Carcinoid syndrome is seen in 2 per cent to 7 per cent of adults; ~ we have not found reports of symptomatic carcinoid syndrome due to this lesion in the paediatric age group although a child has been described with metastatic bronchial eareinoid tumour, elevated plasma serotonin levels and increased urinary 5-hydroxyindole acetic acid excretion.…”

Section: Discussionmentioning

confidence: 99%

Anaesthetic considerations in bronchial adenoma

Murphy

Lockhart

Burrington

1975

Canad. Anaesth. Soc. J.

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BRONCmAL CARClNOID TIJMOR is an unusual tumor which has received considerable attention in the surgical literature; however, the anesthetic management of the tumor has not been previously discussed. CAsE REPOnTA 14-year-old white female was referred for evaluation with a five-week history of malaise, intermittent low-grade fever, and non-productive cough after failure to respond to antibiotic therapy. The only remarkable finding on physical examination was diminished breath sounds over the left posterior chest. Normal laboratory values included complete blood count, urinalysis, liver function tests, serum electrolytes and 24-hour urine 5-hydroxyindole acetic acid excretion. Chest roentgenograms demonstrated atelectasis of the left lower lobe and hyperlucency and hyperexpansion of the left upper lobe, particularly remarkable on expiratory films. An endobronchial mass completely occluding the left lower lobe bronchus and impinging upon the upper lobe bronchus was identified on tomograms. Pulmonary function studies showed increased residual volume and diminished vital capacity (Table I ). Nitrogen washout curves showed slow uneven elimination of nitrogen from the functional residual capacity (Figure 1). A diagnosis of bronchial adenoma was entertained and thoracotomy for resection of the portion of bronchus attached to tumour (sleeve resection) was planned.One hour prior to induction of anaesthesia, morphine 6 mg, diazepam 10 mg, and atropine 0.4 mg was given by intramuscular injection. An intra-arterial cannula for blood gas monitoring, placed after induction of anaesthesia, was used in addition to the usual monitoring devices. After thiopentone induction, spontaneous ventilation with halothane and oxygen was maintained during bronchoscopy. A mass with appearance compatible with bronchial adenoma was visualized in the left mainstem bronchus. It was not manipulated or biopsied. A #7 Fogarty catheter was placed adjacent to the tumour under direct vision and the bronchoscope was removed. A 6.5 mm cuffed tracheal tube was positioned in the trachea above the carina and the patient was turned to the right lateral decubitus position. After thoracotomy the left upper lobe was seen to be markedly emphysematous and gas could not be expressed from it. The lower lobe was completely collapsed with extensive damage secondary to obstruction; therefore sleeve resection was not attempted. The Fogarty balloon was inflated slowly until it could be palpated by the operating surgeon. It was then positioned in the left mainstem bronchus just above the origin of the left upper lobe bronchus. The intermediate bronchus could then be opened and the From:

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Oat-cell carcinoma of the lung. Its origin and relationship to bronchial carcinoid

Cited by 471 publications

References 11 publications

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

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

Array comparative genomic hybridization-based characterization of genetic alterations in pulmonary neuroendocrine tumors

Anaesthetic considerations in bronchial adenoma

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