Small cell lung carcinoma: Clinicopathological, immunohistochemical, and ultrastructural study

Shy, Shya‐Wen; Lee, Wei Hwa; Chou, Ming‐Chih; Lai, Yieh‐Shyong; Tu, Yen-Chang

doi:10.1002/jso.2930450304

Cited by 26 publications

(18 citation statements)

References 73 publications

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“…The spectrum of epithelial cells recognized by 34fE12 monoclonal is relatively wide and includes other tumors having squamous or glandular differentiation. In the current study on biopsy and surgical specimens, we obtained results similar to Morice and Ferreiro [20] rather than those of Shy and coworkers [30]. Thus, we found that both in biopsies and cytologic specimens the 34,E12 CK immunostaining was significantly restricted to non-NE carcinomas, regardless of the histologic type.…”

Section: Discussionsupporting

confidence: 88%

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34βE 12 Cytokeratin Immunodetection in the Differential Diagnosis of Small Cell Tumors of Lung

Viberti¹,

Bongiovanni²,

Croce³

et al. 2000

Int J Surg Pathol

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The group of small cell tumors of the lung includes fine following: (1) small cell carcinoma (SCC) of neuroendocrine (NE) origin, (2) poorly differentiated squamous carcinoma, (3) the rare basaloid (basal cell) carcinomas, and (4) malignant lymphomas, primitive neuroectodermal tumors (PNETs), and rhabdomyosarcomas. The differential diagnosis among these entities carries a heavy therapeutic impact but may be difficult in small biopsy specimens or in cytologic material, especially if necrosis or artifactual alterations are present. The use of additional techniques such as immunostaining for NE markers is not always helpful, since immunoreactive chromogranin A is detectable in only a small percentage of small cell carcinomas. It has recently been reported that in the aerodigestive tract 34betaE12 cytokeratin (CK) immunostaining selectively labels non-NE carcinomas, including squamous cell carcinoma, adenocarcinoma, and the rare basaloid carcinoma. We evaluated the role of such CK immunodetection in the differential diagnosis of small cell lung tumors in cytologic and biopsy specimens. Eighty-one lung tumors diagnosed by means of endoscopic bronchial biopsy, fine needle aspirate, or bronchial washing were collected. They included 43 small cell NE carcinomas and 38 cases used as controls (comprehensive of 2 large cell neuroendocrine carcinomas, 4 carcinoid tumors, 30 cases of non-NE lung carcinomas, 2 cases of bronchial infiltration by non-Hodgkin lymphomas). 34betaE12 CK immunoreactivity was found in 29/30 cases of non-NE carcinomas, but in only 3/43 SCCs. The latter showed positivity in only a few scattered cells. The 2 cases of bronchial infiltration by malignant lymphoma as well as the 4 cases of carcinoid tumors and the 2 cases of large cell neuroendocrine carcinomas were negative. These findings were confirmed in the surgical specimens of operatedon cases. We conclude that, in lung carcinoma biopsies showing a small cell pattern, presence of 34betaE12 CK immunoreactivity favors a non-NE carcinoma, whereas its absence supports the diagnosis of SCC. Int J Surg Pathol 8(4):317-322, 2000

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Section: Discussionsupporting

confidence: 88%

“…This is in contrast with a previous report by Shy et al [30], in which 25% of SCC were positive. The spectrum of epithelial cells recognized by 34fE12 monoclonal is relatively wide and includes other tumors having squamous or glandular differentiation.…”

Section: Discussioncontrasting

confidence: 85%

34βE 12 Cytokeratin Immunodetection in the Differential Diagnosis of Small Cell Tumors of Lung

Viberti¹,

Bongiovanni²,

Croce³

et al. 2000

Int J Surg Pathol

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“…Immunoreactivity for chromogranin is associated with the presence of neurosecretory granules in tumor cells, and many high-grade neuroendocrine carcinomas have absent or aberrant production of such granules. Among primary pulmonary small cell carcinomas, immunopositivity for chromogranin is generally only around 80% 59 and has been reported as low as 23% 60 . Absent or focal chromogranin staining in gastric neuroendocrine carcinomas is also a known phenomenon with reported chromogranin positivity of 40% 61 .…”

Section: Discussionmentioning

confidence: 99%

Three Molecular Subtypes of Gastric Adenocarcinoma Have Distinct Histochemical Features Reflecting Epstein-Barr Virus Infection Status and Neuroendocrine Differentiation

Speck¹,

Tang²,

Morgan

et al. 2015

Applied Immunohistochemistry &Amp; Molecular Morphology

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Current histopathologic classification schemes for gastric adenocarcinoma have limited clinical utility and are difficult to apply due to tumor heterogeneity. Elucidation of molecular subtypes of gastric cancer may contribute to our understanding of gastric cancer biology and to the development of new molecular markers that may lead to improved diagnosis, therapy, or prognosis. We previously demonstrated that Epstein-Barr virus infected gastric cancers have a distinct human gene expression profile compared to uninfected cancers. We now examine the histopathologic features characterizing infected (n=14) and uninfected (n=89) cancers, the latter of which are now further divided into two major molecular subtypes based on expression patterns of 93 RNAs. One uninfected gastric cancer subtype was distinguished by upregulation of three genes with neuroendocrine function (CHGA, GAST, and REG4 encoding chromogranin, gastrin and the secreted peptide REG4 involved in epithelial cell regeneration), implicating hormonal factors in the pathogenesis of a major class of gastric adenocarcinomas. Evidence of neuroendocrine differentiation (molecular, immunohistochemical, or morphologic) was mutually exclusive of EBV infection. EBV infected tumors tended to have solid-type morphology with lymphoid stroma. This study reveals novel molecular subtypes of gastric cancer and their associated morphologies that demonstrate divergent neuroendocrine features.

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“…LNETs are diagnosed by morphologic features such as trabecular, ribbon‐like, and organoid growth and immunohistochemical positivity for neuroendocrine phenotype‐specific molecules such as neural cell adhesion molecule 1 (NCAM1), synaptophysin (SYPT), and chromogranin A (CGA) 1–6 . It has been reported that NCAM1 is expressed in almost all LNETs from typical carcinoid tumors to SCLCs, while SYPT is expressed in 57–74.3% of SCLCs 7–9 . CGA expression has been reported to occur in approximately 100% of typical carcinoid tumors but only 22.9–36% of SCLCs 8–10 .…”

Section: Introductionmentioning

confidence: 99%

Differences of molecular expression mechanisms among neural cell adhesion molecule 1, synaptophysin, and chromogranin A in lung cancer cells

Kashiwagi

Ishii

Sakaeda

et al. 2012

Pathology International

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Neural cell adhesion molecule 1 (NCAM1), synaptophysin (SYPT), and chromogranin A (CGA) are immunohistochemical markers for diagnosing lung neuroendocrine tumors (LNETs). However, the precise expression mechanisms have not been studied in enough detail. The purpose of the present study is to define the molecular mechanisms of NCAM1, SYPT, and CGA gene expressions, using cultivated lung cancer cells and focusing upon NeuroD1 (ND1), achaete-scute homolog-like 1 (ASCL1), and known transcription factors, repressor element 1 (RE1)-silencing transcription factor (REST) and c-AMP responsive element-binding protein (CREB). Promoter assays, chromatin immunoprecipitation, and transfection experiments revealed that ND1 activated NCAM1, that ASCL1 weakly upregulated SYPT expression, and that CGA expression was not regulated by ND1 or ASCL1. REST expression was restricted in non-small cell lung cancer (NSCLC) cells, and knockdown of REST could cause as much SYPT expression as in SCLC cells and weak CGA expression in NSCLC cells. However, CGA gene upregulation via CREB activation was not found in REST-lacking NSCLC cells, indicating the requirement of some additional mechanism for sufficient expression. These results suggest that NCAM1, SYPT and CGA expressions are differently regulated by neuroendocrine phenotype-specific transcription factors and provide a reason why NCAM1 and SYPT are frequently expressed in LNETs, irrespective of malignancy grade.

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Small cell lung carcinoma: Clinicopathological, immunohistochemical, and ultrastructural study

Cited by 26 publications

References 73 publications

34βE 12 Cytokeratin Immunodetection in the Differential Diagnosis of Small Cell Tumors of Lung

34βE 12 Cytokeratin Immunodetection in the Differential Diagnosis of Small Cell Tumors of Lung

Three Molecular Subtypes of Gastric Adenocarcinoma Have Distinct Histochemical Features Reflecting Epstein-Barr Virus Infection Status and Neuroendocrine Differentiation

Differences of molecular expression mechanisms among neural cell adhesion molecule 1, synaptophysin, and chromogranin A in lung cancer cells

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