OV‐TL 12/30 (keratin 7 antibody) is a marker of glandular differentiation in lung cancer

Molengraft, F. J. J. M. Van De; Niekerk, Catharina C. van; Jap, P. H. K.; Poels, L. G.

doi:10.1111/j.1365-2559.1993.tb00066.x

Cited by 30 publications

(14 citation statements)

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“…Its expression is often seen in the major categories of adenocarcinoma, including adenocarcinoma of the breast, lung, ovary, endometrium, thyroid, salivary gland, pancreas, and bile duct (21,25,26). However, there are circumstances in which the determination of CK 7 positivity is useful.…”

Section: Discussionmentioning

confidence: 99%

Cytokeratin 7 and Cytokeratin 20 Expression in Epithelial Neoplasms: A Survey of 435 Cases

2000

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Section: Discussionmentioning

confidence: 99%

Cytokeratin 7 and Cytokeratin 20 Expression in Epithelial Neoplasms: A Survey of 435 Cases

2000

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“…Consistent with this observation, the forced expression of CXCL14 in a lung cancer cell line altered the expression of more than 1,000 genes (42). Functional analysis of the CXCL14-associated gene set revealed a significant enrichment of molecular features related to epithelial differentiation and carcinogenesis, including membrane-tethered mucin genes (MUC1, MUC4, and MUC16), keratin family genes (KRT6 and KRT7), and a diverse set of genes encoding intercellular-junction proteins relevant to the biologic phenotype of AdCa and SqCa, the two major NSCLC subtypes (12,13,(43)(44)(45). Consistent with the activation of cancer-related features within the CXCL14-coexpressed gene set, an analysis of three independent NSCLC datasets revealed a dramatic up-regulation of CXCL14 in AdCa and SqCa, compared with both healthy and COPD airway epithelium.…”

Section: Cxcl14 Links Copd To Lung Cancermentioning

confidence: 99%

Smoking-Induced CXCL14 Expression in the Human Airway Epithelium Links Chronic Obstructive Pulmonary Disease to Lung Cancer

Shaykhiev¹,

Sackrowitz²,

Fukui³

et al. 2013

Am J Respir Cell Mol Biol

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CXCL14, a recently described epithelial cytokine, plays putative multiple roles in inflammation and carcinogenesis. In the context that chronic obstructive pulmonary disease (COPD) and lung cancer are both smoking-related disorders associated with airway epithelial disorder and inflammation, we hypothesized that the airway epithelium responds to cigarette smoking with altered CXCL14 gene expression, contributing to the disease-relevant phenotype. Using genome-wide microarrays with subsequent immunohistochemical analysis, the data demonstrate that the expression of CXCL14 is up-regulated in the airway epithelium of healthy smokers and further increased in COPD smokers, especially within hyperplastic/metaplastic lesions, in association with multiple genes relevant to epithelial structural integrity and cancer.In vitro experiments revealed that the expression of CXCL14 is induced in the differentiated airway epithelium by cigarette smoke extract, and that epidermal growth factor mediates CXCL14 upregulation in the airway epithelium through its effects on the basal stem/progenitor cell population. Analyses of two independent lung cancer cohorts revealed a dramatic up-regulation of CXCL14 expression in adenocarcinoma and squamous-cell carcinoma. High expression of the COPD-associated CXCL14-correlating cluster of genes was linked in lung adenocarcinoma with poor survival. These data suggest that the smoking-induced expression of CXCL14 in the airway epithelium represents a novel potential molecular link between smoking-associated airway epithelial injury, COPD, and lung cancer.Keywords: CXCL14; airway epithelium; smoking; COPD; lung cancerThe airway epithelium, a pseudostratified layer of epithelial cells lining the tracheobronchial tree, is the initial cell population that interacts with inhaled environmental contaminants (1, 2). Among these, cigarette smoke, with its 4,000 compounds and greater than 10 14 free radicals per puff, is a major stressor for airway epithelial cells, and is causally associated with the development of chronic obstructive pulmonary disease (COPD) and lung cancer (1,(3)(4)(5)(6)(7)(8).COPD is a smoking-related disorder defined by irreversible airflow obstruction, associated with structural alterations in the small airways (9, 10), including the small airway epithelium (SAE), which becomes hyperplastic, secretes excessive amounts of mucus, and undergoes metaplastic changes (10-12). In addition to the epidemiological data establishing COPD as a risk factor for lung cancer, several lines of evidence indicate that the molecular mechanisms of COPD pathogenesis are relevant to smoking-induced lung cancer (5,7,8). Importantly, the airway epithelial pathology associated with COPD exhibits remarkable similarities to the pre-neoplastic phenotypes of smoking-induced lung cancer, with a continuum of hyperplastic, metaplastic, and dysplastic changes gradually evolving into an invasive phenotype (13).Studies using mouse models suggest that COPD and lung cancer are both driven, in part, by chronic inflamma...

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“…3 The expression profile of CK7 and CK20 has been thoroughly studied in a range of carcinomas. [3][4][5][6][7][8][9][10][11][12][13][14][15][16] CK7 expression is seen in most carcinomas, with the exception of tumors arising from the colon, prostate, kidney, and thymus; carcinoid tumors of the lung and gastrointestinal tract origin; and Merkel cell tumors of the skin. [4][5][6] On the other hand, CK20 positivity has been detected in the vast majority of adenocarcinomas of the colon, mucinous ovarian tumors, and Merkel cell carcinomas and frequently in transitional cell carcinomas and adenocarcinomas of the stomach, bile duct system, and pancreas.…”

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confidence: 99%

“…6 While assessment of a single CK is of limited diagnostic usefulness, knowledge of the combined CK7/CK20 immunohistochemical profile of specific tumor types has been proven valuable for identifying the tissue of origin of carcinomas of unknown origin, a finding that bears prognostic and therapeutic significance. 3 Characteristic examples include the differential diagnosis between lung, endometrial, nonmucinous ovarian, and breast adenocarcinomas (predominantly CK7 þ /CK20À) and colon adenocarcinoma (mainly CK7À/CK20 þ ), 6,[9][10][11][12] or the distinction of the CK20 þ Merkel cell carcinoma of skin and CK20 þ small cell carcinoma of salivary glands from the CK20À small cell carcinomas of other origins. [6][7][8]13 Carcinomas of salivary gland origin represent an important subset of malignant epithelial tumors.…”

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confidence: 99%

Immunohistochemical expression of cytokeratins 7 and 20 in malignant salivary gland tumors

et al. 2004

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On the basis of the heterogeneity of cytokeratins 7 and 20 expression in malignant epithelial tumors, the cytokeratin 7/20 immunophenotype has served as a useful diagnostic tool for discrimination of primary and/or metastatic carcinomas of unknown origin. However, the expression pattern of these cytokeratins in malignant salivary gland tumors has not been thoroughly studied. Our study material was composed of 84 malignant tumors of primary major or minor salivary gland origin. Nine histologic types of carcinoma were represented, including mucoepidermoid (26 cases), adenoid cystic (25), polymorphous low grade (11), salivary duct (8), acinic cell (4), ex mixed tumor (3), not otherwise specified (3), clear cell (2), and basal cell (2). In all, 13 cases of primary skin or mucosal squamous cell carcinoma with secondary salivary gland involvement were also examined. Immunoreactivity for cytokeratin 7 was evident in all malignant salivary gland tumors; the staining pattern was diffuse and strong in 62 cases, and focal and strong in 22 cases. In contrast, 78 cases were negative for cytokeratin 20, whereas only six cases (two mucoepidermoid, one adenoid cystic, and three salivary duct) displayed focal weak positivity. Overall, 92.9% of malignant salivary gland tumors were characterized by a cytokeratin 7 positive / 20 negative immunoprofile, the remaining 7.1% of cases being positive for both cytokeratins. The latter phenotype was more common in salivary duct carcinomas (Pr0.05). On the other hand, most squamous cell carcinomas (69%) were negative for both cytokeratins, while the remaining cases (31%) were negative for cytokeratin 20 and focally weakly positive for cytokeratin 7. We suggest that assessment of cytokeratin 7/20 immunoprofile may facilitate the differential diagnosis of (a) primary malignant salivary gland tumors from metastatic tumors, (b) metastatic salivary gland tumors, (c) primary salivary gland tumors, especially mucoepidermoid carcinomas, from squamous cell carcinomas, and (d) salivary duct carcinomas from other malignant salivary gland tumors.

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OV‐TL 12/30 (keratin 7 antibody) is a marker of glandular differentiation in lung cancer

Cited by 30 publications

References 4 publications

Cytokeratin 7 and Cytokeratin 20 Expression in Epithelial Neoplasms: A Survey of 435 Cases

Cytokeratin 7 and Cytokeratin 20 Expression in Epithelial Neoplasms: A Survey of 435 Cases

Smoking-Induced CXCL14 Expression in the Human Airway Epithelium Links Chronic Obstructive Pulmonary Disease to Lung Cancer

Immunohistochemical expression of cytokeratins 7 and 20 in malignant salivary gland tumors

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