Clinical and Molecular Features of Small cell Lung Cancer

Campbell, A M; Campling, Barbara G.; Algazy, Kenneth M.; El‐Deiry, Wafik S.

doi:10.4161/cbt.52

Cited by 6 publications

(3 citation statements)

References 37 publications

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“…Clinical SCLC samples were reviewed with staining intensity and extent. Staining intensity was rated as: negative (0), bordering (1), weak (2), and strong (3). Staining extent was rated on the basis of the percentage of positive cells among all cells in the field.…”

Section: Clinical Tissue Samples and Immunohistochemical Analysismentioning

confidence: 99%

“…Clinically, it is distinguished from non-small cell lung cancer (NSCLC) by rapid tumor growth and early onset of metastases. SCLC is thought to carry a variety of molecular abnormalities, including the activation of the Myc and K-RAS oncogenes and inactivation of the p53, Rb, and FHIT tumor suppressor genes (2). However, the underlying mechanisms by which SCLC manifests rapid progression remain to be defined.…”

Section: Introductionmentioning

confidence: 99%

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DNA Methylation-Mediated Repression of miR-886-3p Predicts Poor Outcome of Human Small Cell Lung Cancer

et al. 2013

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Small cell lung cancer (SCLC) is one of the most aggressive types of cancer, yet the pathologic mechanisms underlying its devastating clinical outcome remain elusive. In this report, we surveyed 924 miRNA (miR) for their expressions in the formalin-fixed paraffin-embedded specimens from 42 patients with SCLC, and found that the downregulated miR-886-3p is closely correlated with the shorter survival of SCLC. This correlation was validated with another 40 cases. It was further discovered that loss of miR-886-3p expression was mediated by DNA hypermethylation of its promoter in both cultured SCLC cells and tumor samples. Moreover, miR-886-3p potently repressed cell proliferation, migration, and invasion of NCI-H446 cell in cell culture via suppression of the expression of its target genes: PLK1 and TGF-b1 at posttranscription levels. Forced upregulation of miR-886-3p greatly inhibited in vivo tumor growth, bone/muscle invasion, and lung metastasis of NCI-H446 cells. This newly identified miR-886-3p-PLK1/TGF-b1 nexus that modulates SCLC aggression suggests that both loss of miR-886-3p expression and hypermethylation of the miR-886 promoter are the promising indicators for poor outcome of as well as new therapeutic targets for SCLC. Cancer Res; 73(11); 3326-35. Ó2013 AACR.

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Section: Clinical Tissue Samples and Immunohistochemical Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

DNA Methylation-Mediated Repression of miR-886-3p Predicts Poor Outcome of Human Small Cell Lung Cancer

et al. 2013

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“…Many of the SCLC‐associated antigens are also present in the nervous system, due to the neuroendocrine origin of SCLC. Immune tolerance for these central nervous system antigens is often low, thereby lowering the threshold to involve these antigens in an autoimmune disease 24–26 . Many of these onconeural antibodies have been described in SCLC along with specific PNSs such as the anti‐Hu antibody associated with sensory neuronopathy or the anti‐CV2 antibody associated with encephalomyelitis 27 .…”

Section: Small Cell Lung Carcinoma‐‐associated Antibodies and Pareneomentioning

confidence: 99%

SOX1 antibodies in Lambert–Eaton myasthenic syndrome and screening for small cell lung carcinoma

Lipka

Verschuuren

Titulaer

2012

Annals of the New York Academy of Sciences

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Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder of the neuromuscular synapse. About half of LEMS patients have an associated small cell lung carcinoma (SCLC), which is usually detected after diagnosis of LEMS. This short review summarizes clinical and serological markers shown to predict the presence of SCLC in LEMS patients. SOX1 antibodies are a specific marker for SCLC-LEMS but they are also found in SCLC patients without paraneoplastic neurological syndromes. No relation to any clinical characteristic or survival effect has been found for SOX1-positive patients. Several clinical markers also discriminate between SCLC-LEMS and nontumor LEMS. Detailed analysis of these clinical and demographic characteristics from two independent patient cohorts has led to development of the DELTA-P score. This prediction model has provided for a simple clinical tool to indicate the presence of SCLC early in the course of the disease. The DELTA-P score can be used to guide tumor screening in individual patients.

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