Retention of Chromosome 3 in Extrapulmonary Small Cell Cancer Shown by Molecular and Cytogenetic Studies

Johnson, Bruce E.; Whang‐Peng, Jacqueline; Naylor, Susan L.; Zbar, Berton; Brauch, Hiltrud; Lee, Elaine; Simmons, Alfreda; Russell, Edward K.; Nam, Myong H.; Gazdar, Adi F.

doi:10.1093/jnci/81.16.1223

Cited by 49 publications

(26 citation statements)

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“…Despite the complexity of these alterations, recurrent chromosome gains and losses have been identified by modern cytogenetic and molecular techniques (17,18). In agreement with the current body of literature, extensive 3p deletions have been described as a typical alteration in lung PDECs (19), whereas the same observation has not been shown in very small series of extrapulmonary PDECs (20). In addition, losses of 17p, 5q, 10q, 16q and gains of 1p, 3q, 14q have been identified as very frequent chromosomal alterations in lung PDECs (17).…”

Section: Introductionsupporting

confidence: 58%

Allelotypes and Fluorescence In situ Hybridization Profiles of Poorly Differentiated Endocrine Carcinomas of Different Sites

Furlan

Bernasconi

Uccella

et al. 2005

Clinical Cancer Research

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Purpose: The aim of this work was to investigate the genotypic profiles of 36 poorly differentiated endocrine carcinoma (PDEC) of different sites to verify if their very similar phenotype may reflect similar pattern of genetic anomalies and if useful diagnostic or prognostic markers may be pointed out. Experimental Design: All tumors were microallelotyped at 57 microsatellite on 11 autosomes and the allelotypes of a selected panel of tumors were validated by interphasic fluorescence in situ hybridization with centromeric probes for chromosomes 1, 3, 6, 11, 17, and 18 and a probe specific for p53. Results: Regardless of the primary sites, PDECs exhibit very complex allelotypes (86%) and TP53 allelic imbalance (89%). Among these cases, fluorescence in situ hybridization analysis confirmed the presence of multiple aneusomies and a chromosome instability phenotype. Very low percentage of allelic imbalance (AI) and few aneuploidies were detected in only five PDECs for which an overall longer survival was observed. We found recurrent AI on 3p, 5, and 11q13 in lung PDECs, on 5q21, 8p, and 18q21 in colorectal PDECs and on 7 and 11q22 in gastric PDECs. Significantly better outcome was observed in patients with PDEC exhibiting 8q AIs and absence of AI at chromosome regions 6q25 and 6p. Conclusions: The concurrence of p53 inactivation and aneuploidies or chromosome instability are the main features of PDECs. However, the specific allelotypes observed in relation to primary site support the hypothesis that PDECs and exocrine carcinomas of all sites may share early pathogenetic mechanisms. Molecular markers of potential diagnostic and prognostic values for PDECs of different sites have been identified.

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Section: Introductionsupporting

confidence: 58%

Allelotypes and Fluorescence In situ Hybridization Profiles of Poorly Differentiated Endocrine Carcinomas of Different Sites

Furlan

Bernasconi

Uccella

et al. 2005

Clinical Cancer Research

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“…Expression of the TMPRSS2-ERG fusion gene, which has been suggested to be a marker of an aggressive tumour phenotype found in up to 50% of prostate cancer (Qu et al 2013, Razzak 2013, increased in the NCI-H660 prostate cancer cell line following treatment with an ERA agonist (Setlur et al 2008). NCI-H660 is an AR-negative prostate cancer cell line expressing the TMPRSS2-ERG fusion gene (Mertz et al 2007), derived from the lymph node metastasis of a small-cell prostate tumour with neuroendocrine differentiation (Johnson et al 1989, Lai et al 1995. Expression of ERA and aromatase with the R264C polymorphism has been shown to result in shorter progression-free survival and an increased risk of developing CRPC in a study of 115 men treated with docetaxel (Sissung et al 2011).…”

Section: Er Expression In Prostate Cancermentioning

confidence: 99%

Estrogen receptor beta in prostate cancer: friend or foe?

Nelson¹,

Tilley²,

Neal³

et al. 2014

Endocrine-Related Cancer

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Prostate cancer is the commonest, non-cutaneous cancer in men. At present, there is no cure for the advanced, castration-resistant form of the disease. Estrogen has been shown to be important in prostate carcinogenesis, with evidence resulting from epidemiological, cancer cell line, human tissue and animal studies. The prostate expresses both estrogen receptor alpha (ERA) and estrogen receptor beta (ERB). Most evidence suggests that ERA mediates the harmful effects of estrogen in the prostate, whereas ERB is tumour suppressive, but trials of ERB-selective agents have not translated into improved clinical outcomes. The role of ERB in the prostate remains unclear and there is increasing evidence that isoforms of ERB may be oncogenic. Detailed study of ERB and ERB isoforms in the prostate is required to establish their cell-specific roles, in order to determine if therapies can be directed towards ERB-dependent pathways. In this review, we summarise evidence on the role of ERB in prostate cancer and highlight areas for future research.

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“…However, unlike SCLC, malignant cells from patients with extrapulmonary small cell carcinoma do not exhibit macromolecular 3p deletions, a finding that suggests a different pathogenesis. 17 Nearly all SCLCs are immunoreactive for keratin, epithelial membrane antigen, and thyroid transcription factor-1. Most SCLCs also stain positively for markers of neuroendocrine differentiation, including chromogranin A, neuron-specific enolase, neural cell adhesion molecule (NCAM; CD56), and synaptophysin.…”

Section: Lung Neuroendocrine Tumorsmentioning

confidence: 99%