Daniel Pinkel
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Explore the profile of Daniel Pinkel including associated specialties, affiliations and a list of published articles.
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68
Citations
7152
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Recent Articles
11.
Tokuyasu T, Cotter P, Segraves R, Harris J, Elder M, Gonzales M, et al.
Am J Med Genet A
. 2007 Mar;
143A(9):925-32.
PMID: 17394204
Constitutional submicroscopic DNA copy number alterations have been shown to cause numerous medical genetic syndromes, and are suspected to occur in a portion of cases for which the causal events...
12.
Climent J, Dimitrow P, Fridlyand J, Palacios J, Siebert R, Albertson D, et al.
Cancer Res
. 2007 Jan;
67(2):818-26.
PMID: 17234794
Despite the recent consensus on the eligibility of adjuvant systemic therapy in patients with lymph node-negative breast cancer (NNBC) based on clinicopathologic criteria, specific biological markers are needed to predict...
13.
Chin K, DeVries S, Fridlyand J, Spellman P, Roydasgupta R, Kuo W, et al.
Cancer Cell
. 2006 Dec;
10(6):529-41.
PMID: 17157792
This study explores the roles of genome copy number abnormalities (CNAs) in breast cancer pathophysiology by identifying associations between recurrent CNAs, gene expression, and clinical outcome in a set of...
14.
Neve R, Chin K, Fridlyand J, Yeh J, Baehner F, Fevr T, et al.
Cancer Cell
. 2006 Dec;
10(6):515-27.
PMID: 17157791
Recent studies suggest that thousands of genes may contribute to breast cancer pathophysiologies when deregulated by genomic or epigenomic events. Here, we describe a model "system" to appraise the functional...
15.
Stransky N, Vallot C, Reyal F, Bernard-Pierrot I, Gil Diez de Medina S, Segraves R, et al.
Nat Genet
. 2006 Nov;
38(12):1386-96.
PMID: 17099711
Genetic and epigenetic alterations have been identified that lead to transcriptional deregulation in cancers. Genetic mechanisms may affect single genes or regions containing several neighboring genes, as has been shown...
16.
Thorns C, Bastian B, Pinkel D, Roydasgupta R, Fridlyand J, Merz H, et al.
Genes Chromosomes Cancer
. 2006 Oct;
46(1):37-44.
PMID: 17044049
Angioimmunoblastic T-cell lymphoma (AILT) is a histopathologically well-defined entity. However, despite a number of cytogenetic studies, the genetic basis of this lymphoma entity is not clear. Moreover, there is an...
17.
Mestre-Escorihuela C, Rubio-Moscardo F, Richter J, Siebert R, Climent J, Fresquet V, et al.
Blood
. 2006 Sep;
109(1):271-80.
PMID: 16960149
Integrative genomic and gene-expression analyses have identified amplified oncogenes in B-cell non-Hodgkin lymphoma (B-NHL), but the capability of such technologies to localize tumor suppressor genes within homozygous deletions remains unexplored....
18.
Curtin J, Busam K, Pinkel D, Bastian B
J Clin Oncol
. 2006 Aug;
24(26):4340-6.
PMID: 16908931
Purpose: Melanomas on mucosal membranes, acral skin (soles, palms, and nail bed), and skin with chronic sun-induced damage have infrequent mutations in BRAF and NRAS, genes within the mitogen-activated protein...
19.
Sharp A, Hansen S, Selzer R, Cheng Z, Regan R, Hurst J, et al.
Nat Genet
. 2006 Aug;
38(9):1038-42.
PMID: 16906162
Genomic disorders are characterized by the presence of flanking segmental duplications that predispose these regions to recurrent rearrangement. Based on the duplication architecture of the genome, we investigated 130 regions...
20.
Locke D, Sharp A, McCarroll S, McGrath S, Newman T, Cheng Z, et al.
Am J Hum Genet
. 2006 Jul;
79(2):275-90.
PMID: 16826518
Studies of copy-number variation and linkage disequilibrium (LD) have typically excluded complex regions of the genome that are rich in duplications and prone to rearrangement. In an attempt to assess...