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Diagnosis of Intraabdominal and Mediastinal Sarcoidosis Using Endoscopic Ultrasound Guided Fine Needle Aspiration [Meeting Abstract]

Michael, Hazar; Ho, Sammy; Pollack, Bonnie; Gupta, Mala; Gress, Frank
ISI:000207499900708
ISSN: 0016-5107
CID: 3484222

Methods for Detecting Genetic Abnormalities in Ovarian Carcinoma Using Fluorescence in situ Hybridization and Immunohistochemistry

Chapter by: Huang, Ngan F.; Gupta, Mala; Luke, Sunny
in: HANDBOOK OF IMMUNOHISTOCHEMISTRY AND IN SITU HYBRIDIZATION OF HUMAN CARCINOMAS, VOL 4: MOLECULAR GENETICS, GASTROINTESTINAL CARCINOMA, AND OVARIAN CARCINOMA by ; Hayat, MA
SAN DIEGO : ELSEVIER ACADEMIC PRESS INC, 2006
pp. 307-332
ISBN: 978-0-08-045787-1
CID: 3484252

Functional characterization of core promoter elements: the downstream core element is recognized by TAF1

Lee, Dong-Hoon; Gershenzon, Naum; Gupta, Malavika; Ioshikhes, Ilya P; Reinberg, Danny; Lewis, Brian A
Downstream elements are a newly appreciated class of core promoter elements of RNA polymerase II-transcribed genes. The downstream core element (DCE) was discovered in the human beta-globin promoter, and its sequence composition is distinct from that of the downstream promoter element (DPE). We show here that the DCE is a bona fide core promoter element present in a large number of promoters and with high incidence in promoters containing a TATA motif. Database analysis indicates that the DCE is found in diverse promoters, supporting its functional relevance in a variety of promoter contexts. The DCE consists of three subelements, and DCE function is recapitulated in a TFIID-dependent manner. Subelement 3 can function independently of the other two and shows a TFIID requirement as well. UV photo-cross-linking results demonstrate that TAF1/TAF(II)250 interacts with the DCE subelement DNA in a sequence-dependent manner. These data show that downstream elements consist of at least two types, those of the DPE class and those of the DCE class; they function via different DNA sequences and interact with different transcription activation factors. Finally, these data argue that TFIID is, in fact, a core promoter recognition complex
PMCID:1265815
PMID: 16227614
ISSN: 0270-7306
CID: 68411

Radiology-Pathology Conference: Bilateral renal oncocytomas [Case Report]

Shin, Lewis K; Badler, Ruth L; Bruno, Frank M; Gupta, Mala; Katz, Douglas S
Oncocytoma is an uncommon benign, typically solitary renal tumor first reported in 1942. Renal oncocytomas are rarely multiple and/or bilateral. Accurate preoperative diagnosis and differentiation from renal carcinoma is difficult. We report the radiology and pathology of a patient with bilateral renal oncocytomas and review the literature of this rare presentation.
PMID: 15471666
ISSN: 0899-7071
CID: 3002312

Detection of numerical chromosomal abnormalities in epithelial ovarian neoplasms by fluorescence in situ hybridization (FISH) and a review of the current literature

Huang, Ngan-Fong Tina; Gupta, Mala; Varghese, Sara; Rao, Sujatha; Luke, Sunny
Preliminary retrospective chromosomal analysis was performed using fluorescence in situ hybridization (FISH) with alphoid DNA probes for chromosomes 1, 3, 6, 8, 12, 17, and X. Twenty-four epithelial ovarian tumors were examined in this pilot study, including 8 borderline (LMP) serous tumors, 9 serous carcinoma, and 7 mucinous carcinoma. Hybridization signals were counted to demonstrate the frequency of aneusomy, trace chromosomal progression, and identify the predominance of chromosome copy number abnormalities that are specific to a particular histotype. The preliminary results revealed almost an equal number of mean aneusomies in serous (58.13 +/- 13%) and mucinous (64.33 +/- 10%) carcinoma, both of which were slightly higher than borderline serous tumors (50.57 +/- 17%). Hyposomies 3 and X were significantly higher in mucinous than in serous ovarian carcinomas, and lowest in borderline serous tumors (P<0.05 and P<0.01). Signal losses were a more frequent abnormality in all three histologic subtypes. Mucinous carcinomas showed a loss of chromosomes 8 (45.00 +/- 28%) and 3 (43.14 +/- 16%), in addition to a loss of chromosome X (56.29 +/- 12%). Serous carcinomas showed a gain of chromosome 1 (39.44 +/- 32%), followed by losses of chromosomes 6 (37.00 +/- 20%), 17 (36.44 +/- 19%), and 8 (36.89 +/- 19%). In borderline serous tumors, the most frequent findings were losses of chromosomes 6 (38.00 +/- 17%), 12 (36.88 +/- 17%), and 3 (36.13 +/- 21%). However, further research is necessary to substantiate these preliminary results and elucidate their clinical significance. A brief review of the literature pertaining to interphase cytogenetics in ovarian epithelial tumors is discussed also.
PMID: 12051640
ISSN: 1541-2016
CID: 3484282