WorldCat Identities

Kaiwar, Charu

Overview
Works: 3 works in 3 publications in 1 language and 5 library holdings
Genres: Academic theses 
Roles: Author
Classifications: RC280.L9, 616.994
Publication Timeline
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Most widely held works by Charu Kaiwar
Late onset asymptomatic pancreatic neuroendocrine tumor - A case report on the phenotypic expansion for MEN1 by Charu Kaiwar( )

1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide

De novo variants in FBXO11 cause a syndromic form of intellectual disability with behavioral problems and dysmorphisms by Sandra Jansen( )

1 edition published in 2019 in English and held by 2 WorldCat member libraries worldwide

Deregulation of the notch signaling pathway N B-cell chronic lymphocytic leukemia by Charu Kaiwar( )

1 edition published in 2011 in English and held by 1 WorldCat member library worldwide

B-cell Chronic Lymphocytic Leukemia (B-CLL) is the most common hematological malignancy in United States [1], characterized by CD5 B-lymphocytes in peripheral blood. Deregulation of the Notch signaling pathway has been suggested to contribute to B-CLL pathogenesis [2-4]. Our objective was to characterize the differential expression of the Notch pathway genes in B-CLL cell lines as compared to normal B-cells and to determine if inhibiting the Notch pathway using [gamma]-secretase inhibitors (GSIs would lead to increased death in B-CLL cells. We observed over-expression of Notch pathway genes in three B-CLL cell lines. Treatment with either of the GSIs, DAPT(N-[N-(3, 5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl Ester) or Compound E, failed to have any effect on proliferation or death of these cells. Moreover, there was no alteration in transcription of downstream Notch target genes Hairy and enhancer of split 1, (HES1) Hairy/enhancer-of-split related with YRPW motif 1(HEY1), or Deltex homolog 1 (DTX1) in treated vs. untreated cells. These findings suggest that although Notch pathway genes seem to up regulated in B-B-CLL, inhibition of the pathway does not lead to cell death nor does it alter Notch target gene transcripton. One explanation could be that the Notch receptor is constitutively active in B-CLL as in other hematological malignancies like Tcell-Acute Lymphoblastic Leukemia (T-ALL) [5]. Alternatively, the survival of leukemic cells in B-CLL as well as transcription of the target genes examined, may be a combined result of signaling via the Notch and other signaling pathways such as Jak-STAT, Wnt and Sonic hedgehog, which have roles in B-CLL pathogenesis [6-10]
 
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Audience level: 0.91 (from 0.69 for Deregulati ... to 0.97 for Deregulati ...)

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