The Resource Deregulation of the notch signaling pathway N B-cell chronic lymphocytic leukemia, by Charu Kaiwar, (electronic resource)
Deregulation of the notch signaling pathway N B-cell chronic lymphocytic leukemia, by Charu Kaiwar, (electronic resource)
Resource Information
The item Deregulation of the notch signaling pathway N B-cell chronic lymphocytic leukemia, by Charu Kaiwar, (electronic resource) represents a specific, individual, material embodiment of a distinct intellectual or artistic creation found in University of Missouri Libraries.This item is available to borrow from 2 library branches.
Resource Information
The item Deregulation of the notch signaling pathway N B-cell chronic lymphocytic leukemia, by Charu Kaiwar, (electronic resource) represents a specific, individual, material embodiment of a distinct intellectual or artistic creation found in University of Missouri Libraries.
This item is available to borrow from 2 library branches.
- Summary
- 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]
- Language
- eng
- Extent
- 1 online resource (v, 22 pages
- Note
-
- The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file
- Thesis advisors: Charles W. Caldwell M.D., PhD and Lynda B. Bennett PhD
- "May 2011"
- Label
- Deregulation of the notch signaling pathway N B-cell chronic lymphocytic leukemia
- Title
- Deregulation of the notch signaling pathway N B-cell chronic lymphocytic leukemia
- Statement of responsibility
- by Charu Kaiwar
- Subject
-
- Cell Death -- drug effects
- Cell death
- Cellular signal transduction
- Chronic lymphocytic leukemia
- Dissertations, Academic -- University of Missouri--Columbia -- pathology
- Electronic books
- Electronic bookss
- Electronic dissertations
- Electronic government information -- Missouri
- Endopeptidases -- Inhibitors
- Leukemia, Lymphocytic, Chronic, B-Cell -- metabolism
- Amyloid Precursor Protein Secretases -- antagonists & inhibitors
- Receptors, Notch -- metabolism
- Signal Transduction
- cell death
- gene transcripton
- leukemia
- notch signaling
- Notch proteins -- Metabolism
- Language
- eng
- Summary
- 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]
- Cataloging source
- MMU
- http://library.link/vocab/creatorName
- Kaiwar, Charu
- Degree
- M.S.
- Dissertation year
- 2011.
- Government publication
- government publication of a state province territory dependency etc
- Granting institution
- University of Missouri--Columbia,
- Illustrations
- illustrations
- Index
- no index present
- LC call number
- RC280.L9
- Literary form
- non fiction
- Nature of contents
-
- dictionaries
- bibliography
- theses
- NLM call number
- QZ 350
- http://library.link/vocab/subjectName
-
- Chronic lymphocytic leukemia
- Notch proteins
- Cellular signal transduction
- Endopeptidases
- Cell death
- Leukemia, Lymphocytic, Chronic, B-Cell
- Receptors, Notch
- Amyloid Precursor Protein Secretases
- Cell Death
- Signal Transduction
- Label
- Deregulation of the notch signaling pathway N B-cell chronic lymphocytic leukemia, by Charu Kaiwar, (electronic resource)
- Note
-
- The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file
- Thesis advisors: Charles W. Caldwell M.D., PhD and Lynda B. Bennett PhD
- "May 2011"
- Bibliography note
- Includes bibliographical references
- Carrier category
- online resource
- Carrier category code
-
- cr
- Carrier MARC source
- rdacarrier
- Content category
- text
- Content type code
-
- txt
- Content type MARC source
- rdacontent
- Control code
- 809702821
- Extent
- 1 online resource (v, 22 pages
- Form of item
- online
- Media category
- computer
- Media MARC source
- rdamedia
- Media type code
-
- c
- Note
- MU-HSL: Access is limited to the University of Missouri - Columbia campus.
- Other physical details
- illustrations (some color).
- Specific material designation
- remote
- System control number
- (OCoLC)809702821
- Label
- Deregulation of the notch signaling pathway N B-cell chronic lymphocytic leukemia, by Charu Kaiwar, (electronic resource)
- Note
-
- The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file
- Thesis advisors: Charles W. Caldwell M.D., PhD and Lynda B. Bennett PhD
- "May 2011"
- Bibliography note
- Includes bibliographical references
- Carrier category
- online resource
- Carrier category code
-
- cr
- Carrier MARC source
- rdacarrier
- Content category
- text
- Content type code
-
- txt
- Content type MARC source
- rdacontent
- Control code
- 809702821
- Extent
- 1 online resource (v, 22 pages
- Form of item
- online
- Media category
- computer
- Media MARC source
- rdamedia
- Media type code
-
- c
- Note
- MU-HSL: Access is limited to the University of Missouri - Columbia campus.
- Other physical details
- illustrations (some color).
- Specific material designation
- remote
- System control number
- (OCoLC)809702821
Subject
- Cell Death -- drug effects
- Cell death
- Cellular signal transduction
- Chronic lymphocytic leukemia
- Dissertations, Academic -- University of Missouri--Columbia -- pathology
- Electronic books
- Electronic bookss
- Electronic dissertations
- Electronic government information -- Missouri
- Endopeptidases -- Inhibitors
- Leukemia, Lymphocytic, Chronic, B-Cell -- metabolism
- Amyloid Precursor Protein Secretases -- antagonists & inhibitors
- Receptors, Notch -- metabolism
- Signal Transduction
- cell death
- gene transcripton
- leukemia
- notch signaling
- Notch proteins -- Metabolism
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