Defining causative factors contributing in the activation of hedgehog signaling in diffuse large B-cell lymphoma

Elisa Ramirez, Rajesh R. Singh, Kranthi Kunkalla, Yadong Liu, Changju Qu, Christine Cain, Asha S. Multani, Patrick A. Lennon, Jared Jackacky, Michael Ho, Sity Dawud, Jun Gu, Su Yang, Peter C. Hu, Francisco Vega

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Hedgehog (Hh) signaling pathway is activated in diffuse large B-cell lymphoma (DLBCL). Genetic abnormalities that explain activation of Hh signaling in DLBCL are unknown. We investigate the presence of amplifications of Hh genes that might result in activation of this pathway in DLBCL. Our data showed few extra copies of GLI1 and SMO due to chromosomal aneuploidies in a subset of DLBCL cell lines. We also showed that pharmacologic inhibition of PI3K/AKT and NF-κB pathways resulted in decreased expression of GLI1 and Hh ligands. In conclusion, our data support the hypothesis that aberrant activation of Hh signaling in DLBCL mainly results from integration of deregulated oncogenic signaling inputs converging into Hh signaling.

Original languageEnglish
Pages (from-to)1267-1273
Number of pages7
JournalLeukemia Research
Volume36
Issue number10
DOIs
StatePublished - Oct 1 2012
Externally publishedYes

Fingerprint

Lymphoma, Large B-Cell, Diffuse
Gene Amplification
Aneuploidy
Phosphatidylinositol 3-Kinases
Ligands
Cell Line

Keywords

  • Diffuse large B-cell lymphoma
  • Gene copy number
  • GLI
  • Hedgehog pathway

ASJC Scopus subject areas

  • Cancer Research
  • Hematology
  • Oncology

Cite this

Defining causative factors contributing in the activation of hedgehog signaling in diffuse large B-cell lymphoma. / Ramirez, Elisa; Singh, Rajesh R.; Kunkalla, Kranthi; Liu, Yadong; Qu, Changju; Cain, Christine; Multani, Asha S.; Lennon, Patrick A.; Jackacky, Jared; Ho, Michael; Dawud, Sity; Gu, Jun; Yang, Su; Hu, Peter C.; Vega, Francisco.

In: Leukemia Research, Vol. 36, No. 10, 01.10.2012, p. 1267-1273.

Research output: Contribution to journalArticle

Ramirez, E, Singh, RR, Kunkalla, K, Liu, Y, Qu, C, Cain, C, Multani, AS, Lennon, PA, Jackacky, J, Ho, M, Dawud, S, Gu, J, Yang, S, Hu, PC & Vega, F 2012, 'Defining causative factors contributing in the activation of hedgehog signaling in diffuse large B-cell lymphoma', Leukemia Research, vol. 36, no. 10, pp. 1267-1273. https://doi.org/10.1016/j.leukres.2012.06.014
Ramirez, Elisa ; Singh, Rajesh R. ; Kunkalla, Kranthi ; Liu, Yadong ; Qu, Changju ; Cain, Christine ; Multani, Asha S. ; Lennon, Patrick A. ; Jackacky, Jared ; Ho, Michael ; Dawud, Sity ; Gu, Jun ; Yang, Su ; Hu, Peter C. ; Vega, Francisco. / Defining causative factors contributing in the activation of hedgehog signaling in diffuse large B-cell lymphoma. In: Leukemia Research. 2012 ; Vol. 36, No. 10. pp. 1267-1273.
@article{35a43c9190074e2f8e1a645b89355876,
title = "Defining causative factors contributing in the activation of hedgehog signaling in diffuse large B-cell lymphoma",
abstract = "Hedgehog (Hh) signaling pathway is activated in diffuse large B-cell lymphoma (DLBCL). Genetic abnormalities that explain activation of Hh signaling in DLBCL are unknown. We investigate the presence of amplifications of Hh genes that might result in activation of this pathway in DLBCL. Our data showed few extra copies of GLI1 and SMO due to chromosomal aneuploidies in a subset of DLBCL cell lines. We also showed that pharmacologic inhibition of PI3K/AKT and NF-κB pathways resulted in decreased expression of GLI1 and Hh ligands. In conclusion, our data support the hypothesis that aberrant activation of Hh signaling in DLBCL mainly results from integration of deregulated oncogenic signaling inputs converging into Hh signaling.",
keywords = "Diffuse large B-cell lymphoma, Gene copy number, GLI, Hedgehog pathway",
author = "Elisa Ramirez and Singh, {Rajesh R.} and Kranthi Kunkalla and Yadong Liu and Changju Qu and Christine Cain and Multani, {Asha S.} and Lennon, {Patrick A.} and Jared Jackacky and Michael Ho and Sity Dawud and Jun Gu and Su Yang and Hu, {Peter C.} and Francisco Vega",
year = "2012",
month = "10",
day = "1",
doi = "10.1016/j.leukres.2012.06.014",
language = "English",
volume = "36",
pages = "1267--1273",
journal = "Leukemia Research",
issn = "0145-2126",
publisher = "Elsevier Limited",
number = "10",

}

TY - JOUR

T1 - Defining causative factors contributing in the activation of hedgehog signaling in diffuse large B-cell lymphoma

AU - Ramirez, Elisa

AU - Singh, Rajesh R.

AU - Kunkalla, Kranthi

AU - Liu, Yadong

AU - Qu, Changju

AU - Cain, Christine

AU - Multani, Asha S.

AU - Lennon, Patrick A.

AU - Jackacky, Jared

AU - Ho, Michael

AU - Dawud, Sity

AU - Gu, Jun

AU - Yang, Su

AU - Hu, Peter C.

AU - Vega, Francisco

PY - 2012/10/1

Y1 - 2012/10/1

N2 - Hedgehog (Hh) signaling pathway is activated in diffuse large B-cell lymphoma (DLBCL). Genetic abnormalities that explain activation of Hh signaling in DLBCL are unknown. We investigate the presence of amplifications of Hh genes that might result in activation of this pathway in DLBCL. Our data showed few extra copies of GLI1 and SMO due to chromosomal aneuploidies in a subset of DLBCL cell lines. We also showed that pharmacologic inhibition of PI3K/AKT and NF-κB pathways resulted in decreased expression of GLI1 and Hh ligands. In conclusion, our data support the hypothesis that aberrant activation of Hh signaling in DLBCL mainly results from integration of deregulated oncogenic signaling inputs converging into Hh signaling.

AB - Hedgehog (Hh) signaling pathway is activated in diffuse large B-cell lymphoma (DLBCL). Genetic abnormalities that explain activation of Hh signaling in DLBCL are unknown. We investigate the presence of amplifications of Hh genes that might result in activation of this pathway in DLBCL. Our data showed few extra copies of GLI1 and SMO due to chromosomal aneuploidies in a subset of DLBCL cell lines. We also showed that pharmacologic inhibition of PI3K/AKT and NF-κB pathways resulted in decreased expression of GLI1 and Hh ligands. In conclusion, our data support the hypothesis that aberrant activation of Hh signaling in DLBCL mainly results from integration of deregulated oncogenic signaling inputs converging into Hh signaling.

KW - Diffuse large B-cell lymphoma

KW - Gene copy number

KW - GLI

KW - Hedgehog pathway

UR - http://www.scopus.com/inward/record.url?scp=84865163381&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84865163381&partnerID=8YFLogxK

U2 - 10.1016/j.leukres.2012.06.014

DO - 10.1016/j.leukres.2012.06.014

M3 - Article

C2 - 22809693

AN - SCOPUS:84865163381

VL - 36

SP - 1267

EP - 1273

JO - Leukemia Research

JF - Leukemia Research

SN - 0145-2126

IS - 10

ER -