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

doi:10.1016/j.leukres.2012.06.014

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 journal › Article › peer-review

7 Scopus citations

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 language	English (US)
Pages (from-to)	1267-1273
Number of pages	7
Journal	Leukemia Research
Volume	36
Issue number	10
DOIs	https://doi.org/10.1016/j.leukres.2012.06.014
State	Published - Oct 2012

Keywords

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

ASJC Scopus subject areas

Hematology
Oncology
Cancer Research

MD Anderson CCSG core facilities

Tissue Biospecimen and Pathology Resource

Access to Document

10.1016/j.leukres.2012.06.014

Cite this

Ramirez, E., Singh, R. R., Kunkalla, K., Liu, Y., Qu, C., Cain, C., Multani, A. S., Lennon, P. A., Jackacky, J., Ho, M., Dawud, S., Gu, J., Yang, S., Hu, P. C., & Vega, F. (2012). Defining causative factors contributing in the activation of hedgehog signaling in diffuse large B-cell lymphoma. Leukemia Research, 36(10), 1267-1273. https://doi.org/10.1016/j.leukres.2012.06.014

@article{e5c5464a1fa94b9e8bdc6ae3b69d6c76,

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, GLI, Gene copy number, 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",

note = "Funding Information: This work was supported by funds from The Translational Grant of the Leukemia & Lymphoma Society (to RS and FV) , and K08 Physician-Scientist Award 1 K08 CA143151-01 (NIH) (to FV). The primary tumor samples were provided by the Hematopathology Tissue Bank of the UT MD Anderson Cancer Center (supported by the NCI/NIH Grant CA16672 ). The cytogenetic studies were performed with the collaboration of the Genetic Core laboratory supported by the Cancer Center Core grant CA016672 by the NCI. ",

year = "2012",

month = oct,

doi = "10.1016/j.leukres.2012.06.014",

language = "English (US)",

volume = "36",

pages = "1267--1273",

journal = "Leukemia Research",

issn = "0145-2126",

publisher = "Elsevier Limited",

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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

N1 - Funding Information: This work was supported by funds from The Translational Grant of the Leukemia & Lymphoma Society (to RS and FV) , and K08 Physician-Scientist Award 1 K08 CA143151-01 (NIH) (to FV). The primary tumor samples were provided by the Hematopathology Tissue Bank of the UT MD Anderson Cancer Center (supported by the NCI/NIH Grant CA16672 ). The cytogenetic studies were performed with the collaboration of the Genetic Core laboratory supported by the Cancer Center Core grant CA016672 by the NCI.

PY - 2012/10

Y1 - 2012/10

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 - GLI

KW - Gene copy number

KW - Hedgehog pathway

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

Abstract

Keywords

ASJC Scopus subject areas

MD Anderson CCSG core facilities

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