PMID- 20978342
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130704
LR  - 20200930
IS  - 1523-7834 (Print)
IS  - 1523-7834 (Linking)
VI  - 36
IP  - 3
DP  - 2010
TI  - Examining Hedgehog pathway genes GLI3, SHH, and PTCH1 and the p53 target 
      GLIPR1/GLIPR1L1/GLIPR1L2 gene cluster using fluorescence in situ hybridization 
      uncovers GLIPR1/GLIPR1L1/GLIPR1L2 deletion in 9% of patients with multiple 
      myeloma.
PG  - 111-4
AB  - Mutations in genes regulating cell cycle and apoptosis are considered major 
      culprits for the malignant transformation of cancer cells. Aberrant activation of 
      the Hedgehog (HH) signaling pathway which primarily regulates genes involved in 
      cell growth, proliferation, survival and apoptosis has been demonstrated in 
      multiple myeloma. Mutations resulting in defective components of the p53 pathway, 
      which serves a critical role in mediating cellular stress response by triggering 
      DNA repair, cell cycle arrest, senescence and apoptosis, have also been 
      identified. This study focuses on detecting copy number variations for the 
      GLIPR1/GLIPR1L1/GLIPR1L2 gene cluster of the p53 pathway and three elements of 
      the HH pathway, SHH, PTCH1 and GLI3 in multiple myeloma (MM) using fluorescence 
      in situ hybridization (FISH). In eighteen samples, there was no evidence of 
      abnormal copy number for PTCH1, GLI3 or SHH. Thus, it is unlikely that copy 
      number variations of these genes are linked to multiple myeloma. However, a 
      deletion of the GLIPR1/GLIPR1L1/ GLIPR1L2 gene cluster, all p53 targets, was 
      found in three of 32 samples (9.4%) indicating that these deleted genes may have 
      significant implications in MM. Further studies should be performed to determine 
      the role of the GLIPR1/GLIPR1L1/GLIPR1L2 gene cluster in the pathogenesis of 
      multiple myeloma.
FAU - Tam, Michael
AU  - Tam M
AD  - School of Health Professions, University of Texas at Houston, Texas.
FAU - Lin, Pei
AU  - Lin P
FAU - Hu, Peter
AU  - Hu P
FAU - Lennon, Patrick A
AU  - Lennon PA
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Assoc Genet Technol
JT  - Journal of the Association of Genetic Technologists
JID - 9807282
EDAT- 2010/10/28 06:00
MHDA- 2010/10/28 06:01
CRDT- 2010/10/28 06:00
PHST- 2010/10/28 06:00 [entrez]
PHST- 2010/10/28 06:00 [pubmed]
PHST- 2010/10/28 06:01 [medline]
PST - ppublish
SO  - J Assoc Genet Technol. 2010;36(3):111-4.