PMID- 9787181
OWN - NLM
STAT- MEDLINE
DCOM- 19981130
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 92
IP  - 9
DP  - 1998 Nov 1
TI  - PTEN gene alterations in lymphoid neoplasms.
PG  - 3410-5
AB  - Recently, a novel phosphatase designated PTEN/MMAC1/TEP1 and located on 
      chromosome 10q23.3 has been implicated as a new tumor suppressor gene in human 
      cancer. Allelic loss and mutation of this gene has been reported in epithelial 
      derived tumors, including breast cancer and prostate cancer, and in glioblastoma 
      multiforme. The present study was designed to evaluate the potential involvement 
      of PTEN in the pathogenesis of lymphoid neoplasms. We analyzed 27 hematopoietic 
      cell lines (representing a variety of lymphoid lineages), 65 primary lymphoid 
      tumors (including 24 lymphoblastic leukemia/lymphoma [LBL], 30 large B-cell 
      lymphoma [LBCL], 7 Burkitt's lymphoma [BL], and 4 anaplastic large cell lymphoma 
      [ALCL]), and 25 nonmalignant lymph node controls. Gene deletion and gross 
      rearrangement were evaluated using Southern blot analysis, and mutations were 
      studied by polymerase chain reaction (PCR)-single-strand conformation 
      polymorphism (SSCP) (PCR-SSCP) and sequencing. Six of 27 cell lines (22.2%) and 3 
      of 65 primary lymphomas (4.6%) contained alterations of this gene. A large 
      homozygous deletion spanning exons 2 through 5 was detected in one LBL cell line, 
      and two insertions potentially resulting in premature termination, were detected 
      in a second LBL cell line. Nonconservative nucleotide variations were found in 
      two other cell lines (one LBCL and one BL) and in one primary case of LBCL. In 
      addition, two other cell lines (one BL and one myeloma) and two primary 
      lymphomas, both LBCL, contained small deletions within intron 7. These deletions 
      mapped to a poly-T-rich tract just 5' to the intron 7/exon 8 spice site. Their 
      significance is unclear, as they may represent polymorphisms. Overall, our 
      results suggest that abnormalities of the PTEN gene can contribute to 
      pathogenesis in a small percentage of malignant lymphomas.
FAU - Sakai, A
AU  - Sakai A
AD  - Hematopathology Section, Laboratory of Pathology, National Cancer Institute, 
      National Institutes of Health, Bethesda, MD, USA.
FAU - Thieblemont, C
AU  - Thieblemont C
FAU - Wellmann, A
AU  - Wellmann A
FAU - Jaffe, E S
AU  - Jaffe ES
FAU - Raffeld, M
AU  - Raffeld M
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (DNA, Neoplasm)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 3.1.3.2 (Phosphoric Monoester Hydrolases)
RN  - EC 3.1.3.67 (PTEN Phosphohydrolase)
RN  - EC 3.1.3.67 (PTEN protein, human)
SB  - IM
MH  - Cell Transformation, Neoplastic/genetics
MH  - Chromosomes, Human, Pair 10/*genetics
MH  - DNA, Neoplasm/genetics
MH  - Gene Deletion
MH  - *Genes, Tumor Suppressor
MH  - Hematopoietic Stem Cells/chemistry
MH  - Humans
MH  - Leukemia/*genetics
MH  - Lymphoma/*genetics
MH  - Neoplastic Stem Cells/chemistry
MH  - PTEN Phosphohydrolase
MH  - Phosphoric Monoester Hydrolases/*genetics
MH  - Polymerase Chain Reaction
MH  - Polymorphism, Single-Stranded Conformational
MH  - Tumor Cells, Cultured
MH  - *Tumor Suppressor Proteins
EDAT- 1998/10/27 00:00
MHDA- 1998/10/27 00:01
CRDT- 1998/10/27 00:00
PHST- 1998/10/27 00:00 [pubmed]
PHST- 1998/10/27 00:01 [medline]
PHST- 1998/10/27 00:00 [entrez]
AID - S0006-4971(20)57894-4 [pii]
PST - ppublish
SO  - Blood. 1998 Nov 1;92(9):3410-5.