PMID- 10959095
OWN - NLM
STAT- MEDLINE
DCOM- 20001011
LR  - 20211008
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 29
IP  - 2
DP  - 2000 Oct
TI  - Interstitial deletion of 11q13 sequences in HeLa cells.
PG  - 157-65
AB  - Previous cytogenetic and molecular genetic studies have shown that the HeLa 
      (cervical carcinoma) cell line D98/AH-2 contains two apparently normal copies of 
      chromosome 11 and additional 11q13-25 material translocated onto a chromosome 3 
      marker. To determine the 11q13 breakpoint, we performed fluorescence in situ 
      hybridization (FISH) using 18 different 11q13 specific BAC (bacterial artificial 
      chromosome) and cosmid probes spanning a 5.6 Mb interval. Markers localized to 
      the multiple endocrine neoplasia type 1 (MEN1) gene (menin) were also included in 
      the analysis. The FISH study identified an interstitial deletion between markers 
      D11S449 and GSTP1, an interval of 2.3 Mb, in the marker chromosome. This deletion 
      did not include the MEN1 gene. Because point mutations and methylations can 
      inactivate the MEN1 gene, single stranded conformational polymorphism (SSCP) and 
      Northern and Western blot analyses were performed with MEN1 specific probes and 
      antibody. SSCP did not reveal mutations of the MEN1 gene in HeLa or in seven 
      other cervical cancer cell lines. Northern and Western blot studies revealed 
      normal levels of expression of this gene in the cervical cancer cell lines as 
      well as in HeLa cell derived tumorigenic hybrids. Because deletions of tumor 
      suppressor genes often occur in cancer progression, we hypothesize that the 
      inactivation of a tumor suppressor gene other than MEN1, localized to the 2.3 Mb 
      interval on 11q13, might play a role in the abnormal growth behavior of HeLa 
      cells in vitro or in vivo.
CI  - Copyright 2000 Wiley-Liss, Inc.
FAU - Srivatsan, E S
AU  - Srivatsan ES
AD  - Department of Surgery, VAGLAHS West Los Angeles, UCLA School of Medicine, Los 
      Angeles, California. esrivats@ucla.edu
FAU - Bengtsson, U
AU  - Bengtsson U
FAU - Manickam, P
AU  - Manickam P
FAU - Benyamini, P
AU  - Benyamini P
FAU - Chandrasekharappa, S C
AU  - Chandrasekharappa SC
FAU - Sun, C
AU  - Sun C
FAU - Stanbridge, E J
AU  - Stanbridge EJ
FAU - Redpath, J L
AU  - Redpath JL
LA  - eng
GR  - CA 19401/CA/NCI NIH HHS/United States
GR  - CA 39312/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (MEN1 protein, human)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Proto-Oncogene Proteins)
SB  - IM
MH  - Cell Transformation, Neoplastic/genetics
MH  - Chromosomes, Human, Pair 11/*genetics
MH  - Female
MH  - HeLa Cells
MH  - Humans
MH  - Hybrid Cells
MH  - Multiple Endocrine Neoplasia Type 1/etiology/genetics/metabolism
MH  - Mutation
MH  - Neoplasm Proteins/biosynthesis/genetics
MH  - *Proto-Oncogene Proteins
MH  - *Sequence Deletion
MH  - Tumor Cells, Cultured
MH  - Uterine Cervical Neoplasms/genetics
EDAT- 2000/08/26 11:00
MHDA- 2000/10/14 11:01
CRDT- 2000/08/26 11:00
PHST- 2000/08/26 11:00 [pubmed]
PHST- 2000/10/14 11:01 [medline]
PHST- 2000/08/26 11:00 [entrez]
AID - 10.1002/1098-2264(2000)9999:9999<::AID-GCC1024>3.0.CO;2-P [pii]
AID - 10.1002/1098-2264(2000)9999:9999<::aid-gcc1024>3.0.co;2-p [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2000 Oct;29(2):157-65. doi: 
      10.1002/1098-2264(2000)9999:9999<::aid-gcc1024>3.0.co;2-p.