PMID- 9212742
OWN - NLM
STAT- MEDLINE
DCOM- 19970731
LR  - 20181113
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 151
IP  - 1
DP  - 1997 Jul
TI  - Amplification of CCND1 and expression of its protein product, cyclin D1, in 
      ductal carcinoma in situ of the breast.
PG  - 161-8
AB  - Ductal carcinoma in situ (DCIS) of the breast is a heterogeneous disease 
      clinically and biologically. The few available studies of its natural history 
      implicate DCIS as a non-obligate precursor for invasive carcinoma. We have used 
      fluorescence in situ hybridization (FISH) to detect gene amplification of the 
      cell cycle regulator gene CCND1 in 88 examples of formalin-fixed, 
      paraffin-embedded DCIS. Expression of its protein product cyclin D1 was detected 
      by immunohistochemistry. CCND1 was amplified in 18% of DCIS cases. High grade 
      DCIS was more likely to show amplification than low grade DCIS (32% versus 8%; P 
      = 0.08). Gene amplification was associated with cyclin D1 protein expression (P = 
      0.001), although cyclin D1 was detected in cases that did not demonstrate gene 
      amplification. Overall, cyclin D1 protein was detected in 50% of DCIS cases. 
      Although only 2 of 23 (8%) cases of low grade DCIS had CCND1 amplification, over 
      50% (13/23) of these cases expressed cyclin D1 protein. Low grade DCIS had a 
      higher mean percentage of nuclei expressing cyclin D1 than did intermediate or 
      high grade DCIS (P = 0.007). Mechanisms other than gene amplification may be 
      responsible for increased cyclin D1 protein in DCIS, especially in low grade 
      DCIS. Identifying mechanisms that control cell cycle progression in DCIS may 
      yield clues to its biological behavior.
FAU - Simpson, J F
AU  - Simpson JF
AD  - Division of Pathology, City of Hope National Medical Center, Duarte, California, 
      USA.
FAU - Quan, D E
AU  - Quan DE
FAU - O'Malley, F
AU  - O'Malley F
FAU - Odom-Maryon, T
AU  - Odom-Maryon T
FAU - Clarke, P E
AU  - Clarke PE
LA  - eng
GR  - CA33572/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Cyclins)
RN  - 0 (Oncogene Proteins)
RN  - 136601-57-5 (Cyclin D1)
SB  - IM
MH  - Analysis of Variance
MH  - Breast Neoplasms/*genetics/pathology
MH  - Carcinoma in Situ/*genetics/pathology
MH  - Carcinoma, Ductal, Breast/*genetics/pathology
MH  - Cyclin D1
MH  - Cyclins/*biosynthesis/*genetics
MH  - *Gene Amplification
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization, Fluorescence
MH  - Multicenter Studies as Topic
MH  - Oncogene Proteins/*biosynthesis/*genetics
PMC - PMC1857915
EDAT- 1997/07/01 00:00
MHDA- 1997/07/01 00:01
PMCR- 1998/01/01
CRDT- 1997/07/01 00:00
PHST- 1997/07/01 00:00 [pubmed]
PHST- 1997/07/01 00:01 [medline]
PHST- 1997/07/01 00:00 [entrez]
PHST- 1998/01/01 00:00 [pmc-release]
PST - ppublish
SO  - Am J Pathol. 1997 Jul;151(1):161-8.