Clinicopathologic implications of E-cadherin reactivity in patients with lobular carcinoma in situ of the breast

被引:0
作者
Goldstein, NS
Kestin, LL
Vicini, FA
机构
[1] William Beaumont Hosp, Dept Anat Pathol, Royal Oak, MI 48073 USA
[2] William Beaumont Hosp, Dept Radiat Oncol, Royal Oak, MI 48073 USA
关键词
E-cadherin; lobular carcinoma in situ (LCIS); breast; recurrence; carcinoma; lobular; follow-up;
D O I
10.1002/1097-0142(20010815)92:4<738::AID-CNCR1377>3.3.CO;2-Q
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
BACKGROUND. The current study addressed two questions pertaining to lobular carcinoma in situ (LCIS) of the breast. First, does the risk of a subsequent carcinoma decrease over time after an LCIS biopsy and second, what is the clinical significance of E-cadherin-reactive LCIS? METHODS. Eighty-two consecutive patients with a biopsy containing LCIS only, no prior history of breast carcinoma, and follow-up information available for the period 1955-1976 were reviewed. No patients underwent a mastectomy for LCIS. Four hundred eighty-six sections were stained with E-cadherin. E-cadherin reactivity was correlated with clinicopathologic features of the LCIS and subsequent tumors. The mean number of blocks stained per case was 5.9. The mean follow-up period was 21.6 years. RESULTS. Sixteen patients (19.5%) developed 21 subsequent invasive carcinomas (9 ipsilateral, 2 contralateral, and 5 bilateral carcinomas). The 10-year and 20-year actuarial rates of developing subsequent carcinoma were 7.8% and 15.4%, respectively. Six of the 21 carcinomas (29%) developed after 20 years. Nine LCIS cases (10.9%) had focal E-cadherin reactivity. When compared with patients with nonreactive LCIS, patients with E-cadherin-reactive LCIS more frequently developed a subsequent ipsilateral carcinoma that had a ductal component (55.5% vs. 12.3%; P < 0.01). The subsequent carcinomas also developed after significantly shorter time periods (mean of 7.6 years vs. 19.6 years; P < 0.01). CONCLUSIONS. LCIS appears to confer a persistent, increased risk of subsequent breast carcinoma that does not appear to decrease over time. E-cadherin reactivity appears to identify a subset of LCIS patients with risk factors for subsequent carcinoma similar to those of patients with low-grade intraductal carcinoma. <(c)> 2001 American Cancer Society.
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页码:738 / 747
页数:10
相关论文
共 85 条
[11]  
BENFIELD JR, 1965, ARCH SURG-CHICAGO, V91, P130
[12]   Dysregulation of the E-cadherin/catenin complex by irreversible mutations in human carcinomas [J].
Berx, G ;
Nollet, F ;
Van Roy, F .
CELL ADHESION AND COMMUNICATION, 1998, 6 (2-3) :171-184
[13]  
Berx G, 1998, HUM MUTAT, V12, P226, DOI 10.1002/(SICI)1098-1004(1998)12:4<226::AID-HUMU2>3.0.CO
[14]  
2-D
[15]  
Berx G, 1996, ONCOGENE, V13, P1919
[16]   E-cadherin is a tumour invasion suppressor gene mutated in human lobular breast cancers [J].
Berx, G ;
CletonJansen, AM ;
Nollet, F ;
deLeeuw, WJF ;
vandeVijver, MJ ;
Cornelisse, C ;
vanRoy, F .
EMBO JOURNAL, 1995, 14 (24) :6107-6115
[17]   INTRADUCTAL CARCINOMA - LONG-TERM FOLLOW-UP AFTER TREATMENT BY BIOPSY ALONE [J].
BETSILL, WL ;
ROSEN, PP ;
LIEBERMAN, PH ;
ROBBINS, GF .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1978, 239 (18) :1863-1867
[18]  
Bodian CA, 1996, CANCER, V78, P1024, DOI 10.1002/(SICI)1097-0142(19960901)78:5<1024::AID-CNCR12>3.0.CO
[19]  
2-4
[20]   Breaking the connection: Displacement of the desmosomal plaque protein desmoplakin from cell-cell interfaces disrupts anchorage of intermediate filament bundles and alters intercellular junction assembly [J].
Bornslaeger, EA ;
Corcoran, CM ;
Stappenbeck, TS ;
Green, KJ .
JOURNAL OF CELL BIOLOGY, 1996, 134 (04) :985-1001