Table 1.
Published reports of genomic alterations identified by comparative genomic hybridization in lobular carcinoma
| Cases studied | Noted lobular-specific alterations | ||||||
| Reference | ALH/LCIS | Invasive | Other | Type of CGH | Gain | Loss | Observations |
| Lu and coworkers [41] | ALH and LCIS | IBC (adjacent in 6 cases) | Chromosomal | 6q | 16p, 16q, 17p, and 22q | Alterations were found at a similar high frequency in LCIS and ALH | |
| Buerger and coworkers [45] | LCIS | ILC (adjacent LCIS in 4 cases) | DCIS | Chromosomal | 1q | 16q | LCIS characterized by low average rate of copy number changes; no evidence of amplification in LCIS |
| Gunther and coworkers [46] | ILC and IDC | Chromosomal | 16q, 17q, and 22 | Lower frequency of gain at 8q in ILC compared with IDC; changes of equal frequency include gain at 1q, and loss at 19p and parts of 1p and 11q | |||
| Weber-Mangal and coworkers [47] | ILC and IDC | IBC | Chromosomal | 1q, 8q, and 11q | 16q, 17p, and 22q | Lobular alterations were identified in a table of alterations; however, the study investigated alterations in breast cancer in general | |
| Nishizaki and coworkers [48] | ILC and IDC | Chromosomal | 1q | 16q | Compared ILC with IDC; IDC had higher frequency of gain at 8q and 20q | ||
| Etzell and coworkers [49] | LCIS | Chromosomal | 1q | 8p, 12q24, 16q, and 17p | Correlated 16q loss with loss of expression of E-cadherin by immunohistochemistry | ||
| Mastracci and coworkers [4] | ALH and LCIS | SMRT BAC-array | 2p11.2 and 20q13.13 | 7p11.2, 16q21-q23.1, 19q13.2, and 22q11.1 | Alterations found in common between ALH and LCIS; also identified changes that were specific to either ALH or LCIS | ||
| Loo and coworkers [38] | ILC | IDC | BAC-array | 1q32, 8p23, 11q13, and 11q14 | 16q23 and 16q24 | Found differences between ILC and IDC, stratified by histologic type and estrogen receptor status | |
| Hwang and coworkers [42] | LCIS | ILC (synchronous) | BAC-array | 1q | 11q11-q13, 11q14-qter, and 16q | Clonality was suggested for the genetic relationship between LCIS and ILC | |
| Nyante and coworkers [43] | LCIS | ILC | DCIS | BAC-array | 1p, 16q, and 17p/q | A different profile was identified for DCIS | |
| Morandi and coworkers [44] | ILC | Oligo-array | 1p, 2q, 3p, 6p, 16p, 19p, and 21q | 16q and 19q | Lobular neoplastic lesions are genetically related to ILC and can be categorized as precursors | ||
| Reis-Filho and coworkers [50] | ILC | High-resolution CGH and array-CGH | 1q, 5p, 7q, 11p, 11q, 12q, 14q, 16p, 18p, 19p+q, and 20p+q | 11q, 13q, 16q, 18q, and Xq | Lobular carcinomas have greater genetic complexity and a higher number of recurrent genomic changes than previously reported with other techniques | ||
| Roylance and coworkers [51] | ILC and IDC | 16q BAC-array | 16q (whole chromosome arm) | Alterations on 16q are common to both IDC and ILC; higher grade IDCs have more complex changes on 16q | |||
The 'cases studied' column notes the breast lesion investigated in each study, i.e. ALH/LCIS, Invasive carcinoma or other breast lesions. The 'noted lobular-specific alterations' column notes the chromosomal gains and losses identified in each study. ALH, atypical lobular hyperplasia; BAC, bacterial artificial chromosome; DCIS, ductal carcinoma in situ; IBC, invasive breast cancer; IDC, invasive ductal carcinoma; ILC, invasive lobular carcinoma; LCIS, lobular carcinoma in situ ; LN, lobular neoplasia; SMRT, submegabase resolution tiling array.