Disease relevance of Carcinoma, Lobular

• In such women, a five-year course of tamoxifen reduced the risk of invasive breast cancer by 49%; women with lobular carcinoma in situ or atypical hyperplasia experienced even greater risk reductions [1].
• HIN-1 expression is significantly down regulated in 94% of human breast carcinomas and in 95% of preinvasive lesions, such as ductal and lobular carcinoma in situ [2].
• We found expression of MMP-13 in stromal fibroblast-like cells in all 21 invasive ductal carcinomas studied and in 4 of 9 invasive lobular carcinomas [3].
• As previously observed with lactating adenomas, it is likely that the coexpression of TSP1 and CD36 is related to the secretory activity of invasive lobular carcinoma cells [4].
• In situ lesions of ILCs and pure lobular carcinoma in situ (four cases) were all E-cadherin negative, whereas intraductal carcinomas (11 cases) exhibited mostly strong staining [5].

High impact information on Carcinoma, Lobular

• In human breast cancers, high level of Twist expression is correlated with invasive lobular carcinoma, a highly infiltrating tumor type associated with loss of E-cadherin expression [6].
• We conclude that the vast majority of invasive lobular carcinomas show overexpression of cyclin D1 protein [7].
• Frequent overexpression of the cyclin D1 oncogene in invasive lobular carcinoma of the breast [7].
• We sought to determine the frequency of cyclin D1 protein overexpression in invasive lobular carcinoma, to investigate the cause of the protein accumulation, and to identify the effects of high levels of the protein on the regulation of the cell cycle [7].
• Conversely, the expression of IL6 in invasive lobular carcinoma was enhanced [8].

Chemical compound and disease context of Carcinoma, Lobular

• There was an inverse correlation between aromatase and ER status in invasive ductal carcinoma (P = 0.0213), but not in invasive lobular carcinoma [9].
• In the Study of Tamoxifen and Raloxifene trial, eligible women are at least 35 years of age and postmenopausal, with either lobular carcinoma in situ or a 5-year risk of invasive breast cancer of at least 1.67% [10].
• There was a small, yet significant, increase in 5-methylcytosine content in lobular carcinoma [11].
• The analysis of E-cadherin glycoprotein expression is a powerful tool for distinguishing lobular from ductal carcinomas, because complete loss of E-cadherin expression occurs in most infiltrating lobular tumors and lobular carcinomas in situ, but not in ductal tumors [12].
• Subgroup analysis suggested that high vitamin A intake and high alcohol intake may be associated with risk of ductal but not lobular carcinoma in situ [13].

Biological context of Carcinoma, Lobular

• Each of the four lobular carcinomas with E-cadherin mutations showed tumour-specific loss of heterozygosity of chromosomal region 16q22.1 containing the E-cadherin locus [14].
• Rates that failed to increase after 50 years suggested that menopause had greater impact on medullary and inflammatory carcinomas than on duct NST, tubular, and lobular carcinomas [15].
• Point mutation of the E-cadherin gene in invasive lobular carcinoma of the breast [16].
• In our review of the English literature, this is the 18th case of lobular carcinoma of the male breast to be reported; it is also the first report of lobular carcinoma associated with the use of cimetidine, and the second in a man with documentation of genotype [17].
• A higher frequency of down-regulation of the E-cadherin protein expression was found in invasive lobular carcinomas than in invasive ductal carcinomas, although this difference was of borderline significant (P = 0.084) [18].

Anatomical context of Carcinoma, Lobular

• E-cadherin expression was significantly (P < 0.001) stronger in ductal carcinomas than in lobular carcinomas and stronger (P < 0.01) in low grades than in high grades, but E-cadherin was independent of lymph node status and tumour size [19].
• B7-H4 staining intensity was greater in invasive ductal carcinomas [24.61 relative units (RU)] and in invasive lobular carcinomas (15.23 RU) than in normal breast epithelium (4.30 RU, P = 0.0003) [20].
• Similarly, a lobular carcinoma did not express Cx26 or Cx43, but there was punctate Cx43 in the epithelial cells of a mucoid carcinoma [21].
• During a study of the correlation between the histologic types of breast carcinoma and their hormone receptor contents, eight cases of the alveolar variant of invasive lobular carcinoma were identified, and all had estrogen receptor protein concentrations higher than 400 fmol/mg cytosol protein [22].
• By in situ hybridization, a positive signal for uPA mRNA was in 26 of 28 ductal and four of five lobular carcinomas demonstrated in stromal cells adjacent to nests of cancer cells, whereas only one ductal carcinoma showed a positive reaction in the epithelial component itself [23].

Gene context of Carcinoma, Lobular

• By contrast, TSP1 is codistributed with CD51 in most of the invasive lobular carcinoma cells (40 to 80%) and with CD36 in a subpopulation (30 to 40%) of these invasive tumor cells [4].
• BSP expression was significantly increased in infiltrating ductal carcinoma compared with infiltrating lobular carcinoma (p = 0.0023) [24].
• Patients with lobular carcinoma and ER-negative tumors had serum VEGF levels comparable with those in the controls [25].
• PIK3CA mutation and histological type in breast carcinoma: high frequency of mutations in lobular carcinoma [26].
• We measured, by immunohistochemistry, HMGA1 protein expression in 212 breast tissue specimens: 6 normal samples, 28 hyperplastic lesions (13 with cellular atypia), 11 fibroadenomas, 10 in situ ductal carcinomas, 144 ductal carcinomas, and 13 lobular carcinomas [27].

Analytical, diagnostic and therapeutic context of Carcinoma, Lobular

• RESULTS: Results obtained demonstrated that p53 is a significant predictor of disease-free survival (DFS P < 0.0001) and overall survival (OS P = 0.0002) both in ductal and lobular carcinomas, whereas bcl-2 expression seems to be of prognostic value only in lobular carcinomas (DFS P = 0.01; OS P = 0.02) [28].

References