Why is LCIS Important—Pathological Review

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Abstract

Purpose of Review

Lobular carcinoma in situ (LCIS) encompasses classical LCIS and other rarer and more recently recognised variants, namely pleomorphic LCIS (PLCIS) and florid LCIS. Each of those entities has characteristic histological diagnostic criteria, different rates of underestimation of malignancy and recommended management. In addition, those lesions can mimic a number of benign and malignant breast lesions and can particularly be mistaken for ductal carcinoma in situ (DCIS). Accurate diagnosis of those lesions is critical to ensuring the appropriate patient management.

Recent Findings

Several international guidelines refining the pathological classification, staging and management of those lesions have recently been updated. This review will provide an up-to-date pathological overview of the current knowledge of LCIS with emphasis on the multidisciplinary management implications.

Summary

Close correlation between imaging and pathology in a multidisciplinary pathway is essential in LCIS management. Classical LCIS on core biopsy/vacuum-assisted biopsy (VAB) is coded as B3 and, if without discordant imaging, should further be sampled by vacuum-assisted excision (VAE). PLCIS should be coded and managed as per high-grade DCIS. Florid LCIS is a rare entity that is thought to be more aggressive than classical LCIS. Excision with clear margin is advised.

Related collections

Most cited references 35

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Eighth Edition of the AJCC Cancer Staging Manual: Breast Cancer.

Armando E. Giuliano, Stephen Edge, Gabriel N Hortobagyi (2018)

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Tamoxifen for the prevention of breast cancer: current status of the National Surgical Adjuvant Breast and Bowel Project P-1 study.

André Robidoux, Joseph P Costantino, R. Cecchini … (2005)

Initial findings from the National Surgical Adjuvant Breast and Bowel Project Breast Cancer Prevention Trial (P-1) demonstrated that tamoxifen reduced the risk of estrogen receptor-positive tumors and osteoporotic fractures in women at increased risk for breast cancer. Side effects of varying clinical significance were observed. The trial was unblinded because of the positive results, and follow-up continued. This report updates our initial findings. Women (n = 13,388) were randomly assigned to receive placebo or tamoxifen for 5 years. Rates of breast cancer and other events were compared by the use of risk ratios (RRs) and 95% confidence intervals (CIs). Estimates of the net benefit from 5 years of tamoxifen therapy were compared by age, race, and categories of predicted breast cancer risk. Statistical tests were two-sided. After 7 years of follow-up, the cumulative rate of invasive breast cancer was reduced from 42.5 per 1000 women in the placebo group to 24.8 per 1000 women in the tamoxifen group (RR = 0.57, 95% CI = 0.46 to 0.70) and the cumulative rate of noninvasive breast cancer was reduced from 15.8 per 1000 women in the placebo group to 10.2 per 1000 women in the tamoxifen group (RR = 0.63, 95% CI = 0.45 to 0.89). These reductions were similar to those seen in the initial report. Tamoxifen led to a 32% reduction in osteoporotic fractures (RR = 0.68, 95% CI = 0.51 to 0.92). Relative risks of stroke, deep-vein thrombosis, and cataracts (which increased with tamoxifen) and of ischemic heart disease and death (which were not changed with tamoxifen) were also similar to those initially reported. Risks of pulmonary embolism were approximately 11% lower than in the original report, and risks of endometrial cancer were about 29% higher, but these differences were not statistically significant. The net benefit achieved with tamoxifen varied according to age, race, and level of breast cancer risk. Despite the potential bias caused by the unblinding of the P-1 trial, the magnitudes of all beneficial and undesirable treatment effects of tamoxifen were similar to those initially reported, with notable reductions in breast cancer and increased risks of thromboembolic events and endometrial cancer. Readily identifiable subsets of individuals comprising 2.5 million women could derive a net benefit from the drug.

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E-cadherin inactivation in lobular carcinoma in situ of the breast: an early event in tumorigenesis.

C de Vos, A-M Cleton-Jansen, G. Berx … (1997)

In breast cancer, inactivating point mutations in the E-cadherin gene are frequently found in invasive lobular carcinoma (ILC) but never in invasive ductal carcinoma (IDC). Lobular carcinoma in situ (LCIS) adjacent to ILC has previously been shown to lack E-cadherin expression, but whether LCIS without adjacent invasive carcinoma also lacks E-cadherin expression and whether the gene mutations present in ILC are already present in LCIS is not known. We report here that E-cadherin expression is absent in six cases of LCIS and present in 150 cases of ductal carcinoma in situ (DCIS), both without an adjacent invasive component. Furthermore, using mutation analysis, we could demonstrate the presence of the same truncating mutations and loss of heterozygosity (LOH) of the wild-type E-cadherin in the LCIS component and in the adjacent ILC. Our results indicate that E-cadherin is a very early target gene in lobular breast carcinogenesis and plays a tumour-suppressive role, additional to the previously suggested invasion-suppressive role. Images Figure 1 Figure 2 Figure 3