Lobular carcinoma in situ
|Lobular carcinoma in situ|
|Diagram showing localized and invasive LCIS|
|Classification and external resources|
Unlike ductal carcinoma in situ (DCIS), LCIS is not associated with calcification, and is typically an incidental finding in a biopsy performed for another reason. LCIS only accounts for about 15% of the in situ (ductal or lobular) breast cancers.
Cells of LCIS and invasive lobular carcinoma have the same histology, appearing as single detached cells, as both have loss of expression of e-cadherin, the transmembrane protein mediating epithelial cell adhesion. LCIS often have the same genetic alterations (such as loss of heterozygosity on chromosome 16q, the locus for the e-cadherin gene) as the adjacent area of invasive carcinoma.
Like the cells of atypical lobular hyperplasia and invasive lobular carcinoma, the abnormal cells of LCIS consist of small cells with oval or round nuclei and small nucleoli detached from each other. Mucin-containing signet-ring cells are commonly seen. LCIS generally leaves the underlying architecture intact and recognisable as lobules. Estrogen and progesterone receptors are present and HER2/neu overexpression is absent in most cases of LCIS.
LCIS may be treated with close clinical follow-up and mammographic screening, tamoxifen or related hormone controlling drugs to reduce the risk of developing cancer, or bilateral prophylactic mastectomy. Some surgeons consider bilateral prophylactic mastectomy to be overly aggressive treatment except for certain high-risk cases.
LCIS (lobular neoplasia is considered pre-cancerous) is an indicator (marker) identifying women with an increased risk of developing invasive breast cancer. This risk extends more than 20 years. Most of the risk relates to subsequent invasive ductal carcinoma rather than to invasive lobular carcinoma.
- "Lobular Carcinoma in situ (LCIS)". Breast Cancer. Stanford Cancer Center.
- "Lobular carcinoma in situ: Marker for breast cancer risk". MayoClinic.com.
- "Breast Cancer Treatment". National Cancer Institute.
- Afonso N, Bouwman D (August 2008). "Lobular carcinoma in situ". Eur. J. Cancer Prev. 17 (4): 312–6. doi:10.1097/CEJ.0b013e3282f75e5d. PMID 18562954.
- Cancer, American Joint Committee on (2002). AJCC cancer staging handbook : from the AJCC cancer staging manual (6th ed.). New York: Springer. p. 260. ISBN 9780387952703.
- "Susan G. Komen for the Cure | Understanding Breast Cancer | Breast Facts | Statistics | Breast Cancer Statistics". Retrieved 2013-01-16.
- Hajra KM, Fearon ER (2002). "Cadherin and catenin alterations in human cancer". Genes Chromosomes Cancer. 34 (3): 255–68. doi:10.1002/gcc.10083. PMID 12007186.
- Lakhani SR (2001). "Molecular genetics of solid tumors: translating research into clinical practice. What we could do now: breast cancer". Mol Pathol. 54 (5): 281–4. doi:10.1136/mp.54.5.281. PMC . PMID 11577167.
- Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, MO: Elsevier Saunders. p. 1142. ISBN 0-7216-0187-1.
- "Breast Cancer Treatment (PDQ®) - National Cancer Institute - Lobular Carcinoma In Situ". Retrieved 2013-01-12.
- Page DL, Schuyler PA, DuPont WD, Jensen RA, Plummer WD Jr, Simpson JF (2003). "Atypical lobular hyperplasia as a unilateral predictor of breast cancer risk: a retrospective cohort study". Lancet. 361 (9352): 125–9. doi:10.1016/S0140-6736(03)12230-1. PMID 12531579.