Lobular carcinoma in situ
| Lobular carcinoma in situ |
| Classification and external resources |
Lobular carcinoma in situ, H&E, 20x |
| ICD-10 |
D05.0 |
| ICD-O: |
M8520/2 |
Lobular carcinoma in situ (LCIS) is a condition caused by unusual cells in the lobules of the breast.[1]
It is usually not considered cancer, but it can indicate an increased risk of future cancer.[2][3][4] 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.
Genetics
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.[5] 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.[6]
Morphology
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.[7] 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.[7]
Treatment options
LCIS may be treated with close clinical follow-up and mammographic screening, tamoxifen, or bilateral prophylactic mastectomy.
Prognosis
LCIS confers increased risk of invasive breast cancer. While older studies have shown that the increased risk is equal for both breasts, a more recent study suggests that the ipsilateral (same side) breast may be at greater risk.[8]
See also
References
- ^ "Lobular Carcinoma in situ (LCIS)". Breast Cancer. Stanford Cancer Center. http://cancer.stanford.edu/breastcancer/lcis.html.
- ^ "Lobular carcinoma in situ: Marker for breast cancer risk". MayoClinic.com. http://www.mayoclinic.com/health/lobular-carcinoma-in-situ/DS00982.
- ^ "Breast Cancer Treatment". National Cancer Institute. http://www.cancer.gov/cancertopics/pdq/treatment/breast/HealthProfessional/page6.
- ^ 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. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00008469-200808000-00004.
- ^ 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 1187082. PMID 11577167. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1187082.
- ^ a b 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.
- ^ 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. http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(03)12230-1.