Original contributionLoss of heterozygosity on chromosome 11 q 13 in lobular lesions of the breast using tissue microdissection and polymerase chain reaction☆,☆☆,★
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Cited by (61)
Evaluating agreement, histological features, and relevance of separating pleomorphic and florid lobular carcinoma in situ subtypes
2018, Human PathologyCitation Excerpt :The understanding of lobular carcinoma in situ (LCIS) biology, and its clinical significance, has evolved [1-3]. At one end, instead of just being a risk factor for breast cancer, now, LCIS is considered a non-obligate precursor of invasive disease [1-3]. On the other end, recently, LCIS has been categorized as benign entity [4].
Outcomes of patients with lobular in situ neoplasia of the breast: The role of vacuum-assisted biopsy
2014, BreastCitation Excerpt :Evidence suggests LISN is not simply a generalised risk marker; amongst 252 patient with ALH who underwent surgical biopsy, 20% subsequently developed breast cancer, which was ipsilateral in 68% and contralateral in 24% [8]. Molecular studies add further weight: loss of heterozygosity on the 11q13 chromosome is present in 50% of LCIS associated with invasive lobular carcinoma but rarely in LCIS alone [9]. LISN may therefore be a non-obligate precursor for breast cancer [10].
Lobular carcinoma in situ/atypical lobular hyperplasia on breast needle biopsies: Does it warrant surgical excisional biopsy? A study of 27 cases
2010, Annals of Diagnostic PathologyCitation Excerpt :Therefore, LCIS and ALH have traditionally been considered to be risk factors rather than precursors for the subsequent development of breast carcinoma. However, more recent studies have shown that breast carcinoma is 3 times more prevalent in the ipsilateral breast of LCIS compared with the contralateral breast; and coexistent LCIS and ILC often contain similar genetic alterations, suggesting that at least some LCISs represent actual precursors with progression to carcinoma [6,7]. Because of the uncertainty of the biologic nature of ALH and LCIS and the relatively small number of reports in the literature, the management of these lesions in otherwise benign breast core biopsies remains controversial [8-16].
The impact of large sections on the study of in situ and invasive duct carcinoma of the breast
2007, Human PathologyCitation Excerpt :LCIS and DCIS can be so strictly interrelated that both lesions are occasionally seen intermingled within the same lobule [17-20]. In addition, Lakhani et al [21,22] and Buerger et al [23-25] found genetic similarities between grade 1 DCIS and LN/LCIS, with losses at 16q being the central genetic event, whereas different genetic profile was observed in grades 2 and 3 DCIS [26,27]. Therefore, it seems that there are more similarities than the differences between well-differentiated DCIS/LN, and that this is more than coincidental.
Correlation between core biopsy and excisional biopsy in breast high-risk lesions
2006, American Journal of SurgeryCitation Excerpt :Lakhani et al [18] reported that loss of heterozygosity at chromosomal arms exhibiting imbalance at high frequency in invasive cancer was also detected in LCIS. Nayar et al [19] showed loss of heterozygosity on the 11q13 chromosome in 50% of LCIS associated with invasive lobular cancer, whereas pure LCIS in the absence of invasive lobular cancer had a much lower frequency of loss of heterozygosity. Berx et al [20] reported that 56% of invasive lobular cancers and adjacent LCIS were characterized by loss of expression of E-cadherin adhesion molecule.
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Presented in part at the USCAP Meeting in March 1996, Washington, DC.
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Supported in part by the Elaine Snyder Research Award to Dr Silverberg.
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This is a US government work. There are no restrictions on its use.