Mammographically detected in situ lobular carcinomas of the breast

Sapino, Anna; Frigerio, Alfonso; Peterse, Johannes L.; Arisio, Riccardo; Coluccia, C; Bussolati, Gianni

doi:10.1007/s004280050469

Cited by 83 publications

(41 citation statements)

References 12 publications

(18 reference statements)

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“…21 Furthermore, lobular carcinoma in situ with necrosis can be associated with microcalcifications and can present mammographically like comedo-type ductal carcinoma in situ. 1,8 In contrast to many previous studies on lobular neoplasia, our study does not support routine excision for classic lobular carcinoma in situ or atypical lobular hyperplasia, but does support routine excision for nonclassic lobular carcinoma in situ, including pleomorphic lobular carcinoma in situ and lobular carcinoma in situ with necrosis. Concordance of radiology and pathology findings must be considered when making a decision to recommend excision.…”

Section: Discussioncontrasting

confidence: 99%

“…6 Rosen described 'florid' lobular carcinoma in situ characterized by 'tumor cells that fill and expand the duct lumen' that 'may develop central necrosis and calcifications'. 7 Sapino et al 8 and Fadare et al 9 also have defined in situ lesions with morphologic features of lobular neoplasia but with necrosis as lobular carcinoma in situ. Not only do both pleomorphic lobular carcinoma in situ and lobular carcinoma in situ with necrosis show different morphology, they can also exhibit a more aggressive biologic marker profile compared to classic lobular carcinoma in situ.…”

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confidence: 99%

“…Not only do both pleomorphic lobular carcinoma in situ and lobular carcinoma in situ with necrosis show different morphology, they can also exhibit a more aggressive biologic marker profile compared to classic lobular carcinoma in situ. 6,[8][9][10][11][12] Microinvasive lobular carcinoma has been associated with pleomorphic lobular carcinoma in situ or lobular carcinoma in situ with necrosis, 6,8,9,13 although in routine practice, microinvasive carcinomas have also been observed in association with classic lobular carcinoma in situ. Lobular carcinoma in situ with nonclassic features has also been found to be more frequently associated with adjacent invasive carcinoma, especially invasive lobular carcinoma.…”

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confidence: 99%

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Atypical lobular hyperplasia and classic lobular carcinoma in situ in core biopsy specimens: routine excision is not necessary

Hwang

Barke

Mendelson³

et al. 2008

Modern Pathology

104

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Standardized recommendations for the management of lobular neoplasia in core biopsy specimens are not established. The aim of our study was to define morphologic features of lobular neoplasia in core biopsies that predict the finding of ductal carcinoma in situ or invasive carcinoma in the subsequent excisional specimen. We reviewed 333 cases of atypical lobular hyperplasia or lobular carcinoma in situ without ductal carcinoma in situ or invasive carcinoma diagnosed in core biopsies from 1996 to 2006. Subsequent excision was performed in 41% (136/333) of cases, including atypical lobular hyperplasia (n ¼ 48), lobular carcinoma in situ (n ¼ 39), and lobular neoplasia associated with atypical ductal hyperplasia (n ¼ 49). Upgrades were identified in 2% (1/48) of atypical lobular hyperplasia, 23% (9/39) of lobular carcinoma in situ, and 27% (13/49) of lobular neoplasia associated with atypical ductal hyperplasia cases. When further analyzed, the upgraded cases of lobular carcinoma in situ were associated with radiologic-pathologic discordance in 6/9 cases and with nonclassic pathology (two lobular carcinoma in situ with necrosis and one pleomorphic lobular carcinoma in situ) in the remaining three cases. The frequency of upgrade was 11% (3/26) in classic lobular carcinoma in situ, and 46% (6/13) in nonclassic types (pleomorphic or with necrosis). After excluding cases with discordant imaging/ pathology, there was a 5% upgrade in our excisional specimens. After excluding cases where the upgrade was associated with nonclassic morphology, the upgrade in our study was 1%. Our results suggest that atypical lobular hyperplasia and classic lobular carcinoma in situ with concordant radiology and pathology can be appropriately managed with clinical follow-up without surgery.

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Section: Discussioncontrasting

confidence: 99%

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Atypical lobular hyperplasia and classic lobular carcinoma in situ in core biopsy specimens: routine excision is not necessary

Hwang

Barke

Mendelson³

et al. 2008

Modern Pathology

104

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“…13,[19][20][21][22] They are clinically occult, and although they are often also mammographically silent, a significant minority of lobular neoplasia cases diagnosed on core biopsy have associated microcalcifications. [23][24][25][26] Data derived from the Surveillance, Epidemiology and End Results Program 27 have shown that the ageadjusted, age-specific rates of LCIS among women in the United States has increased fourfold between the late 70s (0.9 per 100 000 person years) and late 90s (3.2 per 100 000 person years). Women aged between 50 and 59 years experienced the greatest absolute increase in incidence from 1978 to 1998.…”

Section: Clinical Featuresmentioning

confidence: 99%

Lobular neoplasia: morphology, biological potential and management in core biopsies

O’Malley

2010

Modern Pathology

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Lobular neoplasia has been traditionally recognized as a marker of increased risk for subsequent breast carcinoma development; however, molecular studies suggest that it also behaves in a non-obligate precursor manner. We do not know, as yet, how to identify the subgroup of cases that is most likely to progress, but the epidemiological data would indicate that this progression occurs after a long period of time. Thus, the current approach of conservative management of these lesions when identified in excision specimens is justified. Recently, several variants of lobular carcinoma in situ (LCIS), most notably pleomorphic LCIS, have been recognized and these can be difficult to differentiate from ductal carcinoma in situ. Application of strict diagnostic criteria and the judicial use of immunohistochemistry, particularly E-cadherin, can be helpful in this differential diagnosis. Another challenging issue is the management of lobular neoplasia when diagnosed on core biopsy. This controversial issue will be discussed in detail. The goals of this review are (1) to describe the morphological criteria used to diagnose the spectrum of lobular neoplastic lesions, including atypical lobular hyperplasia, LCIS and variants of LCIS; (2) to discuss the data exploring the biological potential of lobular neoplasia from an epidemiological and molecular viewpoint; and (3) to outline the recommendations for management of lobular neoplasia when encountered in core biopsies.

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“…In ADH, the presence and role of p53 mutations is still an open field: p53 mutations were initially not documented (Chitemerere et al 1996); subsequently studies pointing to p53 mutations appeared (Kang et al 2001), and, more recently, the presence of mutated p53 in ADH has been demonstrated with the use of laser capture microdissection microscope, singlestranded conformational polymorphism (SSCP) and sequencing (Keohavong et al 2004). Regarding LN, there is scarcity of data: in two studies, no p53 immunoreactivity was demonstrated in LN lesions (Siziopikou et al 1996;Sapino et al 2000), whereas a more recent study on LCIS reported p53 immunoreactivity in one fifth of cases (Mohson et al 2005).…”

Section: P53mentioning

confidence: 99%