Secretory carcinoma of the breast and its histopathological mimics: value of markers for differential diagnosis

Osako, Tomo; Takeuchi, Kengo; Horii, Rie; Iwase, Takuji; Akiyama, Futoshi

doi:10.1111/his.12172

Cited by 50 publications

(44 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…HER2neu status was only reported in 32 SBC patients of whom 31 were negative. These findings are similar to studies by Li et al and Osaka et al . Why earlier and smaller studies found almost exclusively hormone receptor negativity while this larger study from numerous CoC‐approved institutions found many hormone receptor positive SBCs is not clear.…”

Section: Discussionsupporting

confidence: 91%

“…All cases showed positive staining for S‐100 protein and mammaglobin . A recent study by Osaka et al found secretory breast cancer to be positive for S‐100, lysozyme and a‐lactalbumin, and to show vacuolar staining of adipophilin . The abundant secretion and similar growth pattern was also seen in metastatic axillary lymph nodes.…”

Section: Discussionmentioning

confidence: 78%

“…Of interest, cytogenetic identification of chromosomal translocation, t(12;15), was first documented by Murphy et al in 2000 [22]. This led to discovery of a fusion gene, ETV6-NTRK39 reported to be highly specific for SBC, and is associated with the basal-like carcinoma variety [1,[23][24][25][26]. The ETV6-NTRK3 fusion activates RAS-MAP kinases and PI3 K Akt pathways responsible for breast cell proliferation and survival [27].…”

Section: Journal Of Surgical Oncologymentioning

confidence: 99%

See 2 more Smart Citations

Rare breast cancer: 246 invasive secretory carcinomas from the National Cancer Data Base

Jacob

Hodge

Franko

et al. 2016

Journal of Surgical Oncology

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 78%

Section: Journal Of Surgical Oncologymentioning

confidence: 99%

See 1 more Smart Citation

Rare breast cancer: 246 invasive secretory carcinomas from the National Cancer Data Base

Jacob

Hodge

Franko

et al. 2016

Journal of Surgical Oncology

View full text Add to dashboard Cite

show abstract

“…The immunohistochemical features of cases included in this study have been previously described (9, 12), apart from immunohistochemical analysis using antibodies against lysozyme in three MGA cases (MGA4, MGA5 and MGA8), which was performed as previously described (12), with a polyclonal anti-lysozyme antibody (Ventana) using the CC1 mild pretreatment program on a Benchmark XT autostainer (Ventana). Lysozyme was considered positive if cytoplasmic staining was observed in >1% of tumor cells (19). Positive and negative controls were included in each slide run.…”

Section: Methodsmentioning

confidence: 99%

Genetic analysis of microglandular adenosis and acinic cell carcinomas of the breast provides evidence for the existence of a low-grade triple-negative breast neoplasia family

et al. 2017

View full text Add to dashboard Cite

Acinic cell carcinoma is an indolent form of invasive breast cancer, whereas microglandular adenosis has been shown to be a neoplastic proliferation. Both entities display a triple-negative phenotype, and may give rise to and display somatic genomic alterations typical of high-grade triple-negative breast cancers. Here we report on a comparison of previously published data on eight carcinoma-associated microglandular adenosis and eight acinic cell carcinomas subjected to targeted massively parallel sequencing targeting all exons of 236 genes recurrently mutated in breast cancer and/or DNA repair-related. Somatic mutations, insertions/deletions and copy number alterations were detected using state-of-the-art bioinformatic algorithms. All cases were of triple-negative phenotype. A median of 4.5 (1–13) and 4.0 (1–7) non-synonymous somatic mutations per carcinoma-associated microglandular adenosis and acinic cell carcinoma were identified, respectively. TP53 was the sole highly recurrently mutated gene (75% in microglandular adenosis versus 88% in acinic cell carcinomas), and TP53 mutations were consistently coupled with loss of heterozygosity of the wild-type allele. Additional somatic mutations shared by both groups included those in BRCA1, PIK3CA and INPP4B. Recurrent (n=2) somatic mutations restricted to microglandular adenosis or acinic cell carcinomas included those affecting PTEN and MED12, or ERBB4, respectively. No significant differences in the repertoire of somatic mutations were detected between microglandular adenosis and acinic cell carcinomas, and between this group of lesions and 77 triple-negative carcinomas from The Cancer Genome Atlas. Microglandular adenosis and acinic cell carcinomas, however, were genetically distinct from estrogen receptor-positive and/or HER2-positive breast cancers from The Cancer Genome Atlas. Our findings support the contention that microglandular adenosis and acinic cell carcinoma are part of the same spectrum of lesions harboring frequent TP53 somatic mutations, and likely represent low-grade forms of triple-negative disease with no/minimal metastatic potential, of which a subset has the potential to progress to high-grade triple-negative breast cancer.

show abstract

“…AcCCs of the breast are extremely rare. Only 39 cases have been described in the English literature to date, usually as case reports or small case series . In addition to immunoreactivity for serous differentiation markers, AcCCs of the breast have been reported to display a triple‐negative phenotype; interestingly, however, at variance with the common forms of triple‐negative breast cancer (TNBC), breast AcCCs are reported to have indolent clinical behaviour …”

Section: Introductionmentioning

confidence: 99%

Are acinic cell carcinomas of the breast and salivary glands distinct diseases?

et al. 2015

View full text Add to dashboard Cite

Aims Acinic cell carcinomas (AcCC) of the breast have been reported to constitute the breast counterpart of salivary gland AcCCs, based on the similarities of their histological and immunohistochemical features. Breast AcCC is a vanishingly rare form of triple-negative breast cancer (TNBC). Recent studies have demonstrated that in TNBCs, the two driver genes most frequently mutated are TP53 (82%) and PIK3CA (10%). We sought to define whether breast AcCCs would harbour TP53 and PIK3CA somatic mutations, and if so, whether these would be present in salivary gland AcCCs. Methods and results Sanger sequencing of the entire coding region of TP53 and of PIK3CA hotspot mutation sites of 10 breast and 20 salivary gland microdissected AcCCs revealed eight TP53 (80%) and one PIK3CA (10%) somatic mutations in breast AcCCs. No somatic mutations affecting these genes were found in the 20 salivary gland AcCCs analysed. Conclusions Our findings demonstrate that breast AcCCs display TP53 and PIK3CA mutations at frequencies similar to those of common types of TNBCs, whereas these genes appear not to be altered in salivary gland AcCCs, suggesting that despite their similar histological appearances, AcCCs of the breast and salivary glands probably constitute unrelated diseases.

show abstract

Secretory carcinoma of the breast and its histopathological mimics: value of markers for differential diagnosis

Abstract: In this study, we propose a panel of four markers (ETV6 rearrangement, amylase, α-lactalbumin and adipophilin) for distinguishing SC, ACCA, CHC and IDC. This simple but robust panel will serve pathologists well as a practical guide for reaching an appropriate diagnosis.

Cited by 50 publications

References 37 publications

Rare breast cancer: 246 invasive secretory carcinomas from the National Cancer Data Base

Rare breast cancer: 246 invasive secretory carcinomas from the National Cancer Data Base

Genetic analysis of microglandular adenosis and acinic cell carcinomas of the breast provides evidence for the existence of a low-grade triple-negative breast neoplasia family

Are acinic cell carcinomas of the breast and salivary glands distinct diseases?

Contact Info

Product

Resources

About