Suspicious calcifications in benign breast lesions: a radio-pathologic correlation

Nishimura, Rieko; Taira, Naruto; Sugata, Shigenori; Takabatake, Daisuke; Ohsumi, Shozo; Takashima, Shigemitsu

doi:10.1007/s12282-010-0199-4

Cited by 3 publications

(3 citation statements)

References 6 publications

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“…In addition, our mouse model showed premalignant features as reported for FM, including calcifications inside the alveoli [48], collagen fiber deposition [49], lymphocytic infiltrations, and ductal hyperplasia [50]. The transition from benign to malignant structures in our mouse model is potentiated by the heterozygous p53 deletion, which is in accordance with the well-established role of p53 as a tumor suppressor [51].…”

Section: Discussionsupporting

confidence: 84%

Replacement of E-cadherin by N-cadherin in the mammary gland leads to fibrocystic changes and tumor formation

2011

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IntroductionE-cadherin (E-cad; cadherin 1) and N-cadherin (N-cad; cadherin 2) are the most prominent members of the cadherin family of cell adhesion molecules. Although they share many structural and functional features, they are expressed in an almost mutually exclusive manner in vivo.MethodsTo explore functional differences between the two cadherins in vivo, we recently generated a knock-in line in which N-cad is expressed from the E-cad locus. In combination with a conditional gene inactivation approach, we expressed N-cad in the absence of E-cad (referred to as Ncadk.i.) in alveolar epithelial cells of the mammary gland starting in late pregnancy.ResultsWe found that the sole presence of N-cad induces constitutively active fibroblast growth factor (Fgf) signaling and a precocious involution resulting in massive apoptosis of alveolar cells. To block apoptosis, we conditionally deleted one allele of p53 in Ncadk.i. mice and observed a temporal rescue of alveolar morphology and function. However, an accumulation of fibrotic tissue and cysts with increasing age and lactation cycles was observed. This phenotype closely resembled fibrocystic mastopathy (FM), a common disorder in humans, which is thought to precede breast cancer. Concordantly, 55% of Ncadk.i. mice harboring a heterozygous p53 deletion developed malignant and invasive tumors.ConclusionsOur results demonstrate a possible role for N-cad in the formation of fibrosis and cysts in the mammary gland. Moreover, we show that these lesions precede the development of malignant tumors. Thus, we provide a new mouse model to investigate the molecular mechanisms of fibrocystic mastopathy and the transition from benign to malignant tumors.

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Section: Discussionsupporting

confidence: 84%

Replacement of E-cadherin by N-cadherin in the mammary gland leads to fibrocystic changes and tumor formation

2011

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“…Benign breast lesions exhibit calcification similar to breast cancer tissues. Thus, it was feasible in this study to use fibroadenoma breast tissue as a control when studying calcification in breast tumours [ 20 ]. Using immunohistochemistry, extensive expression of CA1 was detected in breast cancer tissues but not in normal tissues.…”

Section: Discussionmentioning

confidence: 99%

CA1 contributes to microcalcification and tumourigenesis in breast cancer

Zheng

Zhao

et al. 2015

BMC Cancer

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BackgroundAlthough mammary microcalcification is frequently observed and has been associated with poor survival in patients with breast cancer, the genesis of calcification remains unclear. Carbonic anhydrase I (CA1) has been shown to promote calcification by catalysing the hydration of CO2. This study aimed to determine whether CA1 was correlated with microcalcification and with other processes that are involved in breast cancer tumourigenesis.MethodsCA1 expression in breast cancer tissues and blood samples was detected using western blotting, real-time PCR, immunohistochemistry and ELISA. Calcification was induced in the cultured 4T1 cell line originating from mouse breast tumours, using ascorbic acid and β-glycerophosphate. Acetazolamide, a chemical inhibitor of CA1, was also added to the culture to determine the role of CA1 in calcification. The MCF-7 human breast cancer cell line was treated with anti-CA1 siRNA and was assessed using a CCK-8 cell proliferation assay, an annexin V cell apoptosis assay, transwell migration assay and a human breast cancer PCR array. The tag SNP rs725605, which is located in the CA1 locus, was genotyped using TaqMan® genotyping.ResultsIncreased CA1 expression was detected in samples of breast carcinoma tissues and blood obtained from patients with breast cancer. A total of 15.3 % of these blood samples exhibited a 2.1-fold or higher level of CA1 expression, compared to the average level of CA1 expression in samples from healthy controls. Following the induction of calcification of 4T1 cells, both the number of calcium-rich deposits and the expression of CA1 increased, whereas the calcification and CA1 expression were significantly supressed in the presence of acetazolamide. Increased migration and apoptosis were observed in MCF-7 cells that were treated with anti-CA1 siRNA. The PCR array detected up-regulation of the androgen receptor (AR) and down-regulation of X-box binding protein 1 (XBP1) in the treated MCF-7 cells. Significant differences in the allele and genotype frequencies of rs725605 were detected in the cohort of patients with breast cancer but not in other tumours.ConclusionThe results of this study suggested that CA1 is a potential oncogene and that it contributes to abnormal cell calcification, apoptosis and migration in breast cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1707-x) contains supplementary material, which is available to authorized users.

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“…Some specific BMC features discernible on mammograms can be indicative of malignancy and raise concerns about the presence of cancerous cells. Several studies focused on fostering an understanding of the link between BMCs and breast cancer [13,29,[39][40][41][42][43][44][45][46][47][48] to clarify those concerning characteristics. They are five main BMC distributions: grouped (or clustered), linear, segmental, regional, and diffuse (Figure 2).…”

Section: Mammography As the Diagnosis Starting Pointmentioning

confidence: 99%

Multiscale approach to provide a better physicochemical description of women breast microcalcifications

Petay¹,

Cherfan²,

Bouderlique³

et al. 2022

Comptes Rendus. Chimie

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Despite the incidence of breast cancer among women, mammography and anatomopathology investigations are still the gold standard method for preventive screening and diagnosis. Several criteria are used to diagnose precisely the severity of the pathology like the distribution and shape of breast microcalcifications (BMCs). However, the link between the different chemical phases of BMCs and the cancer stage remains unclear. As BMCs physicochemical speciation has the potential to help clinicians during their diagnosis, this study aims to propose a methodology using advanced spectroscopical analysis techniques to finely characterize BMCs and uncover the relationship between

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Suspicious calcifications in benign breast lesions: a radio-pathologic correlation

Abstract: Some types of calcifications in mastopathy and fibroadenoma were assessed as borderline by MMG. We should therefore collect data from more benign cases with suspicious calcifications on MMG and elucidate the diagnostic criteria in MMG findings of such calcifications.

Cited by 3 publications

References 6 publications

Replacement of E-cadherin by N-cadherin in the mammary gland leads to fibrocystic changes and tumor formation

Replacement of E-cadherin by N-cadherin in the mammary gland leads to fibrocystic changes and tumor formation

CA1 contributes to microcalcification and tumourigenesis in breast cancer

Multiscale approach to provide a better physicochemical description of women breast microcalcifications

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