scholarly journals Lipogranulomas of the mammary glands: diagnosis and treatment

Author(s):  
Natalia Cara ◽  
◽  
Veronica Svet ◽  
Ion Mereuta ◽  
◽  
...  

Steatonecrosis of the mammary gland is necrosis of its adipose tissue, followed by replacement with scar tissue. Lipogranuloma is known as a benign inflammatory process, necrosis of breast fat occurs due to iatrogenic breast trauma. Most often, fatty necrosis is seen in women with large breasts – in women with small breasts, it develops much less often. It is important to diagnose lipogranulomas because it can often mimic breast cancer. Fat necrosis of the breast is a common pathological condition, with a wide variety of presentations on mammography, ultrasound and MRI. The incidence of fatty necrosis of the breast is estimated at 0.6%, representing 2.75% of all breast lesions.

Author(s):  
Diana Danilov ◽  
◽  
Veronica Svet ◽  
Ion Mereuta ◽  
◽  
...  

About one in two women has symptoms of breast formation. According to various data, the frequency of detection of benign pathologies of the mammary gland is much higher compared to the frequency of referring women to the doctor with these pathologies. Benign tumors of the mammary gland are characterized by a slow, expansive growth (compresses the neighboring tissue), are well encapsulated, most are the result of hormonal changes (hyperestrogenemia, hyperprolactinemia), after excision rarely recur, do not invade local tissues and do not metastasize to others. organs. The basic treatment is surgery – excision of the breast formations. Recurrences rarely occur, do not invade adjacent tissues and do not metastasize to other organs.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ernst Michael Jung ◽  
Friedrich Jung ◽  
Christian Stroszczynski ◽  
Isabel Wiesinger

AbstractThe aim of this present clinical pilot study is the display of typical perfusion results in patients with solid, non-cystic breast lesions. The lesions were characterized using contrast enhanced ultrasound (CEUS) with (i) time intensity curve analyses (TIC) and (ii) parametric color maps. The 24 asymptomatic patients included were genetically tested for having an elevated risk for breast cancer. At a center of early detection of familial ovary and breast cancer, those patients received annual MRI and grey-scale ultrasound. If lesions remained unclear or appeared even suspicious, those patients also received CEUS. CEUS was performed after intravenous application of sulfur hexafluoride microbubbles. Digital DICOM cine loops were continuously stored for one minute in PACS (picture archiving and communication system). Perfusion images and TIC analyses were calculated off-line with external perfusion software (VueBox). The lesion diameter ranged between 7 and 15 mm (mean 11 ± 3 mm). Five hypoechoic irregular lesions were scars, 6 lesions were benign and 12 lesions were highly suspicious for breast cancer with irregular enhancement at the margins and a partial wash out. In those 12 cases, histopathology confirmed breast cancer. All the suspicious lesions were correctly identified visually. For the perfusion analysis only Peak Enhancement (PE) and Area Under the Curve (AUC) added more information for correctly identifying the lesions. Typical for benign lesions is a prolonged contrast agent enhancement with lower PE and prolonged wash out, while scars are characterized typically by a reduced enhancement in the center. No differences (p = 0.428) were found in PE in the center of benign lesions (64.2 ± 28.9 dB), malignant lesions (88.1 ± 93.6 dB) and a scar (40.0 ± 17.0 dB). No significant differences (p = 0.174) were found for PE values at the margin of benign lesions (96.4 ± 144.9 dB), malignant lesions (54.3 ± 86.2 dB) or scar tissue (203.8 ± 218.9 dB). Significant differences (p < 0.001) were found in PE of the surrounding tissue when comparing benign lesions (33.6 ± 25.2 dB) to malignant lesions (15.7 ± 36.3 dB) and scars (277.2 ± 199.9 dB). No differences (p = 0.821) were found in AUC in the center of benign lesions (391.3 ± 213.7), malignant lesions (314.7 ± 643.9) and a scar (213.1 ± 124.5). No differences (p = 0.601) were found in AUC values of the margin of benign lesions (313.3 ± 372.8), malignant lesions (272.6 ± 566.4) or scar tissue (695.0 ± 360.6). Significant differences (p < 0.01) were found in AUC of the surrounding tissue for benign lesions (151.7 ± 127.8), malignant lesions (177.9 ± 1345.6) and scars (1091 ± 693.3). There were no differences in perfusion evaluation for mean transit time (mTT), rise time (RT) and time to peak (TTP) when comparing the center to the margins and the surrounding tissue. The CEUS perfusion parameters PE and AUC allow a very good assessment of the risk of malignant breast lesions and thus a downgrading of BI-RADS 4 lesions. The use of the external perfusion software (VueBox, Bracco, Milan, Italy) did not lead to any further improvement in the diagnosis of suspicious breast lesions and does appears not to have any additional diagnostic value in breast lesions.


2016 ◽  
Vol 371 (1710) ◽  
pp. 20150416 ◽  
Author(s):  
Jacqulyne P. Robichaux ◽  
John W. Fuseler ◽  
Shrusti S. Patel ◽  
Steven W. Kubalak ◽  
Adam Hartstone-Rose ◽  
...  

Left–right (L–R) differences in mammographic parenchymal patterns are an early predictor of breast cancer risk; however, the basis for this asymmetry is unknown. Here, we use retinoid X receptor alpha heterozygous null (RXRα +/− ) mice to propose a developmental origin: perturbation of coordinated anterior–posterior (A–P) and L–R axial body patterning. We hypothesized that by analogy to somitogenesis—in which retinoic acid (RA) attenuation causes anterior somite pairs to develop L–R asynchronously—that RA pathway perturbation would likewise result in asymmetric mammary development. To test this, mammary glands of RXRα +/− mice were quantitatively assessed to compare left- versus right-side ductal epithelial networks. Unlike wild-type controls, half of the RXRα +/− thoracic mammary gland (TMG) pairs exhibited significant L–R asymmetry, with left-side reduction in network size. In RXRα +/− TMGs in which symmetry was maintained, networks had bilaterally increased size, with left networks showing greater variability in area and pattern. Reminiscent of posterior somites, whose bilateral symmetry is refractory to RA attenuation, inguinal mammary glands (IMGs) also had bilaterally increased network size, but no loss of symmetry. Together, these results demonstrate that mammary glands exhibit differential A–P sensitivity to RXRα heterozygosity, with ductal network symmetry markedly compromised in anterior but not posterior glands. As TMGs more closely model human breast development than IMGs, these findings raise the possibility that for some women, breast cancer risk may initiate with subtle axial patterning defects that result in L–R asymmetric growth and pattern of the mammary ductal epithelium. This article is part of the themed issue ‘Provocative questions in left–right asymmetry’.


2003 ◽  
Vol 198 (12) ◽  
pp. 1899-1908 ◽  
Author(s):  
Shuyuan Yeh ◽  
Yueh-Chiang Hu ◽  
Peng-Hui Wang ◽  
Chao Xie ◽  
Qingquan Xu ◽  
...  

Phenotype analysis of female mice lacking androgen receptor (AR) deficient (AR−/−) indicates that the development of mammary glands is retarded with reduced ductal branching in the prepubertal stages, and fewer Cap cells in the terminal end buds, as well as decreased lobuloalveolar development in adult females, and fewer milk-producing alveoli in the lactating glands. The defective development of AR−/− mammary glands involves the defects of insulin-like growth factor I–insulin-like growth factor I receptor and mitogen-activated protein kinase (MAPK) signals as well as estrogen receptor (ER) activity. Similar growth retardation and defects in growth factor–mediated Ras/Raf/MAPK cascade and ER signaling are also found in AR−/− MCF7 breast cancer cells. The restoration assays show that AR NH2-terminal/DNA-binding domain, but not the ligand-binding domain, is essential for normal MAPK function in MCF7 cells, and an AR mutant (R608K), found in male breast cancer, is associated with the excessive activation of MAPK. Together, our data provide the first in vivo evidence showing that AR-mediated MAPK and ER activation may play important roles for mammary gland development and MCF7 breast cancer cell proliferation.


2021 ◽  
Vol 50 (1) ◽  
pp. 50-54
Author(s):  
B. F. Khurasev ◽  
Yu. A. Gurkin

Risk factors for the occurrence of benign diseases and breast cancer were studied in a comparative analysis of the survey data of 321 women who were operated on the mammary gland, had an established histological diagnosis and were registered in the oncology offices of the Kursk polyclinics (main group), and 150 women who did not have any clinical , no objective manifestations of breast pathology (comparison group). To study the frequency of dyshormonal hyperplasias of the mammary glands and risk factors in girls, an in-depth preventive examination of 390 schoolgirls aged 13-17 years was carried out.


2019 ◽  
Vol 23 (4) ◽  
pp. 733-739
Author(s):  
O.Yu. Kruk

Annotation. This article highlights the urgent problem of combined diseases of women's reproductive system. On the basis of theoretical analysis, generalized statistics for recent years are presented. The modern concepts of pathogenesis of diseases of the uterus and mammary glands, their correlation, as well as models of diagnosis and treatment are considered. Indeed, a more in-depth understanding of the problems of the combined pathology of the woman’s reproductive system (diseases of the uterus, ovaries, mammary gland), namely etiopathogenesis, diagnostic and treatment algorithms, will reduce the incidence of women of reproductive and perimenopausal age, as well as improve their quality of life. Only having the fullness of information about the state of the reproductive system of women, the doctor is able to prescribe thoughtful and effective treatment.


2012 ◽  
Vol 2012 ◽  
pp. 1-3 ◽  
Author(s):  
Jun Yamamura ◽  
Norikazu Masuda ◽  
Yoshinori Kodama ◽  
Hiroyuki Yasojima ◽  
Makiko Mizutani ◽  
...  

Carcinoma of an accessory mammary gland is an extremely rare tumor. A 61-year-old male patient presented with a hard mass measuring 85 mm × 51 mm in the left axilla. Incisional biopsy histopathologically showed an adenocarcinoma compatible with breast carcinoma originating in an accessory mammary gland. Systemic examinations revealed no evidence of malignant or occult primary lesion in the bilateral mammary glands or in other organs. Neoadjuvant chemotherapy was performed for the locally advanced axillary tumor and reduced the tumor to 55 mm in size, and, then, he could undergo complete resection with a negative surgical margin in combination with reconstructive surgery to fill the resulting skin defect with a local flap of the latissimus dorsi muscle. The patient has presented with no metastatic lesion in four years since the operation. This unusual case shows that neoadjuvant chemotherapy is an effective and tolerated therapy for advanced accessory breast cancer in the axilla.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A487-A488
Author(s):  
Joshua Philip Mogus

Abstract The mammary gland is a hormone sensitive organ that is susceptible to endocrine disrupting chemicals (EDCs) during several vulnerable periods, including pregnancy and lactation. Mammary gland reorganization during pregnancy and lactation is hormone driven and provides long-term protection against breast cancer risk. It is unknown if EDC exposures during these sensitive windows can alter mammary reorganization to either enhance or offset parity-induced protection against breast cancer. Here, we examined effects of propylparaben (PP), a common preservative used in personal care products and foods with estrogen receptor (ER) agonist properties, on the parous mouse mammary gland. Pregnant BALB/c mice were treated with 0, 20, 100, or 10,000 µg/kg/day PP throughout pregnancy and lactation. These doses were selected for their relevance to human exposures. We also included an unexposed nulliparous female group to evaluate the typical changes associated with parity. Five weeks post-involution (and five weeks after the last PP exposure), mammary glands were collected and assessed for changes in histomorphology, hormone receptor expression, immune cell number, and gene expression. We found that PP reduced many of the typical morphological effects of parity on the mammary gland, resulting in intermediate phenotypes for ductal density and total epithelial structures. Notably, we found increased proliferation in PP-treated mammary glands, despite decreased ductal epithelial volume relative to parous controls. Mammary glands from PP-treated females also had alterations in the expression of ERα-mediated genes, including PgR (the gene that encodes progesterone receptor) and Igf1, with expression levels that were intermediate to both nulliparous and parous control mice. Finally, PP reduced the effect of parity on several immune cell types in the mammary gland including B cells, T-cells, and M2 macrophages. These results suggest that PP, at levels relevant to human exposure, can disrupt the normal response to parity in the mouse mammary gland, including persistent alterations to mammary gland structures. Future studies should address whether PP exposures disturb the protective effects of pregnancy on mammary cancer risk.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Audrey Brenot ◽  
Irina Hutson ◽  
Charles Andrew Harris

Abstract To investigate the role of adipose tissue in the function of the mammary gland (MG) and reproductive system, we have examined lipodystrophic (LD) mice. LD mice of both sexes are sterile, but fertility was restored in both sexes with leptin injections. In addition, leptin was only needed for initial stages of pregnancy and not for parturition. A transplant of mouse embryonic fibroblasts (MEFs) led to the formation of an ectopic fat pad which also rescued the fertility in both sexes. However, pups born to rescued LD mothers died shortly after birth. We therefore examined the mammary glands of these mothers. MGs from LD mice were rudimentary and lacked terminal end buds. Leptin-injected and MEF rescued LD mice were able to become pregnant, showed normal pregnancy-associated glandular proliferation despite a smaller glandular area, were able to produce a small amount of milk that had grossly normal content of milk proteins and neutral lipids, but could not sustain pups to weaning. In order to separate the individual requirements for 1) adipokines such as leptin, 2) estradiol, and 3) epithelial-adipocyte interactions, we performed a series of experiments with both LD and ob (leptin-deficient) mice that received either estradiol or preadipocyte transplant. The resulting fat pad did not rescue the defect in MG development in LD mice. The defect also was not rescued with estradiol pellets. Ob/ob mice, like LD mice, lack leptin and estradiol, but retain adipose tissue. Ob mice have defective MG development. However, in striking contrast to LD mice, reconstitution of a WT fat pad in ob mice rescued the defect in MG development. Estradiol treatment did not rescue MG development in ob mice. Therefore direct interaction between mammary gland epithelia and adipocytes is a requirement for full invasion and expansion of the gland during puberty, but is not required for glandular proliferation during pregnancy and milk production. Given that excess adipose tissue is a risk factor for breast cancer we wanted to determine if breast cancer was affected by the absence of adipose tissue. LD mice were bred to MMTV-PyMT mice that develop spontaneous breast cancer. Remarkably, LD PyMT+ mice had accelerated growth of primary tumors compared to WT PyMT+ mice. Using our MEF transplant model future studies will be directed to understanding whether the accelerated breast cancer growth is due to loss of adipokines or altered epithelial-stromal interactions.


1981 ◽  
Vol 91 (1) ◽  
pp. 81-88 ◽  
Author(s):  
W. H. PEARLMAN ◽  
L.-H. PENG ◽  
M. R. J. PEARLMAN

The study was designed to determine the influence of the physiological state on the invitro uptake and metabolism of glucocorticoid hormone by the mammary gland. [3H]Corticosterone was accordingly incubated with minced mammary glands from pregnant, lactating and post-lactational rats. The total uptake of [3H]corticosteroid was obtained from the concentration of radioactivity by the tissue and the specific activity of the steroid substrate. The extent of 21-acylation was determined as the percentage of the radioactivity in the chromatographed tissue extracts attributable to 21-acyl-[3H]corticosterone. The results indicated that the uptake of [3H]corticosteroid increased with advancing pregnancy, attained a high plateau level during lactation, and steadily declined during the post-lactational period. The extent of 21-acylation of [3H]corticosterone varied from 10 to 40%, fluctuating widely in all physiological states, particularly during the post-lactational period. It was inferred that the stromal elements, presumably the adipocytes, of the mammary gland can also acylate the corticosteroid hormone, a view which gained experimental support from similar studies with minced parametrial adipose tissue from lactating rats.


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