Adenohibernoma of the breast

Kapucuoğlu, Nilgün; Percinel, Sıbel; Angelone, Antonio

doi:10.1007/s00428-007-0553-x

Cited by 10 publications

(17 citation statements)

References 4 publications

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“…Fat accumulation is a major pathogenic factor in sarcopenia, 3 and S100B is found in high abundance in white adipocytes, 55 brown adipocytes, particularly paucilocular and unilocular brown adipocytes, 56 and in breast, cardiac and intraosseous hibernoma. [57][58][59] As shown here, in geriatric muscles S100B co-localizes with UCP-1 + interstitial cells, i.e., bona fide brown adipocytes, and in a subpopulation of medium-sized myofibers and regenerating myofibers. Collectively, our results suggest that ROS/NF-κB-induced S100B might be a major molecular determinant of myoblast-brown adipocyte transition having an important role in the brown adipocyte-like features of myoblasts from sarcopenic humans and a potential therapeutic target.…”

Section: Discussionsupporting

confidence: 71%

Oxidative stress-induced S100B accumulation converts myoblasts into brown adipocytes via an NF-κB/YY1/miR-133 axis and NF-κB/YY1/BMP-7 axis

et al. 2017

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Muscles of sarcopenic people show hypotrophic myofibers and infiltration with adipose and, at later stages, fibrotic tissue. The origin of infiltrating adipocytes resides in fibro-adipogenic precursors and nonmyogenic mesenchymal progenitor cells, and in satellite cells, the adult stem cells of skeletal muscles. Myoblasts and brown adipocytes share a common Myf5 progenitor cell: the cell fate depends on levels of bone morphogenetic protein 7 (BMP-7), a TGF-β family member. S100B, a Ca-binding protein of the EF-hand type, is expressed at relatively high levels in myoblasts from sarcopenic humans and exerts anti-myogenic effects via NF-κB-dependent inhibition of MyoD, a myogenic transcription factor acting upstream of the essential myogenic factor, myogenin. Adipogenesis requires high levels of ROS, and myoblasts of sarcopenic subjects show elevated ROS levels. Here we show that: (1) ROS overproduction in myoblasts results in upregulation of S100B levels via NF-κB activation; and (2) ROS/NF-κB-induced accumulation of S100B causes myoblast transition into brown adipocytes. S100B activates an NF-κB/Ying Yang 1 axis that negatively regulates the promyogenic and anti-adipogenic miR-133 with resultant accumulation of the brown adipogenic transcription regulator, PRDM-16. S100B also upregulates BMP-7 via NF-κB/Ying Yang 1 with resultant BMP-7 autocrine activity. Interestingly, myoblasts from sarcopenic humans show features of brown adipocytes. We also show that S100B levels and NF-κB activity are elevated in brown adipocytes obtained by culturing myoblasts in adipocyte differentiation medium and that S100B knockdown or NF-κB inhibition in myoblast-derived brown adipocytes reconverts them into fusion-competent myoblasts. At last, interstitial cells and, unexpectedly, a subpopulation of myofibers in muscles of geriatric but not young mice co-express S100B and the brown adipocyte marker, uncoupling protein-1. These results suggest that S100B is an important intracellular molecular signal regulating Myf5 progenitor cell differentiation into fusion-competent myoblasts or brown adipocytes depending on its levels.

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Section: Discussionsupporting

confidence: 71%

Oxidative stress-induced S100B accumulation converts myoblasts into brown adipocytes via an NF-κB/YY1/miR-133 axis and NF-κB/YY1/BMP-7 axis

et al. 2017

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“…[21,22]. Albeit rare, the observation of brown fat tumors (hibernomas) in the breast have been described [23-27]. We also acknowledge that activation of BAT tissue within the breasts in female patients undergoing FDG PET/CT is typically not seen.…”

Section: Resultsmentioning

confidence: 99%

A pilot study of FDG PET/CT detects a link between brown adipose tissue and breast cancer

Cao

Hersl

et al. 2014

BMC Cancer

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BackgroundBreast cancer is the second most lethal cancer in women. Understanding biological mechanisms that cause progression of this disease could yield new targets for prevention and treatment. Recent experimental studies suggest that brown adipose tissue (BAT) may play a key role in breast cancer progression. The primary objective for this pilot study was to determine if the prevalence of active BAT in patients with breast cancer is increased compared to cancer patients with other malignancies.MethodsWe retrospectively analyzed data from 96 breast cancer patients who had FDG PET/CT scan for routine staging at the University of Maryland and 96 age- and weight-matched control female patients with other malignancies (predominantly colon cancer) who had undergone FDG PET/CT imaging on the same day. Data on the distribution (bilateral upper neck, supraclavicular and paraspinal regions) and intensity (SUVmax) of active BAT were evaluated by 2 Nuclear Medicine physicians, blinded to the clinical history.ResultsWe found sufficient evidence to conclude that based on our sample data the prevalence of active BAT in breast cancer patients’ group is significantly different from that in the control group. The estimated frequency of BAT activity was 3 fold higher in breast cancer patients as compared to controls with other cancers, (16.7% vs. 5.2%, respectively, p = 0.019). When patients were stratified by age in order to determine the possible impact of age related hormonal changes on active BAT among the younger women (≤ 55 years of age), 25.6% breast cancer patients exhibited BAT activity compared to only 2.8% in control women (p = 0.007). In contrast, among the older women (> 55 years of age), the prevalence of active BAT was similar among breast cancer and control women (10.7% vs 6.7%).ConclusionsIn breast cancer patients prevalence of BAT activity on FDGPET/CT is 3-fold greater than in age- and body weight-matched patients with other solid tumor malignancies; this difference is particularly striking among younger women aged < =55. In summary, our retrospective clinical data provide support to pursue prospective clinical and translational studies to further define the role of BAT in breast cancer development and progression.

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“…1,2 Adenohibernoma is a well-circumscribed nodular mass. It has been reported that these tumors are 3 to 10 mm in diameter.…”

Section: Discussionmentioning

confidence: 99%

“…They suggested that adenohibernoma could be regarded as a new entity and that it was different from fibroadenoma. 2 Garijo et al 8 described a case of mammary hamartoma with brown fat tissue. They considered that their lesion was a variant of hamartoma and it could not be termed as adenohibernoma, since it was not a predominantly fatty tumor.…”

Section: Discussionmentioning

confidence: 99%

Adenohibernoma

2011

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Adenohibernoma of the breast is a very rare tumor composed of brown fat tissue and intermingled glandular tissue. There are only 2 case reports in literature. This study reports the third case of adenohibernoma of the breast, which is not accompanied by breast cancer differing from the previous cases. And, to the best of the authors' knowledge, this is also the first case of adenohibernoma of the breast that has demonstrated adipophilin expression immunohistochemically.

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Adenohibernoma of the breast

Cited by 10 publications

References 4 publications

Oxidative stress-induced S100B accumulation converts myoblasts into brown adipocytes via an NF-κB/YY1/miR-133 axis and NF-κB/YY1/BMP-7 axis

Oxidative stress-induced S100B accumulation converts myoblasts into brown adipocytes via an NF-κB/YY1/miR-133 axis and NF-κB/YY1/BMP-7 axis

A pilot study of FDG PET/CT detects a link between brown adipose tissue and breast cancer

Adenohibernoma

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