Sclerosing Adenosis Research Articles

Sklerosierende Adenose der Prostata Ein Karzinommimikry

Sclerosing adenosis of the prostate is a benign lesion, which was not recognized until a few years ago. As in sclerosing adenosis of the breast, a background of various hyperplastic changes is commonly also present in the prostate. An incidence of 2.8% was reported in one series of resected hyperplastic prostatic glands. As demonstrated in this case report, the main problem lies in the differential diagnosis between sclerosing adenosis and highly differentiated adenocarcinoma of the prostate. Histological diagnosis of sclerosing adenosis based on routine HE sections is supplemented by immunohistochemical methods. Important diagnostic criteria of sclerosing adenosis are the presence of basal cell differentiation, which is demonstrated by cytokeratin 903, and signs of possible myoepithelial differentiation, with expression of S-100 and/or smooth muscle actin. These antibody expressions are lacking with in the presence of adenocarcinoma of the prostate. Nevertheless, in a small number of cases this differential diagnosis remains impossible, even after the application of immunohistochemical methods. Further studies are needed to shed some light on the relations between sclerosing adenosis, atypical adenomatous hyperplasia and adenocarcinoma of the prostate. So far, there appears to be no evidence of a direct relationship between sclerosing adenosis of the prostate and an elevated risk of carcinoma.

Sclerosing Adenosis and the Risk of Invasive Breast Carcinoma

Sclerosing adenosis recently has been implicated as an indicator of mildly increased risk for invasive mammary carcinoma. This article illustrates the confines of definition and morphologic spectrum for sclerosing adenosis, discusses its association with other histologic findings in the breast, and reviews the recently accumulated evidence for inclusion of sclerosing adenosis as an increased risk lesion.

Sclerosing adenosis of the prostate gland. A lesion showing myoepithelial differentiation.

Sclerosing adenosis of the prostate is a rare lesion characterized by the proliferation of variably sized glands in a cellular stroma. We report light microscopic, immunohistochemical, and ultrastructural studies in 22 examples from 15 patients. Two cases were identified in 100 consecutive prostates embedded by a whole organ method, giving a prevalence of 2%. Antibodies directed against the following antigens were used: high-molecular-weight cytokeratin (CKH; 34 beta E12); cytokeratin (CK; AE1/AE3), prostatic acid phosphatase (PAP), prostate-specific antigen (PSA), S-100 protein, muscle-specific actin (HHF35), and vimentin (Vim). Cells within the glandular component demonstrated positive reactivity for CK, CHH, PSA, and PAP, indicating a prostatic epithelial origin. In addition, a distinct population of cells reacting for muscle-specific actin and S-100 protein was identified within this glandular element. Adequate material for ultrastructural study was available in five cases; all showed the presence of flattened cells located between the basement membrane and secretory epithelial cells, which had features typical for myoepithelial differentiation. Although the prostate gland does not normally contain myoepithelial cells, we have documented their consistent presence in this unusual lesion; we believe these cells arise by a metaplastic process from the prostatic basal cells.

A comparison of the results of long-term follow-up for atypical intraductal hyperplasia and intraductal hyperplasia of the breast

Follow-up information was obtained on 199 women with breast biopsy specimens containing intraductal epithelial proliferation. The proliferations were divided into regular or ordinary intraductal hyperplasia (IDH) (117 cases) and atypical intraductal hyperplasia (AIDH) (82 cases). The average length of follow-up was 14 years for the patients with IDH and 12.4 years for the patients with AIDH. Of the 117 patients with ordinary IDH, carcinoma subsequently developed in six (5%); three of these were invasive carcinomas (2.6%). All three invasive carcinomas were in the ipsilateral breast, but of the three intraductal carcinomas (IDCa), two were in the contralateral breast. Of the 82 patients with AIDH, invasive carcinoma subsequently developed in eight (9.8%); six of these were located in the ipsilateral breast and two in the contralateral breast. One of these six patients died of disseminated carcinoma. The average interval to the subsequent carcinoma (intraductal and invasive carcinoma) was about the same in the two groups (8.3 years for AIDH and 8.8 years for IDH lacking atypia). When considering only subsequent invasive carcinomas, the interval was 8.3 years for the AIDH and 14.3 years for the IDH lacking atypia. Of the 14 patients with IDH and a family history of breast carcinoma, invasive carcinoma subsequently developed in one (7%) as compared with two (2%) of the 91 with a negative family history. Among patients with AIDH, invasive carcinoma subsequently developed in two of the 13 (15%) of those with a family history of breast carcinoma as compared with one of 57 (1.8%) of the women with a negative family history. The presence of atypia in epithelial hyperplasia is a significant factor in increasing the likelihood of the development of subsequent invasive carcinoma (P = 0.03; two-tailed test). Of women with AIDH, invasive carcinoma subsequently developed in 17% of those with sclerosing adenosis (SA) as compared with 4.2% of those without it. Therefore, SA may be a contributing factor to increased risk. A positive family history also appears to increase the likelihood of the subsequent development of invasive carcinoma, particularly in patients with AIDH.

Invasive breast cancer risk in women with sclerosing adenosis.

To assess sclerosing adenosis (SA) as an independent risk factor for subsequent invasive breast cancer (IBC), the authors reviewed 10,366 benign breast biopsy specimens (BB) obtained between 1950 and 1968 and identified 547 cases of SA meeting strict histologic criteria of expanded lobular units with whorled compressed acini. Of those women targeted for follow-up (3303, of whom 349 had SA), 84% were successfully followed for an average of 17 years. The relative risk for IBC among patients with SA regardless of the presence of atypical hyperplasia (AH) was 2.1. This risk decreased to 1.7 when patients with AH were excluded, and rose to 6.7 when only those patients with SA and AH were analyzed. The coexistence of a family history of IBC in a first-degree relative did not further elevate risk above that of SA alone when women with AH were excluded. Sclerosing adenosis was found to be positively associated with atypical lobular hyperplasia (ALH) as ALH was present in biopsy specimens with SA 2.7 times more frequently than in other biopsy specimens. Perimenopausal age, histologic calcification, and family history of IBC (FH) were also positively associated with SA. Sclerosing adenosis was most frequent in the perimenopausal period and had a weak association with family history of IBC. No association with atypical ductal hyperplasia (ADH) was identified. The authors conclude sclerosing adenosis represents an independent risk factor for subsequent invasive breast cancer apart from its association with ALH, and the risk (excluding patients with coexistent atypical hyperplasia) is in the range of 1.7, times thereby justifying inclusion of sclerosing adenosis as a component of a group of histopathologically defined lesions termed "proliferative breast disease without atypia" which implies a relative cancer risk of 1.5 to 2.0.

Sclerosing adenosis.

The literature regarding sclerosing adenosis has been reviewed. The pathological and radiological aspects of this benign breast condition have been emphasized since they influence clinical practice. Features of 43 patients diagnosed as having sclerosing adenosis have been reported. Cancer was suspected on mammography in 17, and 25 experienced breast pain. Thus, the lesion is important both as a mimic of malignancy and as a cause of mastalgia. The clinical and radiological features allow the condition to be suspected before biopsy, in which circumstance paraffin histology is greatly preferable to frozen section.

Sclerosing adenosis cancerized by intraductal carcinoma

Sclerosing adenosis is a common proliferative lesion of the mammary lobule which is not associated with an increased risk of developing breast cancer. An unusual case of florid sclerosing adenosis showing extensive cancerization by intraductal carcinoma is reported. The neoplastic nature of the sclerosing lesion can be recognized by the unusual distension of the tubules by cells and the subtle cytological changes, and further confirmed by finding foci of classical intraductal carcinoma.

Real-time sonography of palpable breast masses.

In order to evaluate the clinical usefulness of an electronic real-time linear array scanner in breast diseases, ultrasonography was performed in 148 cases of histologically confirmed palpable breast masses. The real-time images were observed on a television monitor while moving the hand-held transducer probes over the masses. It took only a few minutes to examine and diagnose a palpable mass. Among 45 carcinomas, 39 lesions were correctly diagnosed, four lesions were not detected by ultrasound and two were misdiagnosed as fibroadenomas. On the other hand, ten benign lesions were falsely diagnosed as breast cancers: seven mastopathies (including four sclerosing adenosis), two fibroadenomas and one abscess. The sensitivity and specificity for diagnosing breast cancer were 0.87 and 0.90 respectively. Real-time sonography is a simple, time-saving and useful tool for examining palpable breast masses. However, it should be realised that some breast cancers are difficult to image and differentiate from benign lesions.

Gutartige Veränderungen der Brustdrüse, welche ein Karzinom vortäuschen

Various mammary lesions may offer considerable clinical as well as histological difficulties concerning the biological behaviour. Among them are sclerosing adenosis, ductular papillomas, proliferating types of fibrocystic disease and lobular neoplasia. Between 1975 and 1978 3,243 mammary specimens were examined: 36% were carcinomas and very rare other primary malignancies, 12% sclerosing adenosis, 11% cysts, 12% benign tumors (fibroadenoma etc.), 28% fibrous cystic disease of which 6% were of the proliferating type. Nearly 0.6% were lobular neoplasia (so-called non-invasive lobular carcinoma, lobular carcinoma in situ). Lobular neoplasia shows a higher risk of developing into carcinoma than do the proliferative fibrocystic lesions. However, lobular neoplasia without concomitant carcinoma should not be interpreted as malignant, allowing a more conservative therapy. The histopathologic diagnosis is subject to limitations due to the technique of tissue sampling and examination. Borderline cases deserve extensive and careful scrutiny and should not be judged by intraoperative frozen sections alone.

Electron Microscopy of Sclerosing Adenosis and Infiltrating Duct Carcinoma of the Human Mammary Gland<xref ref-type="fn" rid="fn1">2</xref>

Electron Microscopy of Sclerosing Adenosis and Infiltrating Duct Carcinoma of the Human Mammary Gland<xref ref-type="fn" rid="fn1">2</xref>