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A 33-year-old woman was incidentally found to have a polypoid adenofibroma on MR imaging during the evaluation of carcinoma in situ of the cervix. The position of the polypoid lesion was variable from time to time. Although the lesion was a benign pedunculated one, T2-weighted MR images showed disruption of "junctional zone" in the posterior myometrial wall of the uterus, mimicking myometrial invasion of endometrial carcinoma.
Maffucci's syndrome, a congenital condition of generalized mesodermal dysplasia, is most often associated with multiple enchondromas and soft tissue hemangiomas or lymphangiomas. This case report describes the development of an unusual ovarian fibrosarcoma and subsequent ovarian adenofibroma in a young woman with the syndrome. The importance of aggressive surveillance in this and similar orthopedic syndromes is stressed.
Insulin-like growth factor 1 binding sites were characterized in human benign breast disease. We demonstrated the presence of one high affinity binding site. Chemical cross-linking of [125I]IGF1 to benign breast disease membranes in reducing condition and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) revealed one band with an apparent Mr of 130,000. The specificity of the binding was studied: IGF 2 was a good competitor whereas insulin competed for binding with a potency lower than 1/100 that of IGF1. This IGF1 binding corresponded to the previously described type I IGF receptor (IGF1-R). IGF1-R was assayed in 35 cases of benign breast disease and two samples of normal breast tissue. Forty-three per cent of the lesions were IGF1-R positive. The mean geometric level of specific binding was 1.98% in the whole population, it was significantly lower in adenofibromas (1.55%) than in epithelial hyperplasia (2.5%); it was 2% in dystrophic disease. IGF1-R was undetectable in normal tissue. Considering our previous results showing that almost all the breast cancers contained IGF1-R, these data suggest that the increase in IGF1-R could be a marker of malignant tumor development.
We report a case of asymptomatic mesoblastic nephroma in a 54-year-old woman. The tumor showed immunohistochemical reactions similar to developing nephrons. Electron microscopy showed immature tubules with numerous intracytoplasmic intermediate filaments. Recent studies support the concept of pathogenesis of the mesoblastic nephroma originating from collecting ducts. However, this case exhibited a complex pattern of antigenic expression not restricted to the collecting ducts, but including the glycoprotein CD24 and the neural cell adhesion molecule (NCAM). The following differential diagnoses will be discussed: benign mixed epithelial and stromal tumor, metanephric adenoma, and nephrogenic adenofibroma.
We describe a distinctive benign tumor of the kidney in a 48-year-old woman, which was composed of well differentiated ducts set in the spindle cell stroma which was muscle actin, smooth muscle actin and desmin positive, and was morphologically similar to the ovarian stroma. No immature appearing epithelial renal or mesenchymal tissue was present in the tumor. Histologically, the tumor differed from the nephrogenic adenofibroma and the rare cases of adult Wilms tumors, mesoblastic nephromas and cystic nephromas.
Based on 5 individual cases over a period of 8 years (1 fibroma, 1 angiofibroma, 2 adenofibromas, 1 xanthous neurofibroma) the characteristics of the rare intrapulmonary fibroma and the therapeutic consequences are discussed. Any suspicious tumor demands a thoracotomy with careful preoperative treatment and the subsegment or segment resection depending on the histological diagnosis reported during the procedure.
As a result of health education programs that have stressed self-examination and the importance of early diagnosis and treatment, less than 5 percent of breast lesions seen in clinical practice today are malignant. Nevertheless, breast cancer is the leading cause of deaths due to cancer in women and the second most common breast lesion. Chronic cystic mastitis, the most common breast lesion seen in women, can often be treated conservatively by aspirating the cystic fluid. Close follow-up is necessary so that if carcinoma develops, it can be treated early. Carcinoma is unpredictable but not hopeless. Although controversy exists regarding treatment, radical mastectomy is still the preferred treatment in most cases. Other breast diseases include adenofibroma, a common lesion requiring excisional biopsy for positive diagnosis; nipple discharge, which should be carefully examined cytologically; and relatively rare breast lesions, including intraductal papilloma, adenosis, traumatic fat necrosis, and cystosarcoma phylloides.
We evaluated 41 endometroid neoplasms with features intermediate between a benign endometrioid tumor and endometrioid carcinoma. Although these tumors showed various degrees of epithelial proliferation, they lacked the destructive stromal invasion of carcinoma. Intermediate endometrioid tumors were subdivided into proliferative endometrioid tumors (PET), endometrioid tumors of low malignant potential (ETLMP), and ETLMP with microscopic areas of invasion. PET were adenofibromas with solid aggregates of epithelial proliferation not exceeding 5 mm in any dimension, whereas ETLMP either had noninvasive cytologically malignant epithelium or aggregates of atypical epithelium measuring at least 5 mm in any dimension uninterrupted by fibromatous stroma. Of the seven PET, five were purely adenofibromatous, while two were mixtures of adenofibromatous and papillary components. Of the 31 ETLMP, 12 were adenofibromatous and 19 were either purely papillary or had mixtures of papillary and adenofibromatous components. An additional three ETLMP had one or more areas of microscopic invasion of the stroma in the form of an irregular or cribriform infiltration by atypical glands, often with squamous differentiation. These three neoplasms were designated "ETLMP with microinvasive carcinoma." The only neoplasm with extraovarian implantation at presentation, however, was an ETLMP with mixed adenofibromatous and papillary features, without microinvasion. None of the other patients with ETLMP had a metastasis or developed one within a follow-up period of between 0.8 and 11.2 years. Because they are very low-grade neoplasms, ETLMP should be separated from endometrioid carcinoma and not confused with PET, because PET have no malignant potential.
The clinicopathologic features of neoplasms arising in gastrointestinal endometriosis have not been well characterized. In this series, we report 17 cases of gastrointestinal endometriosis complicated by neoplasms (14 cases) or precancerous changes (three cases). Four patients, one of whom also had hypermenorrhea, presented with chronic abdominal pain and five had obstructive symptoms; one of these also had rectal bleeding. One patient presented with an acute abdomen and fecal peritonitis, one had vaginal bleeding, and one had a progressive change in bowel habits. Nine patients had a long history of endometriosis, 11 patients had had hysterectomies, and eight of these had also received unopposed estrogen therapy. The lesions involved the rectum (6), sigmoid (6), colon, unspecified (2), and small intestine (3), and comprised 8 endometrioid adenocarcinomas (EA), 4 mullerian adenosarcomas (MAS), 1 endometrioid stromal sarcoma (ESS), 1 endometrioid adenofibroma of borderline malignancy (EBA) with carcinoma in situ, 2 atypical hyperplasias (AH), and one endometrioid adenocarcinoma in situ (ACIS). The tumors ranged in size from 2 to 15 cm and all involved the serosa and muscularis propria. Two tumors extended into the mucosa, with mucosal ulceration in one. Follow-up was available in 11 cases. One patient with EA was dead of disease at 1 year, one had two recurrences at 1 and 2 years, and three were alive with no evidence of disease (ANED) at 9 months to 13 years (mean, 68 mos). The patient with the EBA was ANED at 3 months. Two patients with MAS were ANED at 2 and 3 years. The patient with ESS had a recurrence at 3 years and was ANED 6 years after her original diagnosis. One woman with AH was ANED at 60 months and the patient with ACIS was ANED at 16 months. One of the carcinomas was originally misdiagnosed as a primary intestinal adenocarcinoma. The pathologist should be aware of the possibility of a tumor of genital tract type when evaluating intestinal neoplasms in females, particularly if they have a history of endometriosis and have received unopposed estrogen therapy.
Identification of inheritable mutations associated with the development of malignancy has led to prophylactic surgeries to remove tissues at risk. We report seven unrelated patients with family histories of breast and/or ovarian cancer, five of whom underwent prophylactic salpingo-oophorectomy with hysterectomy. Four had proven BRCA-1 or -2 mutations. Malignant cells were found unexpectedly in the peritoneal washings of two patients, leading to the discovery of early-stage fallopian tube carcinoma. After changing the sampling technique at our institution, two more cases of unexpected fallopian tube carcinoma in situ were discovered. Another patient had a significant family history and underwent hysterectomy for uterine fibroids, leading to the discovery of fallopian tube carcinoma. Another patient with BRCA-1 mutation had unexpected widespread primary peritoneal papillary serous adenocarcinoma. The final patient had a borderline malignant clear cell adenofibroma. These cases underscore the importance of peritoneal cytology and thorough sampling in the management of patients undergoing hysterectomy with a family history of breast/ovarian cancer and/or known BRCA-1/BRCA-2 mutations. As prophylactic surgeries are becoming more common secondary to advances in molecular diagnostics, pathologists need to be aware that surgical specimens from these patients may require more rigorous examination to uncover early neoplastic changes.
A case of adenomyofibroma with skeletal muscle differentiation is described. A 55-year-old asymptomatic woman had atypical glandular cells of undetermined significance on a routine Papanicolaou smear. The endometrial biopsy revealed fragments composed of benign endometrial glands and myofibromatous stroma with foci of skeletal muscle differentiation. The stroma exhibited focal mild cytologic atypia and hypercellularity without periglandular cuffing or mitoses. Electron microscopy and immunohistochemical staining for myoglobin confirmed the skeletal muscle differentiation. A diagnosis of low-grade adenosarcoma with heterologous differentiation was made in the biopsy specimen based on the atypical stroma, the skeletal muscle differentiation, and previous observations that adenosarcomas may contain bland areas indistinguishable from an adenofibroma. The patient underwent hysterectomy, bilateral salpingo-oophorectomy, and pelvic lymphadenectomy. The hysterectomy specimen revealed small foci of residual tumor. In light of these findings the diagnosis was revised to adenomyofibroma with skeletal muscle differentiation. Uterine adenomyofibroma with skeletal muscle differentiation should be distinguished from a low-grade adenosarcoma in an endometrial biopsy.
The difficulties of a consistent Müllerian interpretation of the epithelial ovarian tumours include their inconstant hormonal responsiveness, the doubtful nature of the clear cell tumour and the apparent rarity of benign endometrioid forms. The reported frequency figures for the different types of endometrioid tumour suggest that their nature is made evident by proliferation. The appearance of indolent forms is explored by a study of inactive neoplastic areas associated with endometrioid carcinomas, or with proliferating endometrioid tumours or arising in endometriosis. These jointly suggest that most such tumours are identical with inactive 'serous' adenofibromas of glandular pattern and have senile endometrium as their prototype. Increasing proliferation develops more overt endometrioid forms which, if luxuriant, may be associated with corpus carcinoma. The endometrium of pregnancy is probably the prototype of the clear cell tumour, with a corresponding range of cell types. There is tenuous evidence that tumours may respond to steroid hormones if they arise in endometriosis and a difficulty of deducing such an origin is noted. The term 'serous' may be generic and comprise several different tissue types.
A 48-year-old woman with a 14 cm left ovarian mass had total abdominal hysterectomy and bilateral salpingo-oophorectomy. On cut section the tumor had a solid and a cystic component. There was a 2.5 cm nodule attached to the cyst wall. Sections taken from the solid component revealed a tumor composed of interlacing bundles of fusiform cells, resembling a leiomyoma. Smooth muscle actin positivity confirmed the diagnosis. Sections taken from the nodule in the cystic part revealed an adenofibroma. There was an SMA positive area in the cyst wall which we think is the possible origin of the leiomyoma. As far as we know, this is the first case of a co-existing leiomyoma and serous cystadenofibroma in the ovary, and we think it will broaden the histological spectrum of primary ovarian leiomyomas.
We studied one case of atypical polypoid adenomyoma of the uerus immunohistochemically using antisera against keratins, vinentin, S-100 protein, desmin and actin. The stromal cells were reactive with anti-actin and antidesmin antibodies suggesting a muscular phenotype and confirming previous ultrastructural data. Immunohistochemical investigations have proved to be useful in differential diagnosis of APA with invasive adenocarcinoma, adenosarcoma and adenofibroma of the endometrium.
We report an example of metastatic metanephric adenoma containing foci of papillary carcinoma in the primitive tumor arising in the left kidney of an 11-year-old girl. Histology revealed a monomorphous population of small cells with bland cytology arranged in pseudoglandular, tubular, papillary, and glomeruloid structures with frequent psammoma bodies. Intermixed there were foci of and small cavities lined by larger cells with eosinophilic cytoplasm and larger nuclei with small nucleoli. A regional lymph node contained metastatic deposits with the former histologic pattern. By immunohistochemistry the small cells were negative for carcinoembryonic antigen (CEA) and keratin 7 while these antibodies reacted positively in the larger cells. A fluorescent in-situ hybridization (FISH) study for chromosome 17 in imprints from the primitive tumor revealed 3 signals in about 10% of the nuclei while the rest was disomic. Disaggregated cells from the metastatic lymph node consistently revealed 2 signals for chromosomes 7, 16, and l7. Histology of the primitive tumor resembled the epithelial component of the so-called metanephric adenofibroma while the metastatic lymph node exhibited histologic and FISH genomic features of metanephic adenoma. Int J Surg Pathol 9(3):241-247, 2001
During the performance of 2,000 sonomammograms, there were 122 patients with 140 biopsy-confirmed fibroadenomas. Mass lesions or abnormalities were detected on the sonomammograms in 100 of these patients (82%) (118/140 masses), and a retrospective review of the descriptive sonographic criteria tabulated at the initial interpretation of 118 of these masses was undertaken. The most significant sonographic mass features were a round (48%) or oval (37%) shape, a smooth contour (75%), weak internal echoes (80%) in a uniform distribution (88%), and intermediate acoustic attenuation (71%). A pathologist reviewed all the cases, tabulating the gross and microscopic appearance of each specimen. In addition, the average fibrous and epithelial tissue content of 103 tumors (100 fibroadenomas and three adenofibromas) was recorded from a review of five low-power microscopic fields of representative areas of the tumor and correlated with the sonographic features. The sonomammographic features of seven calcified fibroadenomas, five giant fibroadenomas, and one fibroadenoma containing in situ lobular carcinoma and a subgroup having both sonomammograms and radiomammograms are discussed.
Extracellular matrix components of benign ovarian tumours (cystadenoma, adenofibroma, cystadenofibroma) were analysed. The investigated tumours contained twice as much collagen than control ovarian tissues. Significant alterations in mutual quantitative relationships between collagens of various types were observed. The proportion of type I collagen decreased and that of type III collagen increased. The accumulation of collagen was accompanied by a reduction in sulphated glycosaminoglycan content whereas the amount of hyaluronic acid was not changed. Dermatan sulphate was the most abundant glycosaminoglycan component. It is suggested that the accumulation of collagen (natural barrier to the migration of tumour cells) and underexpression of glycosaminoglycans/proteoglycans (binding some growth factors and interleukins) may exert an inhibitory effect on tumour growth.
Daily administration of a brominated triphenylethylene (TBP), to rats which received 20 mg of DMBA p. o. inhibits mammary carcinogenesis. The effect appears even with very small doses (i ppm in the diet) and seems to be dose related. With one exception (an adenofibroma) the tumours in control and treated animals were malignant. Administration of TBP prevents the appearance of corporea lutea in the ovaries but not the usual necrosis of the adrenal cortex.