Search

To investigate racial differences in the presence of leiomyomas, condition severity, associated symptoms and age at diagnosis between black and white hysterectomy patients.This study included 409 black women and 836 white women aged 18 or older who underwent hysterectomy for noncancerous conditions at 28 hospitals in Maryland. Patients were interviewed shortly before surgery, and hospital records were abstracted after discharge.Overall, 89% of the black women and 59% of the white women were found to have leiomyomas. Among those with a confirmed presurgical diagnosis of leiomyomas, the average age at diagnosis was 37.5 years for black women and 41.6 for white women, and the average age at hysterectomy was 41.7 for black women and 44.6 for white women. The average uterine weight for black women with leiomyomas was 420.8 g and for white women was 319.1 g. Black women were more likely to have seven or more leiomyomas (57%) in comparison to white women (36%). Black women with leiomyomas were more likely to be anemic (56%) than white women (38%) and more likely to report having very severe or severe pelvic pain (59%) than white women (41%).Black women having hysterectomy had larger and more numerous leiomyomas, and the leiomyomas were more symptomatic than in white women despite a younger age at diagnosis and hysterectomy.

Apocrine metaplasia is occasionally superimposed on sclerosing adenosis (apocrine adenosis) in breast biopsies, and cytologic atypia is sometimes present (atypical apocrine adenosis). The long term risk of patients developing breast carcinoma subsequent to the diagnosis of this lesion is unknown.Atypical apocrine adenosis was defined as apocrine adenosis with enlarged nucleoli and a greater than threefold variation in nuclear area. Lesions with recognizable cytoarchitectural patterns of intraductal carcinoma were excluded. Surveillance, Epidemiology and End Results (SEER) data were used as the reference population for calculations of relative risk.Thirty-seven women with atypical apocrine adenosis had a mean follow-up of 8.7 years. Four patients developed invasive ductal carcinoma of the breast (3 ipsilateral, 1 contralateral) after a mean of 5.6 years. The relative risk of developing carcinoma was 5.5 (95% confidence interval [CI], 1.9-16). All patients who developed carcinoma were older than age 60 at the time of breast biopsy showing atypical apocrine adenosis, and carcinoma developed at a mean age of 70 years. In the older than 60 years age group (11 patients), the relative risk of developing carcinoma was 14 (95% CI, 4.1-48).Atypical apocrine adenosis confers an increased risk of developing breast carcinoma in women older than age 60, and the risk in younger women is probably low. Some cases of atypical apocrine adenosis may represent in situ apocrine carcinomas that are difficult to diagnose because of the absence of the usual architectural features of intraductal carcinoma.

Primary non-Hodgkin's lymphoma of the breast is a rare neoplasm for which survival data vary among the reported studies. Thirty-one cases of diffuse large B-cell lymphoma of the breast, which had been seen in consultation from 1973 to 1985 at our institution, were reviewed. This represents the largest number of lymphomas of this histologic subtype reported to date in the English literature. Histologic examination and immunophenotypic analysis were performed and the results were correlated with clinicopathologic data. The patient population consisted of 29 females and 2 males with a mean patient age of 58.2 years. At the time of diagnosis, 26 patients had unilateral involvement (16 left, 10 right), and 5 had bilateral disease. Mean tumor size was 3.8 cm. Histologically, all cases showed a diffuse large B-cell lymphoma as classified by the Revised European-American Classification of Lymphoid Neoplasms (R.E.A.L Classification). Immunophenotypic studies on paraffin sections confirmed a B-cell lineage in every case. The majority of patients received chemotherapy and/or radiation therapy. The median survival was 36 months, confirming that this neoplasm has a poor prognosis.

Twenty-eight lipid cell (steroid cell) tumors of the ovary were studied by immunohistochemistry using an avidin-biotin complex detection system; 75% of tumors were vimentin positive, 46% were positive for cytokeratin (CAM5.2 antibody), 37% were positive with the cytokeratin cocktail AE1/AE3 and CK1, and 29% were positive for smooth muscle alpha-actin. Three tumors were positive for CD68 (KP-1), a histiocyte marker, and each of the following markers was positive in two cases: desmin, epithelial membrane antigen, neuron-specific enolase, and S-100 protein. All tumors tested were negative for chromogranin A, CD15 (Leu-M1), myoglobin, neurofilament protein, alpha-fetoprotein, carcinoembryonic antigen, and melanoma-associated antigen (HMB-45 antibody). Immunoreactivity for cytokeratins was usually focal, paranuclear, and globoid, while reactivity for actin and vimentin was diffuse and cytoplasmic. Based on these findings, melanomas and some carcinomas should be distinguishable from lipid cell tumors. However, the immunohistochemical profiles of smooth-muscle tumors, other gonadal stromal tumors (granulosa cell tumors, thecomas), and hepatocellular, renal cell, and adrenocortical carcinomas overlap with that of lipid cell tumors, and therefore these tumors may not be distinguishable from lipid cell tumors using this technique. In 10 cases (36%), negative controls exhibited weak to moderate nonspecific cytoplasmic staining. Evidence obtained using a biotin blocking kit, and a monoclonal antibody against biotin, suggests endogenous biotin-like reactivity as the source of the nonspecific staining.

Teratomas of the uterus are very rare, and a uterine teratoma with pulmonary differentiation has not, to our knowledge, been described previously. In this article, we report such a case in a 33-year-old woman, who presented with heavy vaginal bleeding and a polypoid mass of the uterine cervix. The cervical lesion was composed entirely of mature lung tissue, including bronchial, bronchiolar, and alveolar structures. The presence of well-differentiated respiratory epithelial cells, ie, Clara cells and alveolar type II cells, is confirmed by immunohistochemistry. The patient had no history of dilatation and curettage; therefore, implantation of fetal tissue could be excluded from the differential diagnoses. Since this is a newly developed mass in an adult individual, we favor a neoplastic process over heterotopia and interpret the lesion as unilateral lung development in an extragonadal mature teratoma.

Invasive ductal carcinomas of the breast frequently have an intraductal (in situ) component at the tumor periphery that, in some cases, is included in the measurement of the tumor and thereby increases the size of the tumor beyond that of the invasive component.Thirty-seven ductal carcinomas containing intraductal and invasive components were analyzed. The total tumor size, the size of the invasive component, the percentage of intraductal component, and the estimated tumor volume were assessed for each tumor.The mean size of the invasive component was 6.5 mm in axillary lymph node negative patients and 14.3 mm in those with axillary lymph node metastasis (P = 0.0001). The mean total tumor size was 13.7 mm and 17.6 mm (P = 0.035) and the mean percent of intraductal component was 52% and 26% (P = 0.015) in patients with negative and positive axillary lymph nodes, respectively. Ninety-two and four tenths percent of the difference in mean estimated total tumor volume between patients with negative and positive axillary lymph nodes was attributable to the difference in the volume of the invasive component alone.In small ductal carcinomas of the breast, the size of only the invasive component, as determined by microscopic measurement, is a better predictor of axillary lymph node status than is the total tumor size. The well established prognostic value of total tumor size largely is due to its reflection of the size of the invasive component.

Ovarian carcinoma is the most common cause of death from a gynecologic malignant neoplasm. The typically advanced stage at presentation and aggressive nature of these neoplasms result in an overall 5-year survival rate of less than 40%. Most malignant ovarian neoplasms are of the surface epithelial cell type, which includes serous, mucinous, clear cell, endometrioid, and Brenner tumors. However, among the epithelial neoplasms, benign lesions are more common than malignant neoplasms, and other entities (including nonneoplastic masses) are far more common causes of a pelvic mass. Imaging studies (ultra-sound, computed tomography, and magnetic resonance imaging) can depict the tumor morphology: solid or cystic, unilocular or multilocular cystic, with or without thickening of the walls or septa, with or without papillary excrescences or other soft-tissue elements, and with or without calcifications. Evaluation of these morphologic characteristics allows attempted differentiation among malignant, benign neoplastic, and nonneoplastic lesions. Lesion characterization assists in surgical planning. Malignant neoplasms nearly always require laparotomy, whereas benign neoplasms may be managed laparoscopically. In the case of ovarian carcinoma, treatment is primarily surgical, and most patients also receive chemotherapy. Unfortunately, recurrence is common.

Plexiform tumorlet is a rare lesion usually found in the myometrium and is believed to be a variant of epithelioid leiomyoma. Multiple plexiform tumorlets may have an infiltrative pattern and mimic endometrial stromal sarcoma. Only five cases of multiple plexiform tumorlets of the uterus have been reported, to the best of our knowledge. We now present the sixth case.

Premalignant lesions occur early in neoplastic development, are often small and multiple, lack one or more of the properties of cancers, often regress, and are often easily treatable. Such lesions may be derived from epithelial or nonepithelial cell populations. Many epithelial premalignant lesions can be identified by their confinement by a basement membrane. Mesenchymal, hematologic, and lymphoid premalignant lesions are difficult to recognize as most of these lesions have no defining morphologic features or anatomic boundary that identifies their premalignant nature. We have devised a classification for nonepithelial premalignant lesions, based on biologic behavior rather than morphology, that includes neoplastic lesions that have some but not all of the properties generally attributed to developed cancers. The five categories of nonepithelial premalignant lesions are: (a) lesions delimited by a basement membrane (e.g., melanoma in situ); (b) nonepithelial neoplasms having a low rate of metastasis (e.g., giant cell tumor of bone); (c) early forms of nonepithelial malignancy (e.g., Kaposi's sarcoma, patch stage); (d) indolent neoplasms that regularly progress to malignancies (e.g., chronic lymphocytic leukemia); and (e) certain low-grade neoplasms derived from germ cells (e.g., Grade 1 immature teratoma). Formal classification of the nonepithelial premalignant lesions would allow the pathologist to diagnose these biologically distinct entities as something other than simply benign or malignant, and would direct tumor biologists to study the key molecular properties that control the premalignant phenotype.

Pseudoangiomatous hyperplasia of mammary stroma is a rare, benign mesenchymal proliferation that sometimes mimics angiosarcoma. To our knowledge, it has not been reported in men. We report the first case of this unusual entity in a man. This case was most unusual in that it occurred in a clinical setting of immunosuppression, in axillary gynecomastia, and was growing rapidly.

Ovarian serous tumors of low malignant potential (STLMP) occasionally progress; a small percentage of patients die of the tumor. There is no known way to predict which tumors will progress.Forty STLMP were analyzed by DNA flow cytometry and compared with 26 serous carcinomas.Forty percent of Stage I STLMP and 40% of Stage III STLMP were DNA aneuploid as compared to 54% of serous carcinomas. Aneuploidy was found in 50% of STLMP that progressed and in 38% of neoplasms that did not progress. Four of the 30 Stage I STLMP progressed, and 3 of the 4 were aneuploid; whereas, of the 26 Stage I STLMP that did not progress, 9 were DNA aneuploid. Stage III STLMP were aneuploid in 4 out of 10 instances (40%). Aneuploidy was not related to progression as three of four DNA diploid tumors progressed, and three of six that did not progress were aneuploid. Thirteen of 16 aneuploid STLMP had peridiploid aneuploid populations. The mean follow-up periods were 14.3 years for Stage I STLMP and 8.3 years for Stage III STLMP:DNA aneuploidy in Stages I and III STLMP does not identify neoplasms likely to relapse with sufficient frequency to be useful in identifying those patients at high risk for relapse.

Two cases of synovial sarcoma diagnosed by aspiration cytology are described. A 15-year-old, athletic female presented with a tender midthigh mass clinically thought to be a hematoma. Aspiration cytology revealed numerous clusters of spindle cells admixed with small groups of epithelial cells. Cytokeratin and vimentin stains were positive in the epithelial and spindle components, respectively. Resection of the mass revealed a biphasic synovial sarcoma. Second, a 53-year-old male presented with a recurrent soft tissue mass 10 years after synovial sarcoma of the knee had been resected. Aspiration cytology revealed neoplastic spindle cells. Cytokeratin and vimentin preparations showed focal positivity. Resection revealed a predominantly monophasic synovial sarcoma. These cases demonstrate the utility of aspiration cytology in diagnosing both unsuspected and recurrent synovial sarcoma.

It is unclear whether HER-2/neu proto-oncogene expression in ovarian epithelial neoplasms is related to prognosis.The authors performed immunohistochemical stains on 20 serous tumors of low malignant potential (STLMP) in Stages I and II and 19 serious carcinomas in the same stages. They used three different commercial antibodies to make comparisons.Two of four Stage I STLMP in patients who experienced disease progression showed positive staining for the gene product, whereas none of seven Stage I nonprogressive STLMP showed positive staining. Five of the six Stage III nonprogressive STLMP showed positive staining, whereas none of three Stage III STLMP that progressed showed positive staining. Three carcinomas (one Stage I and two Stage III) also showed positive staining.Expression of HER-2/neu may be associated with high stage in serous ovarian neoplasms, but it is not likely to identify the small fraction of patients with STLMP who will experience disease progression.

Keratoacanthomas (KAs) are rapidly growing cutaneous lesions that frequently look much like well-differentiated squamous cell carcinomas (SCCs) but spontaneously regress. It is uncertain whether KA is a reactive hyperplastic lesion that mimics a neoplasm or a true (but defective) neoplasm that cannot sustain progressive growth. To address this question, we performed DNA flow cytometric analysis on 14 KAs and 10 cutaneous SCCs for comparison. By multiparameter DNA flow cytometry using forward scatter and orthogonal scatter, 10 KAs and 4 SCCs had peridiploid DNA aneuploid populations (DNA indices of 1.03-1.14), and 2 SCCs had grossly aneuploid populations (DNA index, 1.69 and 2.33). Our data thus support aneuploidy in KAs. It is argued that KA is a true neoplasm.

A variant of uterine leiomyosarcoma containing two morphologic bell populations is described. A smooth-muscle component with a mitotic rate of 13 per 10 high-power fields, and a second population of cells mimicking metastatic small-cell carcinoma were both present. The second population was composed of small angulated epithelioid cells with hyperchromatic nuclei and barely discernible cytoplasm growing in tight rows, often in single file between fascicles of smooth muscle. DNA flow cytometry showed a large tetraploid aneuploid tumor cell population, and further suggested that the epithelioid cells probably represent tetraploid tumor cells in S-phase. Thus, this morphologic variant of leiomyosarcoma, unlike previously described variants of smooth-muscle tumors, is explained by the variable appearance of the neoplastic cells in different phases of the cell cycle.

Clear cell dysplasia of the bladder is a well-described morphologic entity that has been found in association with transitional cell carcinoma of the bladder. Its biologic role in bladder tumorigenesis is unknown, and no instances of its polidy analysis have been reported. The authors describe a case of clear cell dysplasia of the bladder found in association with a primary adenocarcinoma of the bladder. Flow cytometric analysis of bladder tissue involved by clear cell dysplasia, adenocarcinoma and cystitis cystica (all from the same bladder) demonstrated no DNA aneuploid populations. Cells from the area of clear cell dysplasia had an S + G2 + M fraction of 7%, indicating that it was a proliferative lesion. Cells from the adenocarcinoma had an S + G2 + M phase of 18%, and cells from an area of cystitis cystica had an S + G2 + M phase of 4%.

Basaloid squamous carcinoma is believed to be a histologically distinct variant of squamous cell carcinoma of the neck region with 11 cases reported. Two cases arising in the pyriform fossa and vallecula are reported, both of which were associated with second primary malignant tumors: esophageal small cell carcinoma and palatal squamous cell carcinoma, respectively. The authors suggest that basaloid squamous carcinoma may be associated with a high incidence of second primary tumors in the upper gastrointestinal tract or larynx.

Pathologists frequently need to judge whether basal cell carcinomas have been excised adequately. Traditionally, excision adequacy is assessed by looking for the presence of tumor at the margins of resection. This time-honored activity has questionable value, since it has been demonstrated that the majority of tumors with positive margins do not recur, and a substantial minority of tumors with negative margins do recur. It is proposed that excision adequacy can be evaluated by considering the pattern of tumor growth. Tumors composed of widely dispersed nests need wider margins than tumors that grow as tight clusters of tumor nests, and this assertion can be evaluated statistically. A morphometric study of 28 basal cell carcinomas (BCCs) was performed, in which the distribution of tumor cell nests seen in cross-section was analyzed. The average distance from the center varied greatly (272 to 2273 microns) among these tumors. Standard deviations were calculated from distances between the tumor center to each nest within the tumor, and one-tailed Student's t tests were used to obtain 90%, 95%, and 99% confidence limits for distances beyond which no additional tumor nests are expected. These distances, in tumor radii, ranged from 0.8 to 1.9 and from 1.03 to 4.89, for 90% and 99% confidence limits, respectively. Conventional methods used to determine margin adequacy do not account for the discontinuous appearance of BCC in histologic sections. This theoretical model demonstrates that an alternate way of assessing excision adequacy can be achieved with a statistical analysis of the pattern of tumor growth, rather than looking for absence of tumor at the resection margin.(ABSTRACT TRUNCATED AT 250 WORDS)

Localized amyloidosis of the seminal vesicles (ASV) is reported as an incidental finding in surgical specimens from three elderly men. In two cases, the amyloid deposits were bilateral, subepithelial, and clinically inapparent, features similar to other cases in the literature. In one case, the diagnosis was made on a transrectal prostatic needle biopsy that included a small portion of seminal vesicle; to our knowledge, this has not been previously reported. Electron microscopy in one case demonstrated nonbranching fibrils characteristic of amyloid, and pretreatment of tissue sections using the permanganate method in two cases showed almost complete ablation of congophilia. Evidence suggests that ASV is a permanganate-sensitive, non-AA (amyloid, protein A) type of amyloid that may be different from all other types of amyloid previously characterized.

3T3 cells have a large, pericellular coat which contains 30 times more hyaluronate than the amount of cell surface hyaluronate associated with simian virus 40-transformed 3T3 (SV-3T3) cells. On the other hand, SV-3T3 cells have high affinity binding sites for exogenously added hyaluronate, whereas 3T3 cells have much lower affinity sites. Removal of cell surface hyaluronate from SV-3T3 cells by treatment with hyaluronidase caused a reproducible increase in their maximum binding capacity for exogenous hyaluronate but no significant change in binding affinity or specificity. For 3T3 cells, however, the maximum amount of binding decreased and the affinity of binding increased after hyaluronidase treatment. When endogenous cell surface hyaluronate was labeled metabolically and then the cells incubated in the presence of exogenous unlabeled hyaluronate, the labeled cell surface hyaluronate was quantitatively displaced from the SV-3T3 cells but was not displaced from the 3T3 cells. Chondroitin sulfate and heparin did not displace cell surface hyaluronate from either cell type. Membranes isolated from SV-3T3 cells bound hyaluronate specifically and with high affinity, whereas membranes from 3T3 cells did not consistently bind a significant amount of hyaluronate. We conclude from these studies that the retention of endogenous hyaluronate on the surface of SV-3T3 cells is mediated by binding sites similar to those detected by the addition of exogenous hyaluronate, and the mechanism of retention of endogenous hyaluronate on the surface of 3T3 cells differs from SV-3T3 cells.

The amniotic band syndrome, a complex collection of asymmetric congenital anomalies, is almost certainly an underdiagnosed entity. No two cases are exactly alike. Two cases are reported, each of which exhibits craniofacial, visceral, body wall, and limb anomalies, the common types of defects seen in this syndrome. The literature is reviewed, and the most commonly accepted theory of pathogenesis is discussed in juxtaposition to another major theory. The importance of recognizing this syndrome is stressed, since it very rarely recurs in families.