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M J Costa

Publications and source records attributed to M J Costa.

At least 37 records · Page 2Linked to original sources
PubMed1997

Vision for a treasured resource. Part 1, Nurse manager role implementation.

The importance of the nurse manager for both quality patient care and organizational effectiveness seems indisputable. With decentralized decision-making, the role of the nurse manager has expanded in both scope and accountability. In this two-part article, role implementation of the nurse manager and associated learning needs are described. This article focuses on interpreting significant incidents related to role implementation in nurse managers' practice. It also shows how the authors used the Manager as Developer Model for organizing and understanding some of the data. Part 2 (April 1997) will describe and interpret significant incidents related to nurse managers' ongoing learning needs.

Boston↗
PubMed1997

Vision for a treasured resource. Part 2. Nurse manager learning needs.

Part 1 in this two-part series focused on the meaning of significant incidents in nurse managers' practice related to role implementation. Explanation of the authors' application of the Manager as Developer Model (MADM) as a useful model for organizing and understanding some of the data was also discussed. Part 2 describes significant incidents in nurse managers' practice related to their ongoing learning needs. The authors address issues of performance counseling and intervention versus coaching and make recommendations for management development programs.

Boston↗
PubMed1997

[Gaucher's disease in pregnancy].

A case of Gaucher's disease associated with pregnancy is reported. Although clinical symptoms were not present, portal hypertension was detected by ultrasound in the 13th week of pregnancy. Maternal anemia implied the use of erythropoietin from the 33rd week onwards. Good perinatal and maternal outcomes were achieved and there were no hemorrhagic complications.

Adult↗
PubMed1996

Epidermal growth factor receptor and c-erbB-2 oncoprotein expression in female genital tract carcinosarcomas (malignant mixed müllerian tumors). Clinicopathologic study of 82 cases.

BACKGROUND: Epidermal growth factor receptor (EGFR) and c-erbB-2 (also known as HER-2/neu) oncoprotein (p185erbB-2) are members of the subfamily of tyrosine kinase, transmembrane receptors often implicated in human carcinogenesis. We hypothesize that expression of EGFR and p185erbB-2 adds useful prognostic and histogenetic information regarding female genital tract carcinosarcomas (FGTCSs). METHODS: Paraffin sections from 82 FGTCS (61 endometrium, 14 ovary, 5 cervix, and 2 fallopian tube), 56% of which exhibited heterologous elements, were stained using anti-EGFR (clone 31G7, Triton Diagnostics, Alameda, CA) and anti-p185erbB-2 (clone CB11, Novocastra Labs, UK). RESULTS: EGFR reactivity was present in 11 (13.4%) FGTCSs (55% carcinomatous component [CC] only, 18% sarcomatous component [SC] only, and 27% in both). EGFR was associated with adenosquamous histology of the CC (P < 0.05) and heterologous rhabdomyosarcomatous differentiation in the SC (P < 0.05); no other histopathologic features were correlated. p185erbB-2 reactivity was present in 79 (87.8% strong [S], 78% membrane [M], and 8.5% weak) FGTCSs (1% CC only, 0% SC only, and 99% in both). p185erbB-2 did not correlate with histopathologic features or EGFR. Seventy-seven patients had clinical follow-up for longer than 12 months. Approximately 49.3% and 72.3% of patients had recurrent disease by 12 and 80 months, respectively; all but 1 were dead from disease. 27% of patients were disease free after 15 to 307 months (median, 77 months; mean, 92 months). EGFR, but not p185erbB-2 expression predicted disease recurrence (P < 0.05). Recurrent disease was associated with Stage greater than I (P < 0.0001), vascular space invasion in resection specimens (P < 0.01), and deep myometrial invasion in hysterectomies (P < 0.05). EGFR was associated with Stage greater than I and did not help predict recurrence in good prognosis groups. CONCLUSIONS: p185erbB-2 overexpression in both CC and SC of FGTCS suggests a common carcinogenic mechanism for both components and supports the conversion-histogenesis hypothesis implicating a dominant role for the CC with the SC arising as a metaplastic change from the CC. EGFR may be expressed in either component and indicates aggressive biologic behavior; however, its prognostic utility is limited by its low predictive value for recurrence (40.3%), inability to foretell recurrence in good prognosis groups, and dependence on stage. High frequency of overexpression and dismal prognosis make FGTCS patients good candidates for trials of therapeutic strategies involving the p185erbB-2 receptor manipulations.

Adult↗
PubMed1996

Fine-needle aspiration cytology of sarcoma: retrospective review of diagnostic utility and specificity.

Fine-needle aspiration cytology (FNA) is useful because of its low cost, quick turn around time, and low incidence of complications. This study investigates the role FNA plays in the evaluation of sarcoma. We reviewed all the pathologic material from patients with sarcoma or a FNA diagnosis suggestive of sarcoma at the University of California-Davis Medical Center (1985-1994). Fifty-two of 196 patients identified (26.5%) were evaluated with FNA exhibiting 46 soft tissue and 6 bone lesions located in the extremities (19), trunk (19), head and neck (8), retroperitoneum (3), and abdominal cavity (3). Among 196 patients identified, those evaluated by FNA had soft tissue rather than bone lesions (P < .001) and primary sites other than in the extremities (P < .001). The primary neoplasms for the 52 FNA patients included 47 sarcomas (10 malignant fibrous histiocytomas and 16 other types), 1 intramuscular myxoma, 2 lymphomas, and 2 spindle cell (sarcomatoid) carcinomas. In 43 patients (22% of total), FNA was used first, before a primary diagnosis. The FNA report showed the correct specific neoplasm in only 20.9%. However, the FNA reports reflected an effective positive diagnosis leading to appropriate diagnostic biopsy in 88.4%, while only 7.0% were misleading (benign or inflammatory) and 4.6% inadequate. Review of FNA slides for 32 of 43 patients in which FNA was used first, in a blinded fashion, exhibited 21.9% specificity for the specific neoplasm, and 88.4% effective positive diagnoses. In 9 patients, FNA was utilized to investigate recurrence. Five out of 5 instances of recurrent sarcoma were identified by FNA. However, FNA misidentified recurrence in 3/4 instances, exhibiting suspicious cells from regenerating skeletal muscle (2) and a traumatic neuroma (1). The specific diagnosis for sarcomas is challenging even with surgical material. FNA usually does not provide a specific diagnosis (only in 20.9% of cases) and review of routinely prepared slides showed the same specificity as reflected by the original FNA report, at times formulated with the benefit of immunohistochemistry or electron microscopy. FNA effectively evaluated lesions in 45 of 52 patients (86.5%), confirming the useful screening role for this technique in sarcomas.

Adult↗
PubMed1996

Transformation in recurrent ovarian granulosa cell tumors: Ki67 (MIB-1) and p53 immunohistochemistry demonstrates a possible molecular basis for the poor histopathologic prediction of clinical behavior.

Ovarian granulosa cell tumors (GCTs) behave unpredictably. Stage I patients suffer recurrences many years after treatment, and histopathologic evaluation of the primary GCT offers only a few clues. Grading, in particular, is largely ineffective. Ki67 (MIB-1) and p53 monoclonal antibodies (active on paraffin embedded tissues) provide insight into nuclear proliferation and control, respectively. In this study, the authors hypothesized that these molecular markers will help predict the clinical behavior of GCTs. Paraffin sections from 68 GCTs (arising in 56 patients: 53 primary and 15 recurrent) including 34 typical and 27 diffuse adult, and seven juvenile types were immunostained for Ki67 (MIB-1 clone; Immunotech, Westbrook, ME) and p53 (DO7 clone; Novacastra Laboratories, UK). The Ki67 proliferation index (Ki67PI = percentage immunoreactive on a count of at least 400 nuclei) ranges from 1 to 50% (mean, = 12.2%; median, 9.3%). Nineteen percent of GCTs exhibited focal p53 immunoreactivity; the number of GCTs and proportion of nuclei decorated were as follows: four, <1%; seven, 1% to 10%; and one, 20%. Ki67PI was higher in recurrent tumors (P<.001) and correlated with mitotic rate (r = .75; P<.0001). p53 staining was associated with juvenile type GCTs (P<.001) and higher Ki67PI (P<.005). Other histopathologic features exhibited no association with p53 staining or Ki67PI. Follow-up was available for 54 of 56 patients: 18 suffered recurrences after 16 to 229 months (mean, 72.1 months; median 59 months), and 36 were disease free 16 to 369 months (mean, 78.2 months; median, 70 months) after diagnosis. Curiously, high Ki67PI and mitotic rates of primary GCT correlated weakly with a disease-free course (P=.03 and .07 respectively). Disease recurrence was associated with stage >I (P<.0005), vessel invasion in the capsule (P<.001), ruptured tumors (P<.005), and older patients (P<.02). p53 staining and size or subtype of GCT exhibited no prognostic value. For 12 patients, paired primary and first recurrence of GCT showed a striking increase in Ki67PI (P<.00005) and mitotic activity (P<.02) in the recurrence. p53 expression also appeared (de novo) in two recurrent GCTs. The interpretation of focal p53 staining (>10% nuclei decorated in only one GCT) is controversial. Some investigators suggest that this represents overexpression of wild type p53 rather than p53 gene mutation. Primary GCTs exhibit a wide spectrum of proliferative activity, and the seven juvenile GCTs (the most proliferative type) demonstrated no recurrences in this study. Recurrent GCTs displayed a transformation of molecular markers to increased proliferative activity and overexpression of p53, fundamentally, by these markers, a different GCT than the primary one. These findings suggest a molecular basis for the lack of histopathologic predictors for recurrence. Factors other than proliferation of the primary GCT (which relates most closely to grading) either extrinsic to the neoplasm (host dependent) or as yet undetectable must determine malignant behavior.

Adolescent↗
PubMed1995

Nephrotoxicity of xenobiotics.

Nephrotoxicity can be grouped by the xenobiotics place of action, by the clinical presentation or by the generic toxic effect. The latter can be dose related, indirect, idiosyncratic or allergic. Nephrotoxicity of lithium, demeclocycline, aminoglycosides, cyclosporine, mercuric ion, nonsteroidal anti-inflammatory drugs, methoxyflurane, ethylene glycol, D-penicillamine and methicillin is reviewed in light of all these three viewpoints, but emphasis is on toxic mechanisms.

Aminoglycosides↗
PubMed1995

Cervical carcinoma with glandular differentiation: histological evaluation predicts disease recurrence in clinical stage I or II patients.

Pathologists confront questions concerning the clinical implications of the more complex, evolving histopathologic classification in cervical carcinoma with glandular differentiation (CCGD) and the associated precursor intraepithelial lesions. Pseudoneoplastic pitfalls, such as microglandular hyperplasia, constitute the subject of recent reports, but the extent of misinterpretation for CCGD is unknown. To address these issues, we retrospectively reviewed all the histopathologic material for 67 patients treated for early clinical stage (I or II) CCGD. Two patients (3%) had pseudoneoplastic glandular lesions (two microglandular hyperplasias). The remaining 65 CCGDs included 35 pure adenocarcinomas (18 mucinous, six serous, five endometrioid, five clear cell, and one adenoid cystic), 26 adenosquamous carcinomas (17 showed > or = 50% and nine showed > 10% but < 50% squamous differentiation-all nonkeratinizing; four were predominantly glassy cell type, and the others showed the following adenocarcinoma component differentiation: 11 mucinous, eight serous, and three endometrioid) and four villoglandular papillary adenocarcinomas (all four were mucinous). In situ carcinoma was identified in 54%. The two patients with pseudoneoplastic lesions were disease free (after 96 and 108 months). Twenty-one patients with CCGD had recurrent disease at 4 to 144 months (mean, 45; median, 18) including three local recurrences, 10 with distant metastasis, and eight with both. Thirty-five patients with CCGD were disease free at 12 to 216 months follow-up (mean, 80.6; median, 65). Adenosquamous (P < .0002, predictive value [PV] = .68) and serous differentiation (P < .05, PV = .61) were the only histological types associated with disease recurrence. Vascular space invasion (P < .0002, PV = .7), deeper invasion (P < .0005), nuclear grade (P = .002, PV = .51), larger tumors on clinical exam (P < .01) or pathological evaluation (P < .01), and presence of pelvic lymph node metastasis at surgery (P < .05, PV = .7) are additional features associated with recurrent disease. A combination of adenosquamous or serous differentiation and vascular space invasion maximized PV for recurrent disease at a level of .75. Mucinous, endometrioid, or clear cell histological types, architectural grade, or the distinction between clinical stages I and II were not associated with recurrent disease. None of the four patients with villoglandular papillary adenocarcinoma exhibited recurrent disease, but confirmation of this histological subtype's prognostic value was hindered by the small number of cases identified (P = .16). Adenosquamous and serous differentiation, nuclear grading, pathological evaluation of vascular space and lymph node involvement, and recognition of pseudoneoplastic glandular lesions helped predict recurrent disease in low clinical stage CCGD in this retrospective study.

Adult↗
PubMed1995

c-erbB-2 oncoprotein overexpression in uterine cervix carcinoma with glandular differentiation. A frequent event but not an independent prognostic marker because it occurs late in the disease.

The c-erbB-2 proto-oncogene (HER-2/neu) codes for a transmembrane, tyrosine kinase, 185 kD oncoprotein (p185erbB2), which is related to the epidermal growth factor receptor. p185erbB2 overexpression occurs in carcinomas at many sites, including the uterine cervix, and predicts poor clinical outcome. The authors hypothesize that p185erbB2 immunohistochemistry will provide additional information in the evaluation of uterine cervix carcinomas with glandular differentiation (CCGD), a difficult and more frequent clinical problem. Paraffin sections from 82 CCGDs including 41 pure adenocarcinomas and 41 adenosquamous carcinomas (7 glassy cell predominant and 34 exhibiting a gland forming component) are immunostained with anti-p185erbB2 (CB11 monoclonal, Novacastra Laboratories, Newcastle upon Tyne, UK). Seventy-seven percent of CCGDs exhibit p185erbB2 immunoreactivity with distinct plasma membrane localization (M) in 50%, the remaining 27% show cytoplasmic staining only. Adjacent benign tissue is negative. The p185erbB2 staining intensity and distribution is as follows: 54.9% strong diffuse (SD, > or = 50% cells positive) with 40.2% M, 17.1% strong focal (SF, < 50% cells positive) with 9.8% M, and 4.9% weak with no M. Immunoreactivity occurs in both squamous and glandular areas of adenosquamous carcinomas. Endometrioid histology is associated with absence of p185erbB2 (P < .01); all other histopathologic features show no association. Follow-up information is available in 77 patients: 37 exhibit recurrent disease (8 pelvic, 15 distant and 14 both) at 1 to 144 months (mean 34, median 16) and 40 were disease free at 12 to 216 months (mean 75, median 64). Strong p185erbB2 immunoreactivity predicts recurrence at 24 months (P < .05) but not overall recurrence at longer follow-up periods. Recurrent disease is associated with nuclear grade (P < .00001); high clinical stage (P < .001); vascular space invasion (P < .001); large size on clinical exam or pathologic evaluation (P < .005); and pelvic lymph node involvement (P < .05). Considering only patients in good prognosis groups, p185erbB2 immunoreactivity does not predict recurrence. Strong p185erbB2 immunoreactivity is associated with stage 3,4 disease (P < .01). p185erbB2 expression is associated with CCGD carcinogenesis but occurs late in the disease, in patients who present at late stage, hindering its prognostic predictive value. p185erbB2 immunolocalization may have a diagnostic role in confirming CCGD in histologically challenging cases, predicting high stage at initial biopsy, and defining therapeutic strategies.

Adenocarcinoma↗
PubMed1995

Immunohistochemical localization of Ad4-binding protein with correlation to steroidogenic enzyme expression in cycling human ovaries and sex cord stromal tumors.

Ad4-binding protein (Ad4BP) has been demonstrated recently as a transcription factor that serves as a general regulator of all steroidogenic P450 genes. We examined the expression of Ad4BP in 32 normal cycling human ovaries and 22 human ovarian sex cord stromal tumors by immunoblotting and immunohistochemistry. Immunoblotting of normal cycling human ovaries revealed a single band of 53 kilodaltons, corresponding to the mol wt of Ad4BP. We also correlated Ad4BP expression with the immunolocalization of the steroidogenic enzymes (side-chain cleavage cytochrome P450, cytochrome P450 17 alpha-hydroxylase, and cytochrome P450 aromatase). Ad4BP immunoreactivity, which was present only in the nuclei, was observed sporadically in the granulosa cells and adjacent stromal cells in the preantral follicles. In the dominant antral follicles, Ad4BP was detected in both granulosa and theca interna cells. However, in the nondominant antral follicles, Ad4BP was observed only in theca interna cells. In the corpus luteum, Ad4BP was present in both luteinized granulosa and thecal cells. Ad4BP was also expressed in some atretic follicles and degenerating corpora lutea. The spatial and temporal localization of Ad4BP in the normal cycling human ovary generally correlated well with that of steroidogenic enzymes. However, expression of the steroidogenic enzymes followed that of Ad4BP during the developing stages of the preantral follicle and vice versa during the process of follicular atresia. In ovarian sex cord stromal tumors, Ad4BP expression was observed in tumor cells that were positive for steroidogenic enzymes, but not in nonsteroidogenic tumor cells. These results, especially the in situ colocalization of Ad4BP and the steroidogenic enzymes, suggest that Ad4BP has the potential to control steroidogenic P450 expression in both normal and pathological human ovaries.

Adult↗
PubMed1995

Angiomatoid features in fibrohistiocytic sarcomas. Immunohistochemical, ultrastructural, and clinical distinction from vascular neoplasms.

The typical example of malignant fibrous histiocytoma (MFH) or dermatofibrosarcoma protruberans (DFSP) does not require ancillary studies for diagnosis. However, hemorrhage with cystic change consisting of blood-filled spaces may closely mimic a vascular neoplasm. Eight fibrohistiocytic sarcomas exhibiting these angiomatoid features, initially mistaken for vascular neoplasms, were identified from personal consultation files and review of 157 consecutive sarcomas (1985 through 1993) at the University of California-(Davis) Medical Center. They included five MFH giant-cell-type sarcomas, two MFH angiomatoid-type sarcomas, and one DFSP. Immunohistochemical analysis of paraffin-embedded material showed vimentin diffuse positive, CD68 (KP-1) diffuse positive, and factor VIII negative in all eight sarcomas; actin HHF-45 focal positive in six, diffuse positive in one, and negative in one sarcoma; desmin focal positive in two and negative in six sarcomas; and S100 protein, cytokeratin AE1:AE3, cytokeratin 10.11, and EMA negative in all eight sarcomas. Electron microscopy of three tumors exhibited neoplastic cells with fibroblastic, myofibroblastic, and histiocytic features. Weibel-Palade bodies or neolumens diagnostic of vascular differentiation were absent. The clinical characteristics and behavior of these sarcomas reflect entities in the spectrum of fibrohistiocytic lineage (MFH subtypes and DFSP) rather than vascular neoplasms. Patients with deep, large, giant-cell-type MFHs did poorly (two of four patients died from disease at 8 and 25 months). Both patients with angiomatoid MFHs showed local recurrences from large incompletely excised head and neck lesions. One died of disease at 21 months and the other is free of disease 12 months following excision of a local metastasis to the opposite side of the neck. The patient with DFSP had an 18-cm locally recurrent scalp tumor that extended into bone. Immunohistochemical and ultrastructural confirmation of fibroblastic, myofibroblastic, and histiocytic lineage and exclusion of vascular differentiation help to establish the correct diagnosis in these fibrohistiocytic sarcomas with angiomatoid features. The clinicopathologic features of these eight cases reaffirm the practical utility of MFH and DFSP as diagnostic entities in the spectrum of fibrohistiocytic sarcomas.

Adult↗
PubMed1995

Squamous differentiation in small-cell carcinoma of the parotid gland.

Small-cell anaplastic carcinomas comprise 1% to 2% of major salivary gland malignant tumors and demonstrate an aggressive clinical course. The initial classification of salivary small-cell anaplastic carcinoma was based on the ultrastructural identification of membrane-bound dense core granules, confirming neuroendocrine differentiation. These neuroendocrine-type small-cell carcinomas were felt to arise from neuroendocrine stem cells that migrated to the salivary gland from the neural crest. Absent neuroendocrine differentiation by ultrastructural evaluation was felt to signify origin from ductal cells. Immunohistochemical study has revised this concept because many small-cell carcinomas express at least one neuroendocrine marker, even in the absence of ultrastructural evidence of neuroendocrine differentiation. In addition, glandular differentiation both by ultrastructural and light microscopic study has been found in cases showing neuroendocrine differentiation. Ultrastructural evidence for squamous differentiation, such as desmosomes and tonofilaments, has also been recognized. These new findings have led to a revision of the old histogenetic hypothesis. All of these small-cell carcinomas are presumed to arise from a hypothetical ductal stem cell that can undergo neuroendocrine, squamous, or glandular differentiation. We report a small-cell anaplastic carcinoma of the left parotid gland in a 61-year-old man with squamous differentiation identified by light microscopy and confirmed by immunohistochemical expression of predominantly high rather than low molecular weight cytokeratins. This tumor is distinctive because it shows an abrupt transition from small-cell anaplastic carcinoma with neuroendocrine differentiation to well-differentiated squamous differentiation, which was identified readily by light microscopy. Our findings support this new hypothesis of a single multipotential stem cell by demonstrating bidirectional neuroendocrine and squamous differentiation.

Carcinoma, Small Cell↗
PubMed1994

Fine-needle aspiration cytology in locally advanced breast adenocarcinoma: a case with complete response to preoperative chemotherapy in association with granulomatous inflammatory reaction.

Preoperative chemotherapy for locally advanced breast carcinoma (stage IIIA,B) is increasingly utilized demonstrating a 70 to 95% objective response and 15 to 35% complete response. A 70-yr-old woman presented with a 9 cm left upper outer quadrant breast mass associated with overlying skin redness and a 2.5 cm left axillary mass. Fine-needle aspiration cytology (FNA) showed a pleomorphic adenocarcinoma in both the breast and axilla. Following three courses of chemotherapy with cyclophosphamide, methotrexate, and 5-fluorouracil (CMF), the patient had a dramatic clinical reduction of tumor, reduction of serum CA 15-3 from 161 to 64 U/ml, and underwent a modified radical mastectomy and axillary dissection. The specimen showed no viable tumor in association with an extensive granulomatous response in both the breast and axillary lymph nodes. This case illustrates two points concerning preoperative chemotherapy for locally advanced breast cancer: (1) The role of FNA v. tissue biopsy is examined. Positive cytology must be conclusive since, as in this case, no viable carcinoma may be present after therapy. (2) Chemotherapy induced host tissue reaction has not been extensively studied. This case showed a remarkable granulomatous reaction in association with tumor elimination. Since this reaction was not present on the original aspiration cytology slides, the chemotherapy treatment must have induced this reaction. Mechanisms for creating this effective host response need further investigation.

Adenocarcinoma↗
PubMed1994

Immunohistochemical phenotype of ovarian granulosa cell tumors: absence of epithelial membrane antigen has diagnostic value.

Granulosa cell tumors (GCTs) represent 1.5% to 3% of primary and 6% to 10% of malignant ovarian neoplasms, and present little diagnostic difficulty in the typical case; however, other primary or metastatic tumors may mimic their various histologic patterns. For this reason, immunohistochemistry can be used to supplement routine histology to help determine a final tissue diagnosis. Previous reports on the utility of antibodies to intermediate filaments vary, as some investigators found keratin to be uniformly negative in GCTs while others reported immunoreactivity for keratin in 20% to 68% of cases. To determine the immunophenotype of granulosa cell tumors and to discover which antibodies are useful in differentiating GCTs from histologic look-alikes, we studied 52 GCTs, including 24 typical cases, 23 cases in which the diffuse pattern predominated, and five juvenile cases, with a panel of commercially available antibodies using an automated immunohistochemistry system. Immunoreactivity for granulosa cells in GCTs was as follows: 17 cases (32.7%) reacted with cytokeratin AE1/AE3, six cases (11.5%) reacted with cytokeratin MAK-6, three cases (5.8%) reacted with cytokeratin CAM 5.2, no case (0%) reacted with epithelial membrane antigen, 52 cases (100%) reacted with vimentin, no case (0%) reacted with desmin, 48 cases (92.3%) reacted with smooth muscle actin, and 26 cases (50%) reacted with S-100 protein. No attempt was made to quantify staining of background thecoma-like or fibroma-like elements in GCTs. Immunoreactivity was independent of the histologic subtype of GCT. Cytokeratin immunoreactivity showed a globoid pattern of staining and was consistent with the expression of 52.5-kD and 45-kD cytokeratins (8 and 18 of Moll's classification). For this reason, the presence of cytokeratin immunoreactivity by itself cannot be used to differentiate a primary or metastatic carcinoma from a GCT. The presence of smooth muscle actin and the absence of epithelial membrane antigen immunoreactivity are additional features that are characteristic of a GCT. S-100 protein immunoreactivity is a finding limited exclusively to GCTs among sex cord stromal tumors, and its presence may have some role in differentiating between Sertoli-stromal cell tumors and GCTs. Since epithelial membrane antigen immunoreactivity is present in many of the histologic look-alikes of GCTs, such as metastatic or primary carcinoma, the absence of staining in GCT has diagnostic value.

Adolescent↗
PubMed1994

Sex steroid biosynthesis enzymes in ovarian sex-cord stromal tumors.

Previous studies on neoplastic and hyperplastic ovarian lesions using paraffin-embedded material have demonstrated immunolocalization of sex steroid biosynthetic enzymes (SSBEs): P-450 side chain cleavage (P-450 SCC), which converts cholesterol to pregnenolone; 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), which converts pregnenolone to progesterone; P-450 17 alpha-hydroxylase and lyase (P-450 17A), which convert progesterone to 17 alpha-hydroxyprogesterone and 4-androstene-3,17-dione; and P-450 aromatase (P-450 AR), which converts 4-androstene-3,17-dione to estradiol. To investigate the utility of immunohistochemical staining for SSBEs, we studied a series of 45 sex cord-stromal tumors of the ovary. P-450 SCC was present in 9 of 11 Sertoli-stromal cell tumors, 3 of 12 granulosa cell tumors, 2 of 7 thecomas, and 1 of 1 stromal luteomas; 3 beta-HSD was present in 5 of 11 Sertoli-stromal cell tumors, 2 of 12 granulosa cell tumors, 2 of 7 thecomas, and 1 of 1 stromal luteoma; P-450 17A was present in 5 of 11 Sertoli-stromal cell tumors, 2 of 12 granulosa cell tumors, 2 of 6 thecomas, and 1 of 1 stromal luteomas; P-450 AR was present in 6 of 11 Sertoli-stromal cell tumors, 2 of 12 granulosa cell tumors, none of 7 thecomas, and 1 of 1 stromal luteoma. SSBEs were not present in 12 fibromas, one sclerosing stromal tumor, and one myxoma. Five of 45 patients with sex cord-stromal tumors showed androgenic effects; 4 of 11 patients with Sertoli-stromal cell tumors and the patient with a stromal luteoma. These five sex cord-stromal tumors contained P-450 SCC, and three of four of the Sertoli-stromal cell tumors contained 3 beta-HSD, P-450 17A, and P-450 AR. Concurrent endometrial histology was available in 25 of 45 sex cord-stromal tumor patients. None of the five sex cord-stromal tumors arising in patients with endometria that showed hyperplasia or adenocarcinoma showed immunoreactivity for SSBEs. Eight patients' endometria were unremarkable, but their sex cord-stromal tumor contained SSBEs. SSBEs were present in areas showing Leydig cell, Sertoli cell, or steroid cell differentiation or luteinized areas; however, the results did not significantly add to the histologic classification of sex-cord stromal tumors. Androgenic hormonal effects could always be explained by synthesis of hormones by SSBEs present in the patient's sex cord-stromal tumor.(ABSTRACT TRUNCATED AT 400 WORDS)

3-Hydroxysteroid Dehydrogenases↗
PubMed1994

Pseudomyxoma peritonei. Histologic predictors of patient survival.

Pseudomyxoma peritonei is uncommon and the histopathologic predictors of patient survival with this disease have not been investigated extensively. The clinicopathologic features of 35 patients with pseudomyxomatous peritoneal implants (implants that produced extracellular mucin) were compared with a control group of 90 consecutive patients with peritoneal implants without extracellular mucin. The histologic patterns of these nonpseudomyxomatous implants were as follows: glandular, 43%; serous, 21%; signet ring, 20%; solid, 13%; and clear cell, 2%. The pseudomyxomatous implants were more likely to have originated from a mucinous epithelial tumor of the appendix (31% vs 1%). Other primary sites produced pseudomyxomatous and nonpseudomyxomatous implants with similar frequency: colon (26% vs 30%), ovary (23% vs 16%), stomach (11% vs 10%), small intestine (3% vs 1%), urinary bladder (3% vs 1%), endometrium (0% vs 10%), prostate gland (0% vs 6%), and unknown (3% vs 15%). Three-year follow-up was available for 29 of 35 and 71 of 90 patients with and without extracellular mucin in their implants, respectively. The patients with pseudomyxomatous implants survived longer (24% vs 4% survival at 3 years). Three-year follow-up was available for 90 of 110 and 10 of 15 patients with and without invasion in the primary tumor or its peritoneal implants, respectively. The patients without invasive tumors survived longer (80% vs 4% survival at 3 years). Invasion in the primary tumor or its implants, present in 21 of 35 pseudomyxomatous implants, eliminated any improved survival associated with the presence of extracellular mucin. Prolonged survival in pseudomyxoma peritonei was associated with the histologic findings of noninvasive implants arising from mucinous epithelial tumors of low malignant potential histology. In our study, such tumors originated in the appendix (eight cases [23%]) and ovary (five cases [14%]) among the total number of 35 patients.

Adult↗
PubMed1994

p53 gene mutation in female genital tract carcinosarcomas (malignant mixed müllerian tumors): a clinicopathologic study of 74 cases.

Mutations of the p53 suppressor gene are involved in carcinogenesis by inactivating p53 protein (p53P), which is involved in normal cell growth control. Mutant p53P, detectable by immunohistochemistry due to longer half-life as compared to wild-type, is a marker for p53 gene mutation. Seventy-four female genital tract carcinosarcomas (FGTCSs) (41 of the heterologous type exhibiting 33 rhabdomyosarcomatous, 13 chondrosarcomatous, one osteosarcomatous, and one liposarcomatous component) were stained using two commercially available monoclonal antibodies: p53P, clone DO7 (p53P-DO7) and p53P, Ab-6 (p53P-P6). p53P-DO7 and p53P-P6 stained 33 and 36, respectively, of 56 endometrial, 8 of 11 ovarian, 2 of 5 cervical, and 2 of 2 fallopian tube carcinosarcomas. Considering all 74 FGTCSs, p53P-DO7 and p53P-P6 stained both the carcinomatous component (CC) and the sarcomatous component (SC) in 46% and 54%, the CC only in 9.5% and 8.1%, and the SC only in 5.4 and 2.7%, respectively. The two antibodies for p53P showed the following concordance for staining of FGTCSs (either CC or SC or both) (p53P-DO7/p53P-P6): +/+, 58%; +/-, 1.3%; -/+, 6.7%; -/-, 34%. p53P immunoreactivity was not associated with histological features or grade of the CC or SC. Clinical follow-up was available in 72 cases, which showed 48.5% and 70.8% of patients recurred or died of disease by 12 and 80 months, respectively. 20.8% of patients were disease-free after 19 to 307 months of follow-up (median, 62; mean, 92). The remaining 8.4% of patients were disease-free but had insufficient follow-up (< 1 year).(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗