[Post operative Caldwell-Luc procedure maxillary cyst: Report of a case]. / Syndrome post Caldwell Luc: à propos d'un cas.

Rare complication of radical surgery (Caldwell Luc procedure) of the maxillary sinus, maxillary cyst can occurred several years after. We describe the case of a patient 56 years old, who came to our consultationfor repeated pain in the right maxillary region with moderate facial asymmetry. In her history we noted a previous sinus surgery (Caldwell Luc) more than 10 years before. The imaging showed an expansive process filled with proteinic tissue of the posterior wall of the maxillary. With the history of the former surgery, we suspected the existence of a mucocele. She underwent an endonasal surgery and the pathological examination of the specimen revealed an intra osseous cyst lined with ciliated respiratory type mucosa post surgery of the maxillary sinus. The diagnosis of a maxillary cyst complicating a Caldwell Luc was established based on the results obtained with the clinico-radiological and pathological results.

Activation of the EGFR/ERK pathway in high-grade mucoepidermoid carcinomas of the salivary glands.

BACKGROUND: Mucoepidermoid carcinoma (MEC) shows differences in biological behaviour depending mainly on its histological grade. High-grade tumours usually have an aggressive biological course and they require additional oncological treatment after surgery. METHODS: In a series of 43 MECs of the salivary glands, we studied the epidermal growth factor receptor (EGFR) gene by using dual-colour chromogenic in situ hybridisation (CISH). Moreover, we assessed the protein expressions of the EGFR and the activated extracellular signal-regulated kinases (pERK1/2) by using immunohistochemistry. These results were correlated with the histological grade of the tumours and the outcome of the patients. RESULTS: The CISH study demonstrated a high-EGFR gene copy number, with balanced chromosome 7 polysomy, in 8 out of 11 high-grade MECs (72.7%), whereas 27 low-grade and 15 intermediate-grade tumours had a normal EGFR gene copy number (P<0.001). The EGFR gene gains correlated with disease-free interval (P=0.003) and overall survival of the patients (P=0.019). The EGFR protein expression had a significant correlation with the histological grade of the tumours but not with the outcome of the patients. The pERK1/2 expression correlated with histological grade of tumours (P<0.001), disease-free interval (P=0.004) and overall survival (P=0.001). CONCLUSIONS: The EGFR/ERK pathway is activated in high-grade MECs with aggressive behaviour. Patients with these tumours who require oncological treatment in addition to surgery could benefit from EGFR and mitogen-activated protein kinase pathway inhibitors.

Laryngeal squamous cell carcinoma in HIV-positive patients: lack of association with human papillomavirus infection.

OBJECTIVES: Neoplasms associated with human papillomavirus (HPV) infection occur at increased frequency in patients with HIV infection/AIDS. Although laryngeal squamous cell carcinomas (LSCCs) in HIV-positive patients are uncommon, a higher incidence of this malignancy in HIV-positive patients than in the general population has been reported. As a proportion of LSCCs are associated with HPV in the general population, the clinicopathological features of a series of LSCCs developing in HIV-positive patients were evaluated to investigate the possible relationship with HPV infection, and infection with other oncogenic viruses. METHODS: All HIV-positive patients with LSCC diagnosed at a single institution from 1998 to 2007 were retrospectively evaluated. The clinicopathological features were analysed and tissues were tested by polymerase chain reaction (PCR), using the short PCR fragment 10 (SPF10) primer, a highly sensitive method for HPV DNA detection. Immunohistochemical studies for HIV p24, p16(INK4a) and p53 were performed. Epstein-Barr virus (EBV) and human herpes virus 8 (HHV-8) were also investigated. RESULTS: Six out of 4987 HIV-infected patients seen in this period in the Infectious Diseases Department developed LSCC (median age 41.5 years; male to female ratio 1:1). All patients were heavy smokers and the tumours presented at an advanced clinical stage. HPV was not detected in any tumour, not even in two patients with coexisting HPV-associated gynaecological neoplasm. Staining for HIV p24 and p16(INK4a) was negative, whereas p53 was positive in half the cases. EBV and HHV-8 were also negative. CONCLUSION: LSCC developing in HIV-positive patients is an infrequent neoplasm, not usually associated with HPV infection. It develops in young, heavy smokers and presents at an advanced clinical stage.

Metastasis to the nasal cavity from primary rectal adenocarcinoma.

We describe a rare case of metastasis to the pa ra - na sal sinuses. The lesion had an immunohistochemical (positivity for cytokeratin 20, negativity for cytokeratin 7, overexpression of p53) and in situ hybridisation profile (neither lesions showed deletion for p53) consistent with metastasis from the earlier rectal adenocarcinoma. The correct typification of intestinal-type neoplasms requires a combination of morphological, immunohistochemical and, sometimes, molecular analysis.

How phenotype guides management of the neuroendocrine carcinomas of the larynx.

OBJECTIVE: This review aimed to critically analyse data pertaining to the clinical presentation and treatment of neuroendocrine carcinomas of the larynx. METHOD: A PubMed search was performed using the term 'neuroendocrine carcinoma'. English-language articles on neuroendocrine carcinoma of the larynx were reviewed in detail.Results and conclusionWhile many historical classifications have been proposed, in contemporary practice these tumours are sub-classified into four subtypes: carcinoid, atypical carcinoid, small cell neuroendocrine carcinoma and large cell neuroendocrine carcinoma. These tumours exhibit a wide range of biological behaviour, ranging from the extremely aggressive nature of small and large cell neuroendocrine carcinomas, which usually have a fatal prognosis, to the less aggressive course of carcinoid tumours. In small and large cell neuroendocrine carcinomas, a combination of irradiation and chemotherapy is indicated, while carcinoid and atypical carcinoid tumour management entails conservation surgery.

Role of ancillary techniques in profiling unclassified laryngeal malignancies.

Laryngeal biopsies, contrary to biopsies from many other sites of the body, very often contain minute amounts of tumour tissue that may consist of morphologically undifferentiated tumour only. In haematoxylin- and eosin-stained sections, there may be no indicative features of what specific tumour entity that is present. In the larynx, particularly small round cell neoplasms, primary or metastatic, often cause a diagnostic dilemma and where an incorrect diagnosis can induce substantial clinical consequences for the patient (e.g., primary neuroendocrine carcinomas vs metastatic variants, certain sarcomas). If sufficient/representative material has been obtained, the application of immunohistochemistry and/or molecular techniques should in virtually every case reveal the true nature of the malignancy. In cases with sparse amount of material, and therefore a limited number of sections to be cut, a careful and thoughtful stepwise approach is necessary to ascertain a reliable diagnosis, or at least guide the clinician to the most likely diagnoses. With today's advanced and widely available technology with an abundance of markers to discriminate different tumours, the use of the term "undifferentiated" should be largely unnecessary. In the exceptional, and indeed exceedingly rare cases, when a classification is not possible, even after repeat biopsy, we suggest that the laryngeal neoplasm is better termed "unclassified malignant neoplasm" rather than "undifferentiated malignant neoplasm".

Induction of mouse lung adenomas by amines or ureas plus nitrite and by N-nitroso compounds: effect of ascorbate, gallic acid, thiocyanate, and caffeine.

Lung adenomas were induced in strain A mice by chronic treatment with N-nitroso compounds (given in drinking water) and with amines or ureas in food plus NaNO2 in drinking water. We studied the effects of varying the concentrations of three N-nitroso compounds and NaNO2 concentration in the morpholine plus NaNO2 and methylurea plus NaNO2 systems. Sodium ascorbate (NaASC) at the highest level tested (11.5 or 23 g/kg food) gave 89-98% inhibition of adenoma induction by the NaNO2 plus piperazine, morpholine, and methylurea systems. In 7 groups, NaASC produced increases of 15-59% in adenoma induction by nitrosomorpholine (NM) and mononitrosopiperazine (MNP), possibly because the mice consumed more of the nitrosamine solution. Adenoma induction by morpholine plus NaNO2 was strongly inhibited by gallic acid, moderately inhibited by caffeine, and unaffected by thiocyanate (all added to the food). Gallic acid inhibited or had no effect on the action of NM and MNP. We discussed the proposal that NaASC (or perhaps gallic acid) be administered with readily nitrosatable drugs.

Spontaneous tumors and common diseases in two colonies of Syrian hamsters. II. Respiratory tract and digestive system.

Spontaneous respiratory tract neoplasms in Syrian hamsters occurred in almost equal frequencies in two colonies: 3% in the Eppley Colony (EC) and 3.6% in the Hannover Colony (HC). Neoplasms were in the nasal cavity, trachea, and lungs, and most were benign; however, 2 adenocarcinomas of the nasal cavity (EC) and 1 adenocarcinoma of the larynx (HC) were found. The incidence of digestive tract tumors showed a more marked difference than that of the respiratory tract: 7% in the EC and 23% in the HC. Digestive tract tumors accounted for 15 and 41% of all tumors in the EC and HC, respectively. All EC digestive tract neoplasms were benign and occurred mostly in males; 19 (83%) were forestomach papillomas and the remaining 4 )17%) were liver hemangioendotheliomas (2) and pancreatic duct adenomas (2). In the HC, almost 50% of the digestive tract neoplasms were malignant and most frequent in females. These tumours include 19(42%) intestinal adenocarcinomas, 18(40%) liver neoplasms (hemangioendotheliomas, cholangiomas, cholangiocarcinomas), 5 (13%) forestomach papillomas, and 2 (4%) gallbladder polyps. The morphology of these neoplasms was reported.

Spontaneous tumors and common diseases in two colonies of Syrian hamsters. I. Incidence and sites.

Syrian hamsters from two colonies [Eppley colony (EC); Hannover colony (HC)] were examined for spontaneous neoplastic and noneoplastic diseases. Significant differences were found in tumor incidence (30%, EC' 42%, HC), occurrence of malignant neoplasms (15%, EC; 32%, HC), appearance of multiple primary tumors in different organs (42%, EC; 30%, HC), average survival rates of tumor-bearing animals, organ distribution and histologic types, and average survival rates of all animals. The frequencies of nonneoplastic diseases also varied between the two colonies. The findings indicated a need for precise histologic evaluation to generate information for comparative purposes regarding the use of hamsters in experimental pathology and carcinogenesis studies.

Spontaneous tumors and common diseases in two colonies of Syrian hamsters. III. Urogenital system and endocrine glands.

The frequency of spontaneously occuring neoplasms in the urogenital system and endocrine organs was examined in two Syrian hamster colonies [Eppley colony (EC); Hannover colony (HC)]. With the exception of a renal adenoma in an EC female, the urinary systems of animals in both colonies were free of neoplastic growths. A single epididymal adenoma of the male fenital system (EC) was found. However, incidences of female genital tract tumors were 10 (EC) and 3.5% (HC) and accounted for 34 and 11%, respectively, of all tumors in females. Among all genital tract tumors, 3 (EC) and 57% (HC) were ovarian, 14% (HC) were in the fallopian tubes, 81 (EC) AND 29% (HC) were uterine, and 16% (EC), vaginal. The overall incidence of endocrine organ tumors was similar in both colonies (EC, 22%; HC, 19%). The distribution of these tumors was as follows: pituitary gland; EC, 3%, HC, 0; thyroid gland: EC, 28%, HC, 31%; parathyroid gland: EC,11%, HC, 18%; adrenal cortex: EC, 42%, HC, 31%; adrenal medulla: EC, 7%, HC, 0; and endocrine pancreas: EC, 10%, HC, 31%. The morphology of these neoplasms is described and the incidence compared with those reported in other colonies.

Spontaneous tumors and common diseases in two colonies of Syrian hamsters. IV. Vascular and lymphatic systems and lesions of other sites.

Spontaneous tumors were found in the vascular and lymphatic systems upon systemic histologic examination of the cardiovascular, hematopoietic, and lymphatic tissues of Syrian hamsters from the Eppley (EC) and Hannover colonies (HC). The incidence of endothelial tumors (hemangioendotheliomas) was similar in both colonies and sexes. The hemangioendotheliomas generally originated in the liver and spleen. Malignant lymphomas developed in high incidences in both colonies; however, their morphology varied. Those in EC hamsters were of histiocytic and, to a lesser extent, plasmacytic types; in the HC lymphocytic and epithelioid cell types were also found. Among tumors of miscellaneous sites, Harderian gland adenomas occurred in almost equal frequencies in EC and HC hamsters, but predominated in males. Tumors of the bone and soft tissue were present only in EC hamsters, whereas skin neoplasms developed solely in HC hamsters.

Effect of beta-oxidized nitrosamines on syrian hamsters. III. 2,2'-Dihydroxydi-n-propylnitrosamine.

2, 2-Dihydroxy-di-n-propylnitrosamine (DHPN), an assumed metabolite of di-n-propylnitrosamine (DPN), injected subcutaneously once weekly for life, was carcinogenic in Syrian hamsters. The main target organs were the respiratory tract, pancreas, liver, and kidneys. In the respiratory system the most affected segments were the nasal cavities and the lungs. Adenomas and adenocarcinomas, mostly of ductal origin, were induced in the pancreas. Liver neoplasms were hemangloendotheliomas, angiosarcomas, hepatocellular adenomas, cholangiomas, and cholangiocarcinomas. Kidney neoplasms were adenomas and adenocarcinomas. The morphology of the induced neoplasms was described, as well as the effects of DHPN, compared to those another possible metabolite of DPN, 2-hydroxypropyl-n-propylnitrosamine (2-HPPN), which is formed in vivo with only 1 aliphatic chain degraded via theta-oxidation.

A new approach for induction of pancreatic neoplasms.

Weekly s.c. injections of equitoxic doses of 2-hydroxy-propyl-n-propylnitrosamine, 2-oxopropyl-n-propylnitrosamine, and methyl-n-propylnitrosamine, assumed metabolites of di-n-propylnitrosamine by beta oxidation, induced low incidences of pancreatic duct adenomas in Syrian golden hamsters. Di-n-propylnitrosamine did not. Application of 2,2'-dihydroxydi-n-propylnitrosamine, another postulated intermediate of di-n-propylnitrosamine, led to development of various types of pancreatic duct adenomas and ductal carcinomas in high percentages of hamsters. In addition, a few acinar-cell carcinomas were found. The morphology of these neoplasms, their latencies, and their distribution in the different segments of the pancreas are described.

Influence of esophagojejunostomy on the induction of adenocarcinoma of the distal esophagus in Sprague-Dawley rats by subcutaneous injection of 2,6-dimethylnitrosomorpholine.

To study the influence of reflux esophagitis on the carcinogenic response of 2,6-dimethylnitrosomorpholine (2,6-DMNM), an experiment was designed, composed of 6 groups of 8-week-old Sprague-Dawley rats, each consisting of 20 males and 20 females. Group 1 served as untreated controls. All animals of groups 2, 4, and 6 underwent an esophagojejunostomy with gastric preservation to produce a chronic reflux esophagitis. 2,6-DMNM was injected s.c. once weekly for life at doses of 1/100 and 1/10 of the 50% lethal dose to groups 3 and 4 and groups 5 and 6, respectively. Carcinogen exposure began in groups 4 and 6 15 days after the esophagojejunostomy. Squamous cell carcinomas were observed in the esophagus of 36 animals, mainly in those receiving the higher dose. Exophytic squamous cell carcinomas, a variety rarely seen in humans, were mostly seen in the groups receiving 2,6-DMNM alone, whereas endophytic squamous cell carcinomas, the variety most frequently seen in humans, mainly developed in the groups receiving the combined treatment. In addition adenocarcinomas with abundant mucin production were found in the distal esophagus of 23 animals. They were found exclusively in animals of groups 4 and 6 which underwent esophagojejunostomy plus 2,6-DMNM exposure. No adenocarcinomas were encountered in groups without experimental reflux esophagitis. These findings may contribute to further understanding of the association between reflux esophagitis and the various histological types of esophageal carcinoma in humans.

PRAD-1/cyclin D1 gene amplification correlates with messenger RNA overexpression and tumor progression in human laryngeal carcinomas.

PRAD-1 is a putative oncogene localized on chromosome 11q13 which encodes cyclin D1, a novel cyclin involved in cell cycle regulation. Amplification of this gene has recently been reported in several human tumors including breast and head and neck carcinomas. In this study we have analyzed the presence of PRAD-1/cyclin D1 gene amplification and mRNA overexpression in a series of 46 matched normal mucosas and squamous cell carcinomas of the larynx. PRAD-1/cyclin D1 was found to be amplified 2- to 12-fold in 17 carcinomas (37%). DNA amplification correlated with advanced local invasion (P = 0.0015), presence of lymph node metastases (P = 0.0078), and stage IV of the tumors (P = 0.0021). mRNA overexpression was found in 15 of the 43 (35%) cases examined and it was also significantly associated with advanced local invasion (P = 0.0025) and stage IV carcinomas (P = 0.0032). A significant association was observed between gene amplification and mRNA overexpression (P < 0.0001) with only 3 discordant cases (2 amplifications with no overexpression and 1 overexpressed carcinoma with no gene amplification). Furthermore, the degree of DNA amplification correlated with the levels of mRNA expression (r = 0.6; P = 0.024). These findings suggest that the PRAD-1/cyclin D1 gene may be an important target of 11q13 amplifications in laryngeal carcinomas and the activation of this gene may be involved in the progression of these tumors. Its association with advanced-stage tumors indicates that PRAD-1/cyclin D1 gene amplification and overexpression may be of prognostic significance.

Loss of heterozygosity of p53 gene and p53 protein expression in human colorectal carcinomas.

The p53 gene is a tumor suppressor gene located on chromosome 17p. Deletions of this chromosome and point mutations of p53 have been implicated in the development of colonic neoplasms. We have analyzed the loss of heterozygosity of the human p53 tumor suppressor gene in 40 cases of colorectal carcinoma using two restriction fragment length polymorphisms detected by BglII and AccII restriction enzymes. p53 gene product expression was studied immunohistochemically in 64 colorectal carcinomas, 18 adenomas, and 40 normal colonic mucosae using an anti-human p53 monoclonal antibody (Pab 1801) and the avidin-biotin-peroxidase complex technique. Twelve of the 40 patients (30%) were polymorphic for the p53 gene. In ten of these informative patients (83%), the tumor samples showed the loss of one allele when compared with normal colorectal samples of the same patient. One of the homozygous patients showed a loss of both p53 alleles. p53 immunostaining was observed in 43 of 64 carcinomas (67%) but only in two adenomas (11%). These two positive adenomas showed areas of carcinoma in situ. The normal mucosa was always negative. No relation could be found between p53 immunostaining and the degree of differentiation, the extension of the tumor, or the Ki-67 proliferative index. Mucinous carcinomas and right-side carcinomas were less p53 immunoreactive (25% and 52%, respectively) than the usual adenocarcinomas (73%) and distal tumors (72%). These findings suggest that p53 may be a target of chromosome 17 deletions and that this gene may play a role in the malignant transformation of adenomas. BglII and AccII restriction fragment length polymorphism analysis of the p53 gene may be a useful and direct technique to detect allelic loss of this gene in tumors.

cdc25 cell cycle-activating phosphatases and c-myc expression in human non-Hodgkin's lymphomas.

cdc25A, cdc25B, and cdc25C are a family of human phosphatases that activate the cyclin-dependent kinases at different points of the cell cycle. cdc25A and cdc25B have been shown to have oncogenic potential, and they have been identified as transcriptional targets of c-myc. To determine the role of cdc25 genes in the pathogenesis of human lymphomas and their possible correlation with c-myc deregulation, we have analyzed the expression of cdc25A, cdc25B, and cdc25C and c-myc genes in a series of 63 non-Hodgkin's lymphomas and 8 nonneoplastic lymphoid tissues. The mRNA levels of the three phosphatases in the nonneoplastic tissues were negative or negligible. cdc25B overexpression was detected in 35 tumors (56%). This overexpression was more frequently found in aggressive (81%) than in indolent lymphomas (36%; P < 0.01). cdc25B overexpression was also significantly associated with a higher proliferative activity of the tumors. No cdc25B gene amplification or rearrangements were detected by Southern blot analysis. A biallelic EcoRI polymorphism of cdc25B gene was identified with a similar distribution in patients with lymphoma and in a normal population. cdc25A was overexpressed in three aggressive lymphomas. No detectable cdc25C mRNA levels were seen in any of the tumors. c-myc was overexpressed in 43% of tumors, and it correlated significantly with the presence of cdc25B up-regulation. Twenty-six of 35 (74%) lymphomas with high levels of cdc25B mRNA also showed c-myc overexpression, whereas 27 of 28 (96%) tumors without detectable or with very low cdc25B expression also had undetectable c-myc levels (P < 0.0001). In addition, a significant linear correlation was found between the cdc25B and c-myc mRNA levels (r = 0.575, P < 0.001). These findings suggest that cdc25B overexpression in non-Hodkin's lymphoma may participate in the pathogenesis of aggressive variants, and it may cooperate with c-myc oncogene in the development of these tumors.

p16MTS1/CDK4I mutations and concomitant loss of heterozygosity at 9p21-23 are frequent events in squamous cell carcinoma of the larynx.

We have examined the presence of p16MTS1/CDK4I gene deletions, mutations and methylation status, and 9p21-23 deletions in a series of 46 squamous cell carcinomas of the larynx and paired normal mucosa previously characterized for cyclin D1 gene amplification and overexpression. pRb expression was also examined by immunohistochemistry. p16MTS1/CDK4I mutations were found in 10/46 (22%) carcinomas and hypermethylation in 2/31 (7%). Loss of heterozygosity at 9p21-23 was found in 24 out of 42 (57%) carcinomas examined. All p16MTS1/CDK4I mutated cases and the two hypermethylated carcinomas showed 9p21-23 loss of heterozygosity. The loss of heterozygosity correlated with advanced local invasion (P=0.0045), lymph node metastases (P=0.0326), stage IV of the tumors (P=0.0058), and existence of cyclin D1 amplification/overexpression (P < 0.03). Only one out of 37 carcinomas was negative for pRb expression. No alterations in p16 gene or 9p21-23 loss of heterozygosity were detected in this case. These findings indicate that p16MTS1/CDK4I is frequently inactivated by gene mutation, hypermethylation, and allelic deletions in a significant subset of squamous cell carcinomas of larynx. Since 9p21-23 loss of heterozygosity was more frequently detected than p16MTS1/CDK4I mutations, and mutated carcinomas invariably had loss of heterozygosity, allelic losses probably precede the p16MTS1/CDK4I mutations. Their association with cyclin D1 deregulation in advanced carcinomas could indicate a possible cooperative effect in the progression of these neoplasms.

Intraabdominal desmoplastic small round cell tumor with EWS/ERG fusion transcript.

This report describes an intraabdominal small cell tumor in a 37-year-old woman, with clinical, topographic, and morphologic features highly suggestive of the desmoplastic small round cell tumor. Immunohistochemical analysis revealed a polyphenotypic profile consistent with this tumor--positivity for keratin, epithelial membrane antigen, neuron-specific enolase, vimentin, and desmin--but, in addition, a strong membranous immunoreactivity for CD99 (MIC2 protein). Reverse transcription polymerase chain reaction revealed a EWS/ERG fusion transcript characteristic of the Ewing's sarcoma/peripheral primitive neuroectodermal tumor group of tumors, rather than the EWS/WT1 chimeric transcript typical of the desmoplastic small round cell tumor. This is the third report of a hybrid tumor with features of the desmoplastic small round cell tumor and Ewing's sarcoma/peripheral primitive neuroectodermal tumor, and the first one with the EWS/ERG fusion gene. Our case shows the existence of some overlap between these two groups of tumors, which are considered to be histogenetically different, and the need for further studies of molecular characterization of small cell tumors, especially in those with atypical morphologic or immunohistochemical features.

Mesonephric adenocarcinoma of the uterine corpus: CD10 expression as evidence of mesonephric differentiation.

Mesonephric (wolffian) neoplasms of the female genital tract are infrequent and found in sites where embryonic remnants of wolffian origin are usually detected, such as the uterine cervix, broad ligament, mesosalpinx, and ovary. Their diagnosis is difficult because of the absence of specific immunohistochemical markers for mesonephric derivatives. We present the first report of adenocarcinoma of mesonephric type arising as a purely myometrial mass without endometrial or cervical involvement in the uterine corpus of a 33-year-old woman. The tumor showed a combination of patterns, with retiform areas, ductal foci, and small tubules with eosinophilic secretion, which merged with solid sheets of cells with a sarcomatoid appearance. Immunohistochemically, neoplastic cells were diffusely positive for cytokeratin 7, epithelial membrane antigen, and CD15 and focally positive for BerEP4 and vimentin. A hitherto unreported feature was the positivity for CD10 in neoplastic cells, which was also present in a large number of control tissues obtained from male mesonephric derivatives and female mesonephric remnants and tumors. Furthermore, CD10 was negative in controls from müllerian epithelia of the female genital tract and in their corresponding tumors. Therefore, the expression of CD10 by mesonephric remnants may be useful in establishing the diagnosis of tumors with mesonephric differentiation.