Unusual Clinical Presentation of Gastrointestinal Clear Cell Sarcoma.

Background: Use of molecular assays is gradually becoming a mandatory part of the clinical management of soft tissue tumors, however the choice and the interpretation of these tests may present a challenge.

Summary: This report demonstrates an unusual presentation of sarcoma, which was initially diagnosed as a tumor of unknown primary site. Given the presence of vimentin, Fli-1, CD99 and S100 markers, lack of immunostaining for melan A, HMB45, MITF, synaptophysin, CD56, myf4, CKAE1/3 and WT-1, as well as the presence of EWSR1 translocation determined by a break-apart FISH assay, Ewing's sarcoma (ES) diagnosis seemed to be well justified.

Novel ALK fusion partners in lung cancer.

Detection of ALK rearrangements in patients with non-small cell lung cancer (NSCLC) presents a significant technical challenge due to the existence of multiple translocation partners and break-points. To improve the performance of PCR-based tests, we utilized the combination of 2 assays, i.e.

Invasion and genome reproduction of the trophoblast cells of placenta junctional zone in the field vole, Microtus rossiaemeridionalis.

In the field vole Microtus rossiaemeridionalis, like in other rodents, invasive secondary giant trophoblast cells (SGTC) form a continuous layer at the foeto-maternal interface in the beginning of placentation. However, in the field vole, at midgestation, clusters of junctional zone (JZ) trophoblast non-giant cells interrupt SGTC layer and progressively replace SGTC at the border of decidua basalis. As a result, 'border' cells form a continuous stratum of cytokeratin-positive glycogen-rich cells at the foeto-maternal interface.

Aromatase, CYP1B1 and fatty acid synthase expression in breast tumors of BRCA1 mutation carriers.

Numerous experimental evidence suggest that BRCA1-associated breast carcinomas may have distinct endocrine and metabolic features, however these peculiarities are poorly evaluated in clinical settings. Here we comparatively analyzed for the first time aromatase, estrogen 4-hydroxylase (CYP1B1) and fatty acid synthase immunohistochemical expression in breast tumors obtained from 12 BRCA1 mutations carriers and 22 non-carriers. Aromatase expression was higher in mutation carriers than in sporadic cases (p = 0.

Signs of proinflammatory/genotoxic switch (adipogenotoxicosis) in mammary fat of breast cancer patients: role of menopausal status, estrogens and hyperglycemia.

The abundance of fat tissue surrounding normal and malignant epithelial mammary cells raises the questions whether such "adipose milieu" is important in the local proinflammatory/genotoxic shift, which apparently promotes tumor development and worsens prognosis, and what conditions stimulate this shift, or "adipogenotoxicosis." We studied 95 mammary fat samples from 70 postmenopausal and 25 premenopausal breast cancer (BC) patients at a distance of 1.5-2.

Distinct prevalence of the CYP19 Delta3(TTTA)(7) allele in premenopausal versus postmenopausal breast cancer patients, but not in control individuals.

The CYP19 gene encodes the enzyme aromatase, which plays a key role in the conversion of androgens to oestrogens. A polymorphism in CYP19 in intron 4 (TTTA)n has been reported to be associated with breast cancer (BC) risk, although conflicting evidence has also been published. Here, we employ a non-traditional, highly demonstrative design of a molecular epidemiological study, where the comparison of BC cases and healthy middle-aged female donors was supplemented by an analysis of groups with extreme characteristics of either BC risk (bilateral breast cancer (biBC) patients) or cancer tolerance (tumour-free elderly women aged >or=75 years).

Concordance of allelic imbalance profiles in synchronous and metachronous bilateral breast carcinomas.

Bilateral breast cancer (biBC) is a common form of breast cancer; however, it has not been subjected to systematic comparative genetic studies. We allelotyped 28 biBCs on 14 chromosomal arms, addressing 2 lines of questions: (i) does comparison of genetic profiles disclose contralateral metastases misdiagnosed as second primaries? and (ii) do shared environmental and host factors drive the development of true biBC along similar genetic routes? Allelotyping provided unambiguous proof for distinct clonality in 23 of 28 cases. In another 4 biBCs, the genotyping data did not exclude the hypothesis of metastatic spread, whereas clinical and histologic data were in favor of bilaterality.

Tissue transglutaminase expression in breast carcinomas.

Tissue transglutaminase (tTG) is known to participate in multiple cellular processes, including apoptosis, cellular adhesiveness etc. Alterations of tTG expression could contribute to the development of several categories of diseases, including AIDS, cancer etc. The aim of the study was to test the pattern and relevance of tTG expression in a subset of breast carcinomas.

Evidence for microsatellite instability in bilateral breast carcinomas.

The molecular pathogenesis of various categories of breast cancer (BC) has been well described, but surprisingly few reports have appeared on analysis of somatic mutations in bilateral BC. We have performed a polymerase chain reaction (PCR)-driven investigation of chromosomal regions showing common loss of heterozygosity (LOH) in 23 cases (46 tumors) from patients diagnosed with bilateral BC. LOH was observed in 15/46 (33%) informative tumors for chromosome 1p, 5/32 (16%) for 5q, 12/44 (27%) for 11q, 15/40 (38%) for 13q and 4/24 (17%) for 17p.

High benzo[a]pyrene diol-epoxide DNA adduct levels in lung and blood cells from individuals with combined CYP1A1 MspI/Msp-GSTM1*0/*0 genotypes.

Levels of anti-benzo[a]pyrene diol-epoxide DNA adducts were analysed by high-pressure liquid chromatography/fluorimetric detection in non-tumorous lung tissues from 20 lung cancer patients and in white blood cells from 20 polycyclic aromatic hydrocarbon exposed coke oven workers. All were current tobacco smokers. CYP1A1 mutations (MspI at 6235 nt, Ile-Val462) and GSTM1 deletion polymorphisms in each individual were analysed in genomic DNA by PCR/restriction fragment length polymorphism.

Wild type neu transgene counteracts mutant homologue in malignant transformation of rat Schwann cells.

Mutational activation of the neu (erbB-2) receptor protein tyrosine kinase gene appears to be the triggering event in the process of oncogenesis induced by N-ethyl-N-nitrosourea (EtNU) in immature Schwann cells of the rat peripheral nervous system. Subsequent loss of the wild-type neu allele may represent a critical secondary step towards malignancy. Developmentally-regulated expression of a wild-type rat neu transgene (neu cDNA under the control of the rat Po promoter) in the Schwann cells of transgenic BDIX and Sprague-Dawley rats exposed to EtNU on postnatal day 1 results in a lower incidence of early atypical proliferates in the trigeminal nerve.

Aromatase in breast cancer tissue--localization and relationship with reproductive status of patients.

The precise place of local estrogen production in mammary cancer is still controversial. In this investigation localization of aromatase (the key enzyme of estrogen biosynthesis) was studied in breast cancer tissue by immunohistochemical method using polyclonal rabbit antibodies. The cytoplasmic staining was found in different cell types, but the most intensive specific staining was found in malignant cells and it was stronger (P < 0.

Development of malignant fibrous histiocytoma induced by 7,12-dimethylbenz[a]anthracene in the rat: characterization of early atypical cells.

Morphologically atypical cells were first detected in the adjacent connective tissue 98 days after implanting a paraffin pill containing 2 mg of 7,12-dimethylbenz[a]anthracene (DMBA) into the subcutaneous tissues of rats. These cells subsequently formed groups and finally produced gross malignant fibrous histiocytomas (MFH). Early atypical cells were located between proliferating fibroblasts and histiocytes in the center of a fibrous capsule surrounding the DMBA pill.

Effect of metabolic inhibitors, methylxanthines, antioxidants, alkali metals, and corn oil on 1,2-dimethylhydrazine carcinogenicity in rats.

The effect of the oral administration of 10 compounds on 1,2-dimethylhydrazine (DMH) carcinogenesis was investigated in 180 male Wistar rats and 510 male BD6 rats. DMH, administered s.c.

Rat model of the human "Triton" tumor: direct genetic evidence for the myogenic differentiation capacity of schwannoma cells using the mutant neu gene as a cell lineage marker.

Spontaneous myogenic differentiation was observed in 2 out of 15 cases when cells from schwannomas induced in the offspring of BDIX rats by transplacental exposure to N-ethyl-N-nitrosourea (EtNU) were grown in monolayer culture following fluorescence-activated cell sorting with monoclonal antibody (Mab) 217c. Myotubes and numerous mononucleated cells no longer expressed the Schwann cell antigens 217c and S-100 protein, but rather revealed the presence of desmin, the alpha-sarcomeric form (alpha-sr) of actin, and the cell surface antigen specified by Mab RB21-7, a 250 kD glycoprotein sharing an epitope with the neural cell adhesion molecule (N-CAM). Subcutaneous reimplantation of such cells into syngeneic animals led to the appearance of tumors composed of both S-100 positive Schwann cells and desmin and alpha-sr-actin positive rhabdomyoblasts, thus closely resembling the human "Triton" tumor.

Effect of exogenous beta-glucuronidase on the carcinogenicity of 1,2-dimethylhydrazine in rats: evidence that carcinogenic intermediates form conjugates and act through their subsequent enzymatic release.

Albino, outbred 3-month-old rats were given a single s.c. dose of 1,2-dimethylhydrazine dihydrochloride (DMH; 100 mg/kg) and, 6 or 24 h later, an i.

Study of kinetics of epithelial cell populations in normal tissues of the rat's intestines and in carcinogenesis. III. Changes in kinetics of enterocyte populations in the course of experimental intestinal tumour induction in rats.

A stage-by-stage study of disturbances in enterocyte proliferation in the ileum and descending colon in the course of tumour induction by treatment with 1,2-dimethylhydrazine was performed. Even at early stages, an expansion of the zone of epithelial cell proliferation in the crypts and migration of dividing cells as far as to the crypt mouth, which is a manifestation of enterocyte differentiation disturbances, were observed. Enterocytes of the crypts chiefly proliferated through a short cycle, the mean duration of which was slightly greater than in normal intestinal tissue.

Effects of misclerone (clofibrate) on dimethylhydrazine-induced intestinal carcinogenesis in rats.

Intestinal tumors were induced by treatment with dimethylhydrazine (DMH) (14 mg with reference to base/kg body weight, weekly, s.c., for 20 weeks) in male rats supplied by Rappolovo Animal Farm.

Study of kinetics of epithelial cell populations in normal tissues of the rat's intestines and in carcinogenesis. II. Peculiarities of kinetics of enterocyte populations in experimental tumours of the colon.

Cell proliferation in adenocarcinomas induced in the rat's colon by parenteral injection of 1,2-dimethylhydrazine was compared with that in normal colonic epithelium by means of autoradiographs. The distinct zone of proliferation, typical of the intestines, was not observed in the tumours, and cells replicated nearly in all segments of neoplasms. Tumour enterocytes were found to have a longer short mitotic cycle (16 instead of 11 hrs), due, chiefly, to an extension of G1-period duration.

Study of kinetics of epithelial cell populations in normal tissues of the rat's intestines and in carcinogenesis. I. A comparison of enterocyte population kinetics in different segments of the small intestine and colon.

The peculiarities of enterocyte proliferation in the duodenum, jejunum, ileum, caecum, ascending, transverse and descending colon in the rat were studied by different methods of analysis of cell population kinetics (percentage-labelled mitosis curves, cumulative labelling curves, distribution of labelling index curves, etc.). The majority of proliferating cells in the small intestine are homogenous, as far as mitotic cycle mean duration (11-12 hrs) is concerned.