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Janina Kulka

Publications and source records attributed to Janina Kulka.

12 recordsLinked to original sources
PubMed2006

Detection of HER-2/neu gene amplification in breast carcinomas using quantitative real-time PCR - a comparison with immunohistochemical and FISH results.

The aim of our study was to evaluate the value of quantitative real-time-PCR (qPCR) in the determination of HER-2/neu amplification status of human breast carcinomas by comparing qPCR, FISH and immunohistochemistry results from the same samples. A total of 210 breast carcinomas were examined. Ready-to-use CB11 antibody was applied to detect HER-2/neu oncoprotein expression. In 76 out of 210 cases FISH was performed, and 162 cases were investigated with qPCR. Seventy-five tumors were 2+ or 3+ positive with immunohistochemistry, while 135 samples were either completely negative or 1+. In 45 cases results from all three methods were available. Out of these, in twenty negative and sixteen positive cases both FISH and qPCR led to similar results. The mean qPCR amplification ratio in the concordant positive cases was 5.424 while in the qPCR+/FISH- group the mean ratio was 2.765. Out of 121 samples with scores of 0 or 1+ immunohistochemical result, analyzed also with qPCR, 26 showed HER-2/neu gene amplification. In these cases the mean amplification ratio was 2.53. Comparison of FISH and qPCR together with immunohistochemistry shows that qPCR is more sensitive to detect HER-2/neu gene amplification in tumors scored as 2+ with immunohistochemistry, but the diagnostic cut-off ratio should be defined above 2.7 to avoid high number of false positive cases. Amongst the immunohistochemistry score 2+ cases, 10 of 18 showed gene amplification by qPCR while 10 of 26 by FISH. In conclusion, a well calibrated HER-2/neu qPCR assay may serve as useful alternative to FISH in breast cancer patients.

Adenocarcinoma, Mucinous↗
PubMed2006

Divergences in diagnosing nodular breast lesions of noncarcinomatous nature.

Nodular breast lesions of noncarcinomatous origin are often of fibroepithelial origin. They may cause classification problems when they are hypocellular or hypercellular; the latter setting may also raise the differential diagnosis of phyllodes tumors. Thirty equivocal nodular breast lesions were collected and one hematoxylin and eosin slide from each was assessed by six pathologists with special interest in breast pathology. The overall reproducibility of classifying these lesions into categories of fibroadenoma, phyllodes tumor or anything else was moderate (kappa value: 0.48). The lack of a uniform nomenclature was not felt disturbing for hypocellular lesions, but the discordant diagnosis of tumors resembling or representing phyllodes tumors was acknowledged to require intervention, such as more obvious implication of guidelines and quality assurance programs aiming at assessing diagnoses and prognostic parameters.

Adenofibroma↗
PubMed2006

[The results of cetuximab treatment of a patient with multiple pretreated, irinotecan resistant metastatic colorectal cancer].

AIM: The case of a patient with heavily pretreated, irinotecan-resistant, metastatic colorectal cancer is presented by the authors, and they would like to point to the effectiveness of a new therapeutic option, cetuximab treatment. Additionally, they would like to call attention to the need of performing EGFR determination from all of the biopsy samples (primary tumor, lymph nodes and metastases) to start the treatment. A weak EGFR-positivity of the primary tumor in fact does not mean the contraindication of cetuximab treatment, since the metastases, which are usually treated, could be strongly positive. The therapeutic answer could be excellent in this case, as it occurred in our case.

Antibodies, Monoclonal↗
PubMed2005

[Oncocytic tumor of the adrenal gland].

Oncocytic tumor of the adrenal gland. The authors describe a case of a rare tumor arising in the adrenal gland. The tumor 6 cm in diameter, connected to the right adrenal gland, was found incidentally in a healthy young man of 34 years of age, who suffered an accident and had a rib fracture. No pathological hormone production was detected on laboratory tests. The right adrenal gland with the tumor was removed by laparoscopic surgery. Histopathological examination revealed an oncocytic adenoma of the adrenal cortex. The authors describe the morphology and the differential diagnosis of this rare tumor of the adrenal gland.

Adenoma, Oxyphilic↗
PubMed2005

Claudin-1, -3 and -4 proteins and mRNA expression in benign and malignant breast lesions: a research study.

INTRODUCTION: We compared levels of protein and mRNA expression of three members of the claudin (CLDN) family in malignant breast tumours and benign lesions. METHODS: Altogether, 56 sections from 52 surgically resected breast specimens were analyzed for CLDN1, CLDN3 and CLDN4 expression by immunohistochemistry. mRNA was also analyzed using real-time PCR in 17 of the 52 cases. RESULTS: CLDNs were rarely observed exclusively at tight junction structures. CLDN1 was present in the membrane of normal duct cells and in some of the cell membranes from ductal carcinoma in situ, and was frequently observed in eight out of nine areas of apocrine metaplasia, whereas invasive tumours were negative for CLDN1 or it was present in a scattered distribution among such tumour cells (in 36/39 malignant tumours). CLDN3 was present in 49 of the 56 sections and CLDN4 was present in all 56 tissue sections. However, CLDN4 was highly positive in normal epithelial cells and was decreased or absent in 17 out of 21 ductal carcinoma grade 1, in special types of breast carcinoma (mucinous, papillary, tubular) and in areas of apocrine metaplasia. CLDN1 mRNA was downregulated by 12-fold in the sample (tumour) group as compared with the control group using GAPDH as the reference gene. CLDN3 and CLDN4 mRNA exhibited no difference in expression between invasive tumours and surrounding tissue. CONCLUSIONS: The significant loss of CLDN1 protein in breast cancer cells suggests that CLDN1 may play a role in invasion and metastasis. The loss of CLDN4 expression in areas of apocrine metaplasia and in the majority of grade 1 invasive carcinomas also suggests a particular role for this protein in mammary glandular cell differentiation and carcinogenesis.

Adult↗
PubMed2005

The expression of five different claudins in invasive breast carcinomas: comparison of pT1pN1 and pT1pN0 tumors.

The evaluation of the role of claudins (CLDNs) in breast carcinogenesis has recently begun. We investigated the expression of CLDNs 1, 2, 3, 4, and 7 in pT1pN0 and pT1pN1 invasive ductal breast carcinomas. Tissue arrays of 30-30 pT1pN0 and pT1pN1 invasive ductal breast carcinomas of different grades were constructed, and the expression of CLDN 1, 2, 3, 4, and 7 proteins was analyzed using standard and immunofluorescent immunohistochemistry. The results were evaluated by light and confocal microscopy. Regarding CLDN 1, 4, and 7 expressions, differences were noted between normal and tumor cells and also between tumors of different grades, while no remarkable differences were noted between pT1pN0 and pT1pN1 tumors. CLDNs 1 and 7 were found to be downregulated in tumor cells compared to the normal epithelium, while CLDN 4 expression was decreased in grade 1 tumors. CLDN 7 protein was abundant in normal epithelia, and the staining decreased in grade 3 tumors. There were no differences between normal and neoplastic cells regarding CLDN 2 and 3 expressions. As a preliminary result, our observations suggest that the analyzed CLDNs do not promote tumor metastasis. On the basis of our findings, it seems that CLDN 1, CLDN 4, and CLDN 7 may rather have an important role in tumorigenesis or in cell-to-cell adhesion.

Axilla↗
PubMed2003

[Tenascin-C expression in human breast tumors].

INTRODUCTION: Increased amounts of extracellular matrix proteins have been described in breast tumours, which are normally present in embryonal connective tissue, in adults however, these occur only in pathological conditions: one of which is tenascin. Within the tenascin family the most examined and most controversial member is tenascin-C. It has been suggested that tenascin-C decreases cell adhesion, promotes invasion and metastases, and may play role in pathological angiogenesis. MATERIAL AND METHODS: Authors investigated 62 primary breast carcinomas and in further 20 cases both the primary and the recurrent or second primary tumours were examined. In the latter group the main question was whether tenascin-C was of prognostic significance. The newly formed vessels were visualised using CD31 antibody. RESULTS AND CONCLUSIONS: Tenascin-C positivity in the tumour cells was shown in the 10 of the 62 primary carcinomas and in 7 from the second group of cases (20 patients). Of all cases examined, in five specimens tenascin-C positivity was present in normal ductal epithelial cells. In variable amount, in the stroma of invasive tumours, tenascin-C was present in every case. The presence of tenascin-C within tumour cells, at the periphery and also in the stroma of tumours, within the proliferating ducts, around tumour cell nests and in situ carcinomas, furthermore, in the epithelial cells of normal ducts suggests that tenascin-C may promote detachment and migration of carcinoma cells. There was no correlation, however, between tenascin-C expression and the occurrence of recurrences in this small group. Correlation was found between increased stromal tenascin-C expression and angiogenesis. Authors conclude that tenascin-C might have a role in angiogenesis.

Adult↗
PubMed2003

[New TNM classification of breast tumors].

INTRODUCTION: The TNM classification of breast carcinomas has substantially changed. Both the newly implemented Hungarian breast cancer screening programme and the national cancer registry require the adequate reporting of the disease with particular emphasis on its extent. AIMS: The purpose of this article is to introduce the new TNM classification. METHODS: Description of the breast cancer related definitions and of the general guidelines that have to be applied for the staging of breast carcinomas. The TNM categories are presented in a practical, partly tabulated format with examples and background information. CONCLUSION: Breast cancers are advised to be reported according to the new TNM classification from January 2003.

Breast Neoplasms↗
PubMed2002

[Role of osteopontin in the formation of microcalcifications in breast cancer].

INTRODUCTION: Osteopontin, a non-collagen, Ca-binding phosphoprotein, plays roles in both physiological and pathological mineralisation processes. Its expression may be severely altered in malignant tumours. AIM: To investigate the presence of this protein in breast tumours showing mammographic microcalcifications. MATERIAL: In this study the authors investigated immunohistochemically the osteopontin expression in 26 breast tumours. The elemental composition of the microcalcifications of the same tumours was also examined with energy dispersive spectrometer linked to a scanning electron microscope. RESULTS: Osteopontin expression was found within the tumours in the tumour cells, in vascular smooth muscle cells, in the myoepithelial cells of the normal ducts, and in macrophages. Extracellular osteopontin positivity was seen around calcified foci. There was no correlation between osteopontin positivity and the examined prognostic factors: grade, type and size of the tumour, axillary lymph nodes status, or age. Two types of microcalcifications were seen: 1. Ca-phosphate only, 2. Those composed of various other elements. CONCLUSION: The presence of osteopontin in the vicinity of calcified foci and in the vessel walls seems to support the hypothesis that osteopontin takes part in calcification process.

Adult↗
PubMed2002

Extracellular matrix components in breast carcinomas.

A malignant process interferes with the normal 'programme' of extracellular matrix biosynthesis and can modify extensively the structure and composition of the matrix. This effect appears to be attributable to several processes such as direct production of some selected matrix macromolecules by malignant cells or indirectly by the production of factors by malignant cells interfering with the regulation of normal matrix production. Other possibilities may also exist, such as the direct action of an environmental carcinogen on otherwise normal mesenchymal cells. The result is a more or less profound modification of tissue structure and composition with possible feedback effects on the malignant process. Some examples will be discussed such as elastin production by some tumours as well as the biosynthesis of some other selected matrix macromolecules as tenascin and osteopontin by breast tumours. Although the detailed mechanisms of these specific matrix productions is not yet completely elucidated, the rapidly increasing knowledge on the regulation of specific matrix production process and deranged matrix production might represent a new area of crosstalk between cancer research and matrix biology.

Animals↗