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The objective of our study was to investigate the effect of weight loss on the crevicular microflora following bariatric surgery. Crevicular fluid samples were taken from 57 subjects: 22 were in the normal control group; 18 in the obese control group; and 17 patients had had bariatric surgery, who underwent a repeat sampling 6 to 12 months after the operation. Crevicular fluid samples were analyzed by MALDI-TOF MS analysis. After surgery and weight loss, the mean germ count increased, albeit not significantly. Also, Candida albicans and non-albicans Candida species: C. dubliniensis, C. kefyr, and C. lusitaniae appeared after surgery (p < 0.05) in subjects where Neisseria was either absent throughout or eliminated after surgery. However, periodontitis did not develop during this time in our subjects.

Background: In acute myeloid leukemia (AML), the internal tandem duplication (ITD) in the juxtamembrane domain of the FLT3 (Fms-like tyrosine kinase 3) gene is one of the most frequent genetic alterations associated with poor prognosis. Methods: A complex evaluation of the analytical properties of the three most frequently used detection methods -PCR followed by agarose (AGE), polyacrylamide (PAGE) or capillary electrophoresis (CE) -was performed on 95 DNA samples obtained from 73 AML patients. Results: All the three methods verifi ed the presence of a mutant allele in 20 samples from 18 patients. AGE and PAGE could detect the presence of 1 % -2 % mutant allele, while the detection limit of CE was 0.28 % . However, acceptable reproducibility (inter-assay CV < 25 % ) of the mutant allele rate determination was only achievable above 1.5 % mutant/ total allele rate. The reproducibility of the ITD size determination by CE was much better, but the ITD size calculated by PeakScanner or GeneScan analysis was 7 % lower as compared to values obtained by DNA sequencing. The presence of multiple ITD was over-estimated by PAGE and AGE due to the formation of heteroduplexes.

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hMSH2 gene might be responsible for the development of colon cancers. In family members where the exon 7 mutation is not coupled with this missense mutation, colon cancer appears after the age of 40. The association of these two mutations seems to decrease the age of manifestation of the disease into the early thirties. INTRODUCTIONAccording to published data, about 15-20 % of colorectal carcinomas (CRC) follow a familial pattern. Familial adenomatous polyposis coli syndrome (FAP) and its subtypes are responsible for only about 1 % of all CRCs, while hereditary nonpolyposis colon cancer (HNPCC) accounts for approximately 3-8 % of cases [1][2][3] . The characteristic presentation of HNPCC is frequently right-sided localization, the presence of synchronous and metachronous CRCs, and its association with other HNPCC-related extracolonic tumors, including gastric, endometrial, and urinary and biliary tract cancers in afflicted families [2,3] . Compared to sporadic colorectal carcinomas, HNPCC has an earlier age of onset, Crohn's disease-like lymphocytic infiltration in tumor tissues, increased mucin production, and a lower degree of histological differentiation [3][4][5] . The classic adenoma-carcinoma sequence can be observed in HNPCC patients as well, but the conversion of polyps to malignant proliferation is accelerated, taking only 1-3 years, as opposed to sporadic adenomas, where this can take as long as 10-15 years [1] . The number of polyps in the colon is not so high as in cases of FAP. The genetic background of HNPCC has been identified in the germline defect of DNA mismatch repair genes (MMR Abstract AIM: To screen a suspected Hungarian HNPCC family to find specific mutations and to evaluate their effect on the presentation of the disease. METHODS:The family was identified by applying the Amsterdam and Bethesda Criteria. Immunohistochemistry was performed, and DNA samples isolated from tumor tissue were evaluated for microsatellite instability. The identification of possible mutations was carried out by sequencing the hMLH1 and hMSH2 genes. RESULTS:Two different mutations were observed in the index patient and in his family members. The first mutation was located in exon 7, codon 422 of hMSH2, and caused a change from Glu to STOP codon. No other report of such a mutation has been published, as far as we could find in the international databases. The second mutation was found in exon 3 codon 127 of the hMSH2 gene, resulting in Asp→Ser substitution. The second mutation was already published, as a non-pathogenic allelic variation. CONCLUSION:The pedigree analysis suggested that the newly detected nonsense mutation in exon 7 of the