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Copyright of Der Pathologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Der Pathologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Der Pathologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The German Bladder Cancer Association (DFBK) invited its members to the 3rd annual meeting 2012 in Hannover 4 years after the official founding. The meeting was directed to discuss the progress of ongoing and newly initiated projects and collaborations. In this article we will introduce current research activities and collaborations of the DFBK and would like to invite interested researchers to join this national interdisciplinary research association. The aim of the DFBK is to initiate interdisciplinary collaboration and to support scientific discussions among its members. For further information please visit our website at www.forschungsverbund-blasenkarzinom.de.

Bladder cancer may be caused by external factors like tobacco smoking, but may also be familial. We report on a father and son who developed this tumour at the ages of 45 and 35. Testing various genetic markers including the mismatch repair proteins MLH1, MSH2 and MSH6, whose loss is associated with a higher risk for hereditary non-polyposis colorectal cancer (HNPCC, Lynch syndrome), did not point to a familial disease. Thus the heavy smoking habits of the two patients must be considered as causal.

Plasmacytoid carcinoma is a rare variant of urothelial carcinoma and is characterised by distinct histopathological and clinical characteristics. The incidence varies between 2.7% and 3.1% of all muscle-invasive urothelial carcinoma. It is an aggressive, high-grade tumor with poor prognosis. Negative E-cadherin expression seems to be important for exact diagnosis. Systemic chemotherapy of plasmacytoid carcinoma could lead to prolonged patient survival.

Aims: The clonality of multiple urothelial carcinomas (UC) is subject to debate and affects treatment. Evidence derived from X-chromosome mosaicism and patterns of molecular alterations supports both a mono- and polyclonal relationship. In contrast to most UC, tumours with the mutator phenotype have frequent mutations in repetitive sequences (MSI) and promoter methylation. The aim of this study was to investigate the clonality of multifocal UC with MSI., Methods: We have screened 400 UC for MSI and found it to occur in 1% of bladder and 15% of upper tract UC. Of these, 9 patients, whose tumours had MSI, developed or presented with multiple UC. A total of 32 UC (occurring over 0-6 years, 2-12 TCC per patient), 2 cases of CIS and 9 normal urothelial samples were screened for MSI at 17 loci and aberrant promoter methylation at 7 genes., Results: In 8 of 9 patients, the pattern of microsatellite mutation and promoter methylation suggested that the multiple tumours had a clonal origin. Patterns of aberrant methylation in multiple tumours were more similar than microsatellite mutations, suggesting an earlier carcinogenic timing. MSI and promoter methylation were present in macroscopically normal urothelium from these patients., Conclusions: Aberrant promoter methylation occurs before microsatellite alteration in UC with mutator phenotype. The majority of recurrent UC with MSI are monoclonal in origin and macroscopically normal urothelium harbours multiple molecular abnormalities. Thus, at the time of apparently successful treatment, there is molecular evidence of residual tumour that subsequently develops into recurrent disease.

The present investigation was concerned with the impact of prenatal and perinatal complications (biological risks) and of family adversity (psychosocial risks) on developmental status at age 4 1/2. In a prospective study the developmental course of 362 children (including 210 high-risk children) was followed from birth to age 4 1/2 years. A multilevel approach was used to assess all relevant domains of functioning (i.e. motor, cognitive and social-emotional development). The goal was to obtain information about the effects of biological and psychosocial risks alone and together on outcome in the different domains of functioning. The results show that psychosocial risk factors posed the greatest threat to normal development. Children with psychosocial risks were significantly behind those without such risks in all areas of functioning. Biological risks mainly affected motor development, their negative effects on cognitive and social-emotional functioning having been largely compensated for by age 4 1/2. The extent of an adverse outcome was related to both the degree of risk load and the number of risk factors, whereas interactions among risks were of only minor relevance. An adverse outcome is not inevitable, however: Despite the risks most of the at-risk children showed normal development at age 4 1/2.

In a prospective longitudinal study the development of N = 362 children will be followed over four time points (T1-T4) from birth to school age utilizing a comprehensive battery of instruments. Aims of the study are the description of the developmental course of children born at differing degrees of biological and psychosocial risk, the identification of early predictors of developmental disorders and their compensation, as well as the analysis of the processes and mechanisms underlying differential developmental patterns. The results of waves 1 and 2 show that early development from 3 to 24 months is quite unstable. Depending on the examined domain of development up to 3/4 of the disturbances of infancy have remitted by the later age, whereas nearly a fifth of the hitherto well children developed new disturbances. Both risks have a marked negative effect on development. While biological risks go hand in hand with impaired motor functioning, psychosocial risks adversely affect cognitive and social-emotional competence. However, the relative weight of risk factors changes during the first two years with biological risks becoming less important and psychosocial risk factors gaining influence. Single risk factors identified as being prognostically very unfavourable are very low birth weight and neonatal seizures. Of the psychosocial risks a pattern of unfavourable family characteristics such as low educational level, history of broken home or mental health problems of parents and chronic difficulties is related most strongly to poor outcome.