Biomedical subjects

Tom Böhling

Publications and source records attributed to Tom Böhling.

23 records · Page 2Linked to original sources

PubMed2002

Transforming growth factor beta released from natural coral implant enhances bone growth at calvarium of mature rat.

Earlier studies have shown that transforming growth factor beta (TGF-beta) has the capability of enhancing bone formation after a single application to an orthotopic site. We investigated whether 1, 5, or 25 microg of recombinant human TGF-beta1 added to porous natural coral (NC) blocks could promote bone ingrowth in a critical size defect (CSD) model in nongrowing rats. A 6-mm CSD in the parietal bone of Wistar rats was filled with NC disks, which were retrieved at 3 and 8 weeks. We prepared undecalcified sections for microscopy and histomorphometry to study bone formation in the implants. The differences in the means of the measured variables were compared with a one-way analysis of variance and Tukey's Student range test, and p values smaller than 0.05 were considered statistically significant. Bone formation was enhanced in all the TGF-beta1-treated implants at 8 weeks in comparison with the controls, but none of the implants showed complete bridging across the defect. The number of macrophages and giant cells was reduced in the TGF-beta1 implants, which showed less resorption and more intact structure than the coral controls. Void areas without any fibrous tissue ingrowth were found only in the TGF-beta1-treated implants, which may partly explain the reduced resorption. The data suggested that TGF-beta1 induced enhanced but limited bone formation in mature rats and prevented resorption of the coral calcium carbonate matrix, possibly by hindering reactive cell formation and fibrous tissue ingrowth.

Animals↗

PubMed2002

Recurrent DNA sequence copy losses on chromosomal arm 6q in capillary hemangioblastoma.

Capillary hemangioblastomas (CHB) of the central nervous system, the most common tumor in von Hippel-Lindau (VHL) disease, usually show mutations in the VHL tumor suppressor gene on chromosome 3p25-p26. Because little is known concerning the cytogenetic changes in these tumors, we studied 22 cases through comparative genomic hybridization to screen for DNA copy number changes in both sporadic and VHL-associated CHB. Our analysis revealed that 6 of 22 samples (27%) contained DNA copy number losses, whereas no gains were observed. The most recurrent finding was loss of chromosomal arm 6q, seen in five cases. In two of these cases also loss of chromosome 3 was noted. The third aberration observed was loss of chromosome 8, seen in one case. No differences were noted between VHL-associated and sporadic tumors, nor did the cytogenetic aberrations correlate with the clinical outcome. The loss of 6q, seen in this study and previously in other VHL-associated tumors (renal cell carcinomas and pheochromocytomas) and other tumors, suggest that this chromosome area may contain tumor suppressor genes involved in the early steps of tumorigenesis.

Adult↗

PubMedDate not supplied

Neuroendocrine differentiation in primary Merkel cell carcinoma--possible prognostic significance.

BACKGROUND: The aim of this study was to examine the level of neuroendocrine differentiation to determine its association with clinicopathological parameters. PATIENTS AND METHODS: Twenty-five primary MCC samples were evaluated for neuroendocrine differentiation profiles by immunohistochemistry using antibodies to chromogranin-A, microtubule associated protein-2 and synaptophysin. The data were compared with clinical parameters to find out whether their expression correlates with prognosis. RESULTS: In general, MCC shows a high degree of neuroendocrine differentiation. A higher expression of chromogranin-A and synaptophysin associated with benign behaviour. Chromogranin-A appeared to be the most important one in predicting the course of disease. CONCLUSION: Low levels of neuroendocrine differentiation in MCC associates with poor prognosis. Chromogranin-A could be used to identify patients who might benefit from oncological treatments.

Aged↗

PubMedDate not supplied

Cyclooxygenase-2 expression in human soft-tissue sarcomas is related to epithelial differentation.

BACKGROUND: Cyclooxygenase-2 (Cox-2) is expressed by several types of epithelial malignancies, i.e., carcinomas, and inhibition of Cox-2 may have a therapeutic role in chemoprevention and treatment of cancer. The role of Cox-2 in non-epithelial malignancies, however, is unclear. MATERIALS AND METHODS: We investigated, by immuno- histochemistry, the expression of Cox-2 in 103 human soft-tissue sarcomas. RESULTS: All 10 biphasic synovial sarcomas were positive for Cox-2, but positivity was observable only in the epithelial component of these tumours. Excluding sarcomas with epithelial differentation, uniform staining of the tumour was observed in only 2 samples. In addition, positivity for Cox-2 appeared in tumour cells in only 18 samples around necrotic areas. CONCLUSION: In human soft-tissue sarcomas, Cox-2 expression seems to be associated with epithelial differentation and, in some types of sarcomas, to be expressed in otherwise negative tumours at sites of necrosis.

Adult↗

PubMedDate not supplied

Cell cycle control by p21, p27 and p53 in Merkel cell carcinoma.

Merkel cell carcinoma (MCC) is an aggressive dermal tumour of neuroendocrine origin with poor prognosis. The role of cell cycle-regulatory proteins (p53/p21/p27) in MCC pathogenesis and their prognostic importance were evaluated. Twenty-four primary MCC specimens with corresponding clinical data were analysed by immunohistochemistry for p21, p27 and p53 antibodies. The stainings were evaluated semi-quantitatively and the results analysed statistically. p53 was negative in 80% and p21 in 71% of the samples. Positive staining for p27 was evident in 92% of the samples. However, the expression of these antibodies did not correlate with the outcome of the patient. The proportion of p53- and p21-negative samples seems to indicate that correction processes after DNA damage are not activated during MCC pathogenesis, a supposition that is supported by the aggressive nature of this tumour. Therefore, the expressions of the three studied cell cycle regulators cannot serve as prognostic markers for survival.

Biomarkers, Tumor↗