Biomedical subjects

Udo Döbbeling

Publications and source records attributed to Udo Döbbeling.

4 recordsLinked to original sources

PubMed2006

[Perspective of cutaneous lymphoma reserach].

Primary cutaneous lymphomas are characterized by an expansion of hematopoietic cells in the special microenvironment of the skin. They represent a special challenge both for researches and for clinicians who treat patients with these disorders. New research data concerning the biology of lymphocytes and the cutaneous microenvironment have increased our knowledge of these diseases in the last decades. The new WHO/EORTC classification definitely will facilitate a more detailed investigation of the various subtypes.

Biomedical Research↗

PubMed2006

Cutaneous malignant lymphomas: update 2006.

Cutaneous lymphomas represent a unique group of lymphomas and are the second most frequent extranodal lymphomas. As with other neoplasias, the pathogenesis is based mainly on a stepwise accumulation of mutations of suppressor genes and oncogenes caused by genetic, environmental or infectious factors. The diagnostic work-up includes clinical, histological, imaging and hematological investigations and in many cases immunohistochemical and molecular biological analyses. The current WHO/EORTC classification of cutaneous lymphomas differentiates "mature T-cell and NK-cell lymphomas", "mature B-cell lymphomas" and "immature hematopoietic malignancies", their variants and subgroups. It is compatible with the WHO classification for neoplasias of the hematopoietic and lymphoid tissue and respects the organ-specific peculiarities of primary cutaneous lymphomas. The assignment of the various types of cutaneous lymphomas into prognostic categories (pre-lymphomatous "abortive" disorders; definite malignant lymphomas of low-grade malignancy; definite malignant lymphomas of high-grade malignancy) provides essential information on the biological behavior and allows an appropriate planning of the therapeutic strategy, which may be topical or systemic and aggressive or non-aggressive. Besides the classical options for therapy, there are new and "experimental" strategies, the efficacy of which has to be studied in clinical trials.

Dermatology↗

PubMed2003

Expression of apoptosis regulators in cutaneous T-cell lymphoma (CTCL) cells.

This study examined cutaneous T-cell lymphoma (CTCL) cell lines and cutaneous lesions for the presence of Bcl-2 gene family members and found that the two apoptosis-inhibiting members Bcl-xL and Mcl-1 and the two apoptosis-supporting members Bad and Bax were expressed. However, Bad was at least partially inactivated by phosphorylation. In skin lesions, the translocation of Bad from the nucleus to the cytoplasm may reflect the Bad inactivation by phosphorylation identified in vivo. Bax is also ineffective, as the non-steroidal anti-inflammatory drug sulindac, whose cytotoxic effect is mediated by Bax, could not induce apoptosis in CTCL cell lines. The expression of Bcl-2, Bcl-xL, and Mcl-1 may therefore be sufficient to guarantee the survival of malignant CTCL cells. The Bcl-x, Mcl-1, Bad, and Bax proteins were also expressed in all CTCL skin lesions tested. In two patients from whom two biopsies from two different time points of the disease were available, a significant increase in Mcl-1 expression was found in the later-stage skin lesion. Overexpression of Mcl-1 and synthesis of non-functional Bax may be responsible for the resistance of CTCL cells to the anti-cancer drugs chlorambucil and sulindac.

Aged↗

PubMed2002

From inflammation to neoplasia: new concepts in the pathogenesis of cutaneous lymphomas.

Mycosis fungoides is a clinicopathologic term which describes a neoplasm of cerebriform T lymphocytes that form plaques and tumors. We further suggest that mycosis fungoides arises in a background of chronic inflammation or as a response to chronic antigenic stimulation. Subsequently, a series of mutations results in the stepwise progression from eczematous patches, to plaques, tumors and eventual hematogenous dissemination. The pathogenetic process is driven by various, probably individually different, exogenous factors, e.g. environmental foreign antigens, bacterial superantigen, and/or endogenous factors, e.g. autocrine cytokine loops, CD40/CD40L and B7/CD28 interaction.

Humans↗