LYMFKLIERKANKER. Non-Hodgkinlymfomen en ziekte van Hodgkin

Informatie over actuele ontwikkelingen in zowel reguliere als alternatieve en/of aanvullende behandelingen en middelen bij lymfklierkanker - non-Hodgkin lymfomen en ziekte van Hodgkin in alle stadia.

In linkerkolom staan recente artikelen min of meer op alfabetische volgorde gerubriceerd

Ervaringen van kankerpatienten met complementaire aanpak zijn te vinden onder ervaringsverhalen en er zijn op onze website ook een aantal video's van ervaringen van kankerpatienten met complementaire aanpak te zien. Aan te klikken via videoknop linksbovenaan op deze pagina. Of ga naar de website van het SNFK waar voorlichtingsfilmpjes zijn te zien over complementaire aanpak bij kanker.

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PDT - fotodynamische therapie doodt lymfklierkankercellen en laat T-cellen in tact.

8 september 2004: Bron: Hodgkin Contactgroep.

Meer informatie over PDT = Photodynamische Therapie onder Wat is PDT

[4643] Preferential Induction of B Cell Apoptosis Using Photodynamic Therapy. Session Type: Publication Only

Gorazd Krosl, Pascale Dube, Nancy Dallaire, Marc Vaillancourt, Denis- Claude Roy. Hematology-Immunology, Maisonneuve-Rosemont Hospital Research Centre, Montreal, QC, Canada; Celmed BioSciences, Montreal, QC, Canada Apoptotic cell death in cancer cells promotes antigen presentation and favors the development of an anti-tumor vaccination effect. While lymphoma cells can easily be obtained from lymph nodes or peripheral blood, these malignant cells usually co-localize with normal hematopoietic T lymphocytes, rendering the selective induction of apoptosis in malignant B cells particularly difficult.

We have found that photodynamic therapy (PDT) using the photosensitizer 4-5 dibromorhodamine methyl ester (TH9402) and visible light (514 nm) can be used to preferentially eliminate malignant B-lineage non-Hodgkin's lymphoma cells (mean of 3-4 logs) over T lymphocytes.

As a rhodamine derivative, TH9402 cellular efflux is mediated through the P-glycoprotein (Pgp) pump. However, the preferential elimination of B cells over resting T cells could not be ascribed to Pgp inactivation and we found no difference in intracellular retention of TH9402 between B and T cells.

In order to understand the molecular events leading to such high B cell susceptibility to PDT, we then investigated the nature of death pathways involved. To determine whether apoptosis was the preponderant mechanism leading to the rapid elimination of B cells, we measured the binding of Annexin V (AnnV) in 7-aminoactinomycin D (7AAD) negative (i.e. live) B and T cells using flow cytometry, and quantified DNA fragmentation and caspase 3 and 9 activity in isolated CD3+ and CD19+ PDT treated and untreated cells.

We found that B cells demonstrated high levels of apoptosis after PDT, with 53?1.3% (mean?SE) AnnexinV+/7AAD- cells compared to 30?1.9% in T cells (p< 0.05). The extent of DNA fragmentation, as determined by the TUNEL reaction, was extensive in B cells (33.7?9.8%)(mean?SE) but not T cells (2.3?0.1%) when measured at 4 hours post PDT (p<0.01).

After PDT, catalytic caspase 3 levels were also 4-fold higher in CD19+ cells than CD3+ cells (p<0.01). In contrast, caspase 9 levels remained low for both cell types. The induction of apoptosis translated into the elimination of more than 90% of B cells within 4 hours after PDT, while the majority of T cells were not affected. Importantly, similar elimination of B-lineage cell lines and patient cells was observed, using a limiting dilution assay, whether cells overexpressed the anti-apoptotic bcl-2 protein or not. Thus, these results indicate that the predominant caspase 3 apoptotic pathway is specifically implicated in PDT-induced B cell death, and its early activation explains the rapid and profound sensitivity of B lymphocytes to PDT. This strategy could promote tumor cell vaccination in the context of autologous TH9402-purged stem cell transplantation for patients with B-lineage malignancies. In addition, preferential B cell targeting could take advantage of the crucial immunomodulatory role of apoptosis for the treatment of patients with autoimmune B cell disorders. Abstract #4643 appears in Blood, Volume 104, issue 11, November 16, 2004