Arterial, portal or combined arterio-portal regional chemotherapy in experimental liver tumours?

The most appropriate route for regional administration of chemotherapeutic drugs to liver tumours was studied in a standardized rodent model: cells of Novikoff hepatoma were transplanted into the central liver lobe of Sprague-Dawley rats. From day 5 to day 12 after transplantation, the liver was continuously perfused with 420 mg/kg 5'-fluoro-2-deoxyuridine by subcutaneous osmotic micropumps via the hepatic artery (n = 20), the portal vein (n = 20) or both vessels together (n = 12). The tumour multiplication factor (TMF) and the vascularization of the tumour were evaluated. Arterial and combined infusion led to a highly significant reduction in TMF, but combined infusion was not more effective than arterial alone. Portal infusion had no significant effect. There was no correlation between vascularization and tumour response in arterial infusion, but a strong correlation in portal infusion. Thus chemotherapy via the portal route may be effective in selected tumours with considerable portal vascularisation.

The nature of Hodgkin and Reed-Sternberg cells, their association with EBV, and their relationship to anaplastic large-cell lymphoma.

This review focuses on the cellular origin of Hodgkin and Reed-Sternberg (HRS) cells, their association with the Epstein-Barr virus (EBV), and their relation to Ki-1+ anaplastic large-cell (ALC) lymphoma. The tingibility of HRS cells in paraffin sections for polyclonal immunoglobulin represents a staining artifact and thus can no longer serve as an argument for the histiocytic nature of HRS cells. Immunolabeling studies do not support the putative relationship of HRS cells to cell types such as macrophages or interdigitating reticulum cells, but instead suggest: a) that lymphocyte-predominant (LP) Hodgkin's disease (HD) represents a B-cell neoplasm which is distinct from non-LP HD, and b) that non-LP HD constitutes a syndrome rather than a disease entity, with the existence of T-cell types and B-cell types. HRS cells (and the tumor cells in ALC lymphomas) frequently display an immature genotype in association with late activation markers, leading to the assumption that the tumor cells in many cases of HD (and some cases of ALC lymphoma) may be derived from immature lymphoid cells that are infected by a virus that superimposes characteristics of mature activated lymphocytes on these cells. Southern blotting, in situ hybridization, and polymerase chain reaction (PCR) experiments revealed an association of EBV with HRS cells in a significant proportion of HD cases, suggesting that EBV may be responsible for the dissociation between genotype and phenotype in HRS cells, because EBV is a strong inducer of the activation antigens CD30 and CDw70.(ABSTRACT TRUNCATED AT 250 WORDS)