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[Invasive, metastatic growth of lymphoblastoid B cells in immunodeficient SCID mice]
A Burkitt's lymphoma (BL, EBV +, 8/22 translocation), the EBV immortalized lymphoblastoid cell line from the same individual (LCL) and somatic cell hybrids (HYB) between both cell lines were inoculated in immunedeficient scid mice. Subcutaneous injected BL cells produced local tumor masses without distant metastases. In contrast LCL and hybrids show invasive and disseminated growth. Peripheral lymph nodes and thymic tissue were preferentially colonized. A detailed phenotypic analysis of BL, LCL and 3 different hybrids was performed using differntiation and adhesion molecules. The preferential "homing" of LCL and hybrids seem to be correlated with the expression of the lymphocyte homing receptor (CD44). The growth of LCL in scid mice shows, that additional genetic alterations are not necessary to cause a malignant phenotype. Activation of myc seem to play a minor role, because hybrids mimic the LCL phenotype and distribution pattern.
A Burkitt's lymphoma (BL, EBV +, 8/22 translocation), the EBV immortalized lymphoblastoid cell line from the same individual (LCL) and somatic cell hybrids (HYB) between both cell lines were inoculated in immunedeficient scid mice. Subcutaneous injected BL cells produced local tumor masses without distant metastases. In contrast LCL and hybrids show invasive and disseminated growth. Peripheral lymph nodes and thymic tissue were preferentially colonized. A detailed phenotypic analysis of BL, LCL and 3 different hybrids was performed using differntiation and adhesion molecules. The preferential "homing" of LCL and hybrids seem to be correlated with the expression of the lymphocyte homing receptor (CD44). The growth of LCL in scid mice shows, that additional genetic alterations are not necessary to cause a malignant phenotype. Activation of myc seem to play a minor role, because hybrids mimic the LCL phenotype and distribution pattern.