Cancer is one of the three leading causes of premature death worldwide. Lymphomas are a group of neoplasms originating from B or T lymphocytes of the peripheral lymphoid organs, with 85 to 90 % of lymphomas arising from B lymphocytes. The aim of this master’s thesis was to establish and evaluate the tumour component of a syngeneic B-cell lymphoma model using the A20_CD19+ and A20_CD19_KO cell populations, and to molecularly validate the modification of the Cd19 gene in the A20_CD19_KO cell population. The A20_CD19+ cells represent a murine B-cell lymphoma line with preserved expression of the surface antigen CD19, whereas the A20_CD19_KO cells have been genetically modified to exhibit reduced or absent expression of the CD19 protein. Female BALB/cAnNCrl mice were subcutaneously injected with A20_CD19+ or A20_CD19_KO cells at doses of 0,5 × 10⁶, 1 × 10⁶ and 2 × 10⁶ cells. Tumour incidence and growth, body weight, feed and water intake, as well as haematological and blood metabolic parameters, were monitored. Molecular validation was performed using Sanger sequencing, and the results were analysed using the ICE and TIDE software packages. Tumours developed in all mice injected with either A20 cell populations, although spontaneous tumour regression occurred in 11 % of the animals. The dose of 1 × 10⁶ cells was associated with the most rapid tumour growth. Both cell populations demonstrated comparable tumour-forming capacity, while sequence analysis confirmed the presence of the intended modifications at the Cd19 gene-editing site in the A20_CD19_KO cell population. The findings of this study represent an important step towards the establishment of a syngeneic model for immunotherapy research. The successfully established tumour component provides a valuable platform for further investigations of CD19-targeted immunotherapies and the mechanisms of tumour immune escape associated with the loss of CD19 expression.
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