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Background  Apoptosis plays an important role in the development and homeostasis of multicellular organisms and its deregulation may result in many serious diseases, including cancer. Now it is clear that some oncogenic mutations disrupt apoptosis, leading to tumour initiation, progression or metastasis. Here, expression of apoptotic genes in context of drug resistance was investigated.    Methods  We examined total of 102 samples from leukemic patients (n = 60) and patients with solid tumours (n = 42). We used RT-PCR to determine the levels of mRNA expression and the in vitro chemoresistance of leukemic cells was evaluated using the MTT assay.    Results  We found statistically significant increase in mRNA expression of all investigated proteins (p53, BAX, Bcl-2 and Bcl-XL) between the leukemia samples and leukocytes from healthy volunteers. We did not find any significant difference in mRNA levels among the solid tumour samples. Notably, we showed a significant positive correlation in both leukemic and solid tumour patient groups between  p53  and  BAX  mRNA. We found that the highest values for the  Bcl - 2/BAX  ratio were in solid tumours in comparison to leukemic cells or normal leukocytes. Moreover, we assessed the impact of  p53  and  BAX  mRNA levels on the sensitivity of the leukemic cells to selected cytostatics.    Conclusions  Elevated levels of  p53  and  BAX  mRNA may indicate cellular response to possible changes in genomic DNA integrity associated with malignant transformation. We suggest that the  BAX  gene is regulated by the p53 protein but the initiation of apoptosis through the transcription activation of  BAX  is blocked by the high levels  of Bcl - 2 . Given that the apoptosis resistance mechanisms are different among oncological patients as well as stages of identical malignancy cases, personalized and specific combination therapy is proposed to be more effective in clinical application.

Differential mRNA expression of the main apoptotic proteins in normal and malignant cells and its relation to in vitro resistance