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The evaluation of the efficacy and toxicity of targeted treatment in non-small cell lung cancer patients – single centre experience

100%

Kardas J., Buraczewska A., Chrom P., Waśko-Grabowska A., Młot B., Szczylik C.

OncoReview

2017

vol. 7

issue 2

92-97

Introduction: Tyrosine kinase inhibitors (TKI) are the standard of treatment in patients with advanced non-small cell lung cancer (NSCLC) with EGFR (endothelial growth factor receptor) gene activating mutation. Objective: The evaluation of the efficacy and toxicity of TKI drugs in NSCLC patients treated in single centre. Material and methods: NSCLC patients treated with TKI (gefitinib, erlotynib, afatinib) between 2012– 2016 were retrospectively analysed. We evaluated: overall response rate (ORR) which is the sum of complete responses (CR) and partial remissions (PR), progression free survival (PFS), overall survival (OS) and adverse events (AE) according to CTCAE (Common Terminology Criteria for Adverse Events) scale. Results: The study group were 16 patients ORR was 50% (CR: 1, PR: 7). Median PFS and OS was 8,7 and 22,9 months respectively. Adverse events observed mainly in stage 1 and 2 were related to hyponatraemia, hyperbilirubinemia, skin toxicity and mucositis. There was one death reported due to infectious complications. Conclusion: The efficacy and toxicity of TKI in study group were found to be similar to those described in the literature.

Role of anti-apoptotic pathways activated by BCR/ABL in the resistance of chronic myeloid leukemia cells to tyrosine kinase inhibitors

75%

Danisz K., Blasiak J.

2013

vol. 60

issue 4

503-514

Chronic myeloid leukemia (CML) is a hematological stem cell disorder characterized by the excessive proliferation of the myeloid lineage. In its initial chronic phase, the myeloid progenitor cells expand and demonstrate apparently normal differentiation. The disease may then transform into the accelerated phase, usually associated with resistance to therapy, and finally, into acute leukemic progression phase - blast crisis. Abnormal myeloid cells produce progenitors, which have lost their ability to differentiate, but retain the capacity to proliferate. The molecular hallmark of CML is the Philadelphia chromosome, resulting from reciprocal chromosome translocation, t(9;22)(q34;q11), and containing the BCR/ABL fusion gene, producing the BCR/ABL protein with a constitutive tyrosine kinase activity. BCR/ABL-positive cells have faster growth and proliferation over their normal counterparts and are resistant to apoptosis. Introduction of imatinib (IM), a tyrosine kinase inhibitor, revolutionized the therapy of CML, changing it from a fatal disease into a chronic disorder. However, some patients show a primary resistance to IM, others acquire such resistance in the course of therapy. Therefore, a small number of leukemic stem cells retains self-renewal capacity under IM treatment. Because BCR/ABL is involved in many signaling pathways, some of them may be essential for resistance to IM-induced apoptosis. The PI3K/AKT, Ras and JAK/STAT signaling pathways are involved in resistance to apoptosis and can be activated by BCR/ABL. Therefore, they can be candidates for BCR/ABL-dependent pro-survival pathway(s), allowing a fraction of CML cells to withstand treatment with tyrosine kinase inhibitors.

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1 Acta Biochimica Polonica

1 OncoReview

1 2017

1 2013

1 Blasiak J.

1 Buraczewska A.

1 Chrom P.

1 Danisz K.

1 Kardas J.

1 Młot B.

1 Szczylik C.

1 Waśko-Grabowska A.

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The evaluation of the efficacy and toxicity of targeted treatment in non-small cell lung cancer patients – single centre experience

Role of anti-apoptotic pathways activated by BCR/ABL in the resistance of chronic myeloid leukemia cells to tyrosine kinase inhibitors