OncohematologyOncohematologyОнкогематология1818-83462413-4023Publishing House ABV Press77710.17650/1818-8346-2009-0-3-57-60HEMATOLOGIC MALIGNANCIES: TREATMENT, SUPPORTIVE CAREГЕМОБЛАСТОЗЫ: ЛЕЧЕНИЕ, СОПРОВОДИТЕЛЬНАЯ ТЕРАПИЯBCR-ABL gene amplification in patients with chronic myeloid leukemia and imatinib resistanceАмплификация гена BCR-ABL у пациентов с хроническим миелоидным лейкозом, рефрактерных к иматинибуKutzevS. I.КуцевС. И.
Russian Federation

Rostov-on-Don

Сергей Иванович Куцев

Ростов-на-Дону

kutsev@mail.ruMordanovS. V.МордановС. В.
Russian Federation

Rostov-on-Don

Ростов-на-Дону

Rostov state medical universityРостовский государственный медицинский университет270820093576027112022271120222009https://oncohematology.abvpress.ru/ongm/article/view/777

The treatment of Ph-positive chronic myeloid leukemia (CML) has achieved significant progress with the tyrosine kinase inhibitor (TKI) imatinib. Complete cytogenetic remission is a standard for patients treated in chronic phase. Nevertheless, primary and acquired resistance has been observed in few CML patients. Imatinib resistance in patients is related to heterogeneous mechanisms. The role of the BCR-ABL-related mechanism of imatinib resistance —BCR-ABL gene ampliphication in primary resistant cases was studied. The BCRABL gene ampliphication was established in 18% refractory to imatinib patients. Decreasing probability of complete cytogenetic response was revealed in these cases.

У больных хроническим миелоидным лейкозом (ХМЛ), получающих терапию иматинибом, с высокой частотой достигается полный цитогенетический ответ. Тем не менее у некоторых пациентов наблюдается первичная или приобретенная резистентность к иматинибу. В данной работе исследовано значение амплификации гена BCR-ABL в развитии первичной резистентности к иматинибу у пациентов с ХМЛ. Амплификация гена BCR-ABL выявлена у 18% больных ХМЛ, рефрактерных к иматинибу. Показано достоверное снижение вероятности достижения полного цитогенетического ответа у пациентов с амплификацией гена BCR-ABL.

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