Thesis

IFM is a Potential Key Player in AML Cell Survival and CML Cell Resistance to Tyrosine Kinase Inhibitor

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Myeloid leukemia is characterized by the excessive proliferation of myeloid cells within the bone
marrow. It is categorized into acute (AML) and chronic (CML) myeloid leukemia, with distinct etiologies
and therapeutic complexities. The genetic heterogeneity of AML contributes to varying treatment
responses, leading to a high mortality rate. One gene that has been identified as an adverse prognostic
factor in AML is IFM, although its exact role remains unelucidated. IFM belongs to the group of IFN-
related DNA damage-resistant signature (IRDS) genes, which is associated with resistance to DNA-
damaging therapies across various types of cancer. However, the involvement of IRDS genes,

particularly IFM, in tyrosine kinase inhibitor (TKI) resistance in CML remains unclear. Thus, this study
sought to investigate the impact of IFM on AML cell survival and its expression level in TKI-resistant
CML cells in vitro. It was observed that IFM knockdown induced apoptosis in AML cells due to the
elevation in DNA damage level. Moreover, IFM expression is induced in TKI-resistant CML cells,
indicating its potential role in TKI resistance. These findings suggest a pro-tumoral role for IFM in both
acute and chronic myeloid leukemia.

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Availability

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Detail Information

Series Title

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Call Number

BM 24-037

Publisher

i3L, Jakarta : i3L Press., 2024

Collation

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Language

English

ISBN/ISSN

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Classification

NONE

Content Type

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Media Type

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Carrier Type

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Edition

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Subject(s)

leukemia
AML
CML
IRDS
resistance

Specific Detail Info

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Statement of Responsibility

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