WordNet

(genetics) a segment of DNA that is involved in producing a polypeptide chain; it can include regions preceding and following the coding DNA as well as introns between the exons; it is considered a unit of heredity; "genes were formerly called factors" (同)cistron, factor
the 22nd letter of the Roman alphabet (同)v
informal term for information; "give me the gen on your new line of computers"

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1. 慢性骨髄性白血病の細胞生物学および分子生物学 cellular and molecular biology of chronic myeloid leukemia
2. 慢性骨髄性白血病の分子遺伝学 molecular genetics of chronic myeloid leukemia
3. 血液悪性腫瘍およびリンパ悪性腫瘍の遺伝的異常 genetic abnormalities in hematologic and lymphoid malignancies
4. 急性骨髄性白血病の分子遺伝学 molecular genetics of acute myeloid leukemia
5. 好中球増多症の原因 causes of neutrophilia

A novel mouse model identifies cooperating mutations and therapeutic targets critical for chronic myeloid leukemia progression.

Giotopoulos G1, van der Weyden L2, Osaki H1, Rust AG3, Gallipoli P1, Meduri E1, Horton SJ1, Chan WI1, Foster D1, Prinjha RK4, Pimanda JE5, Tenen DG6, Vassiliou GS7, Koschmieder S8, Adams DJ2, Huntly BJ9.
The Journal of experimental medicine.J Exp Med.2015 Aug 24. pii: jem.20141661. [Epub ahead of print]
The introduction of highly selective ABL-tyrosine kinase inhibitors (TKIs) has revolutionized therapy for chronic myeloid leukemia (CML). However, TKIs are only efficacious in the chronic phase of the disease and effective therapies for TKI-refractory CML, or after progression to blast crisis (BC),
PMID 26304963

Bagca BG1, Ozalp O, Kurt CC, Mutlu Z, Saydam G, Gunduz C, Avci CB.
Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine.Tumour Biol.2015 Aug 23. [Epub ahead of print]
Ruxolitinib is the first agent used in myelofibrosis treatment with its potent JAK2 inhibitory effect. In this novel study, we aimed to discover the anti-leukemic effect of ruxolitinib in K-562 human chronic myeloid leukemia cell line compared to NCI-BL 2171 human healthy B lymphocyte cell line. Cyt
PMID 26298727

Genetic variations of hOCT1 gene and CYP3A4/A5 genes and their association with imatinib response in Chronic Myeloid Leukemia.

Vaidya S1, Ghosh K1, Shanmukhaiah C2, Vundinti BR3.
European journal of pharmacology.Eur J Pharmacol.2015 Aug 21;765:124-130. doi: 10.1016/j.ejphar.2015.08.034. [Epub ahead of print]
There is an increasing body of evidence demonstrating that mechanisms independent of BCR/ABL gene also contribute to imatinib resistance in Chronic Myeloid Leukemia (CML). It has been extensively reported that polymorphisms of the genes associated with imatinib metabolization and imatinib influx/eff
PMID 26300393