Results 111 to 120 of about 1,603 (142)
Some of the next articles are maybe not open access.
2019
???????????????????????? 3???8 ?????????????? ???????????????????? ???????? bcr/abl ?????????????????? ?????????????? ?????????????? ??'?????????? ???????????? (108 ??????????????????????) ?? ?????????????? ???? ?????????????? ?????????????????????????? ???????????? ?? ???????????????? ?? ?????????????? M-bcr. ???????????????????????????? ???????? ?????
openaire +3 more sources
???????????????????????? 3???8 ?????????????? ???????????????????? ???????? bcr/abl ?????????????????? ?????????????? ?????????????? ??'?????????? ???????????? (108 ??????????????????????) ?? ?????????????? ???? ?????????????? ?????????????????????????? ???????????? ?? ???????????????? ?? ?????????????? M-bcr. ???????????????????????????? ???????? ?????
openaire +3 more sources
Malignant transformation by abl and BCR/ABL
1993Activated abl oncogenes have been implicated in causing pre-B lymphoma in mice via Abelson murine leukemia virus, fibrosarcoma in cats via Hardy-Zuckerman feline sarcoma virus II, and, through the Philadelphia chromosome, are linked with the myeloproliferative syndrome chronic myelogenous leukemia and with acute lymphoid and myeloid leukemia in humans.
openaire +2 more sources
Bailliere's clinical haematology, 1997
The 1982 discovery that in chronic myeloid leukaemia (CML) the ABL proto-oncogene is translocated to the BCR gene located on chromosome 22 initiated many studies on the structural organization and function of these genes. The nucleotide sequence of the entire BCR and major parts of the ABL gene has now been determined.
J, Groffen, N, Heisterkamp
openaire +1 more source
The 1982 discovery that in chronic myeloid leukaemia (CML) the ABL proto-oncogene is translocated to the BCR gene located on chromosome 22 initiated many studies on the structural organization and function of these genes. The nucleotide sequence of the entire BCR and major parts of the ABL gene has now been determined.
J, Groffen, N, Heisterkamp
openaire +1 more source
2006
The hallmark of chronic myelogenous leukemia (CML) is the expression of Bcr-Abl, a constitutivelyactive form of the Abl tyrosine kinase. Imatinib, a 2-phenyl aminopyrimidine Bcr-Abl inhibitor developedby Novartis and marketed under the tradename of Gleevec (Glivec), is highly effective in treating CML patientswith early stage disease. However, patients
openaire +1 more source
The hallmark of chronic myelogenous leukemia (CML) is the expression of Bcr-Abl, a constitutivelyactive form of the Abl tyrosine kinase. Imatinib, a 2-phenyl aminopyrimidine Bcr-Abl inhibitor developedby Novartis and marketed under the tradename of Gleevec (Glivec), is highly effective in treating CML patientswith early stage disease. However, patients
openaire +1 more source
2017
We report the results of BCR/ABL translocation analysis on interphase leukemic cells of 33 acute myeloid leukemia (AML) patients by fluorescence in situ hybridization. Of these, there were 13 persons exposed to ionizing radiation due to the Chernobyl accident with radiation-associated AML and 20 patients with spontaneous disease.
openaire +1 more source
We report the results of BCR/ABL translocation analysis on interphase leukemic cells of 33 acute myeloid leukemia (AML) patients by fluorescence in situ hybridization. Of these, there were 13 persons exposed to ionizing radiation due to the Chernobyl accident with radiation-associated AML and 20 patients with spontaneous disease.
openaire +1 more source
Involvement of Jak2 tyrosine phosphorylation in Bcr–Abl transformation
Oncogene, 2001Shanhai Xie +2 more
exaly