Results 231 to 240 of about 125,674 (260)
Some of the next articles are maybe not open access.
Bailliere's clinical haematology, 1997
The BCR-ABL hybrid gene, the main product of the t(9;22)(q34;q11) translocation, is found in the leukaemic clone of at least 95% of CML patients. The fusion protein encoded by BCR-ABL varies in size, depending on the breakpoint in the BCR gene. Three breakpoint cluster regions have been characterized to date: major (M-bcr), minor (m-bcr) and micro (mu ...
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The BCR-ABL hybrid gene, the main product of the t(9;22)(q34;q11) translocation, is found in the leukaemic clone of at least 95% of CML patients. The fusion protein encoded by BCR-ABL varies in size, depending on the breakpoint in the BCR gene. Three breakpoint cluster regions have been characterized to date: major (M-bcr), minor (m-bcr) and micro (mu ...
openaire +2 more sources
Blood, 2007
In Ph+ chronic myeloid leukemia (CML), the constitutively active Bcr-Abl kinase leads to the up-regulation and activation of multiple genes, which may subsequently result in the expression of leukemia-associated antigens. In this study, we investigated the immunogenicity of Bcr-Abl–regulated antigens by stimulating CD8+ T lymphocytes with autologous ...
Florian, Scheich +3 more
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In Ph+ chronic myeloid leukemia (CML), the constitutively active Bcr-Abl kinase leads to the up-regulation and activation of multiple genes, which may subsequently result in the expression of leukemia-associated antigens. In this study, we investigated the immunogenicity of Bcr-Abl–regulated antigens by stimulating CD8+ T lymphocytes with autologous ...
Florian, Scheich +3 more
openaire +2 more sources
2019
???????????????????????? 3???8 ?????????????? ???????????????????? ???????? bcr/abl ?????????????????? ?????????????? ?????????????? ??'?????????? ???????????? (108 ??????????????????????) ?? ?????????????? ???? ?????????????? ?????????????????????????? ???????????? ?? ???????????????? ?? ?????????????? M-bcr. ???????????????????????????? ???????? ?????
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???????????????????????? 3???8 ?????????????? ???????????????????? ???????? bcr/abl ?????????????????? ?????????????? ?????????????? ??'?????????? ???????????? (108 ??????????????????????) ?? ?????????????? ???? ?????????????? ?????????????????????????? ???????????? ?? ???????????????? ?? ?????????????? M-bcr. ???????????????????????????? ???????? ?????
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International journal of hematology, 1995
A strong association between the Philadelphia chromosome (Ph1) and chronic myelogenous leukemia (CML) suggests that the Ph1 translocation plays a significant role in pathogenesis of CML. For this reason, Ph1-positive leukemias have been well studied from the molecular, clinical and cell biological perspective.
T, Tauchi, H E, Broxmeyer
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A strong association between the Philadelphia chromosome (Ph1) and chronic myelogenous leukemia (CML) suggests that the Ph1 translocation plays a significant role in pathogenesis of CML. For this reason, Ph1-positive leukemias have been well studied from the molecular, clinical and cell biological perspective.
T, Tauchi, H E, Broxmeyer
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Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells
Nature Medicine, 1996B. Druker +7 more
semanticscholar +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
Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
Science, 2001M. Gorre +6 more
semanticscholar +1 more source
Der Einfluss von BCR-ABL auf STAT5 in BCR-ABL-positiven Leukämiezellen
2010[no abstract]
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