「MYELOID」の共起表現一覧(1語右で並び替え)
該当件数 : 52件
chest weakness, anaemia, some suppression of | myeloid activity and abdominal pains. |
Myeloid and erythroid nuclear termination stage-speci | |
gene is expressed in B-cell but not T-cell or | myeloid cell lines. |
greatly induced under conditions suitable for | myeloid cell differentiation. |
e and rat suggest that this gene may regulate | myeloid cell activity and delivers an inhibitory sign |
, endothelial cells, platelets, monocytes and | myeloid cell lines, blood T-lymphocytes and B-lymphoc |
h affinity counter-receptor for P-selectin on | myeloid cells and stimulated T lymphocytes. |
is reported to promote survival of progenitor | myeloid cells through the insulin receptor substrate- |
rotein is responsible for preventing immature | myeloid cells from differentiating into more mature c |
kin grafts upon ligation of CD200 receptor on | myeloid cells |
inhibitory CD32B is expressed on B cells and | myeloid dendritic cells. |
ene suggest that this interaction may control | myeloid function in a tissue-specific manner. |
Spi-1 regulates | myeloid gene expression during haemopoietic developme |
in mammals, CALM, (Clathrin-assembly lymphoid | myeloid leukaemia protein) is named after its associa |
are among the most common mutations in acute | myeloid leukaemia due to internal tandem duplication |
bine is mainly used in the treatment of acute | myeloid leukaemia, acute lymphocytic leukaemia (ALL) |
ncipal use is in acute leukaemias and chronic | myeloid leukaemia. |
ced that Todd had been diagnosed with chronic | myeloid leukaemia. |
under development for the treatment of acute | myeloid leukaemia. |
-inducing agent in malignant glioma and acute | myeloid leukaemia. |
ity to induce the terminal differentiation of | myeloid leukaemic cells. |
to be administered in the diagnosis of acute | myeloid leukemia to demonstrate that the leukemic cel |
A potential link to leukemia including acute | myeloid leukemia has also been described. |
hibitor undergoing clinical studies for acute | myeloid leukemia (AML) and myelodysplastic syndrome ( |
being investigated for the treatment of acute | myeloid leukemia (AML) and myelodysplastic syndrome ( |
s of age and older with newly diagnosed acute | myeloid leukemia (AML). |
CR-ABL inhibitor for the treatment of chronic | myeloid leukemia (CML). |
When diagnosed with acute | myeloid leukemia and informed that traditional treatm |
by Seattle Genetics as a treatment for acute | myeloid leukemia (AML), a condition which results in |
exemplified by their treatment-related acute | myeloid leukemia (AML), which is uncommon for antimet |
mmer for The Brakes, was diagnosed with acute | myeloid leukemia in August, 2007 and he died on May 4 |
cell surface antigen expressed by CD34+ acute | myeloid leukemia cell lines, T-cell lines, activated |
may increase risk for myelofibrosis and acute | myeloid leukemia in the long term. |
or of Bcr-Abl kinase induces death of chronic | myeloid leukemia (CML) cells.This work led to the dev |
s laevis proteins Xr1 and Xr11; human induced | myeloid leukemia cell differentiation protein MCL1 an |
it was reported that Burr was diagnosed with | myeloid leukemia, which may require a bone marrow tra |
ancer, mostly metastatic breast cancer, acute | myeloid leukemia, and non-Hodgkin's lymphoma. |
In acute | myeloid leukemia, especially in the M2 subtype, the t |
is a common site of retroviral integration in | myeloid leukemia, and may function as a leukemia dise |
ing this gene have been associated with acute | myeloid leukemia. |
has an inherent risk of transforming to acute | myeloid leukemia. |
his receptor is restricted to the surfaces of | myeloid lineage cells and the receptor-substrate inte |
mbrane glycoprotein present on the surface of | myeloid lineage cells such as neutrophils, monocytes, |
against JAK2 for relapsed lymphoma, advanced | myeloid malignancies, myelofibrosis and CIMF |
l abnormality associated with therapy-related | myeloid malignancies. |
cythemia vera, essential thrombocythemia, and | myeloid metaplasia with myelofibrosis. |
He died in 1967 of | myeloid metaplasia, a rare blood disease. |
xpression also occur in certain cell lines of | myeloid origin (e.g. the immature myeloid cell lines |
They differentiate from | myeloid precursor cells in response to the cytokines |
nduction of growth arrest and/or apoptosis of | myeloid precursor cells |
1), although the underlying genetic defect in | myeloid precursor cells is not entirely elucidated, m |
T cells, activated B cells, some thymocytes, | myeloid precursors, and oligodendrocytes that associa |
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