戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 een in 27 patients; no patients had grade IV bone marrow toxicity.
2 ality associated with neutropenia and marked bone marrow toxicity.
3 r frequencies and resistance to 5-FU-induced bone marrow toxicity.
4 ses beyond those levels which produce severe bone marrow toxicity.
5 gBRCA mutations or HRD status, with moderate bone marrow toxicity.
6 locyte colony-stimulating factor to minimize bone marrow toxicity.
7 Ci/m2 of 125I-mAb A33 did not cause bowel or bone marrow toxicity.
8  = 0.009), generally for gastrointestinal or bone marrow toxicity.
9 ns to other participants, but none developed bone-marrow toxicity.
10     Camptothesome markedly reduced the acute bone marrow toxicity and gastrointestinal mucositis asso
11 Cs may be responsible for increased risks of bone marrow toxicity and leukemia.
12 assess the whole-body dose as a surrogate of bone marrow toxicity and tumor (absorbed) dose per unit
13  appears generally limited to mild transient bone marrow toxicity and xerostomia because of uptake of
14                                              Bone-marrow toxicity as a consequence of chronic irradia
15 ty profile, including no genotoxicity and no bone marrow toxicity at the highest evaluated concentrat
16                                     However, bone marrow toxicity during cyclophosphamide treatment o
17  significant hematologic, renal, hepatic, or bone marrow toxicity, even at high or repeated doses.
18 ations for the use of mouse models to assess bone marrow toxicity for DNA-damaging agents and inhibit
19 ceiving combined MMF and tacrolimus therapy; bone marrow toxicity in 24% of recipients receiving MMF
20 or migration in vitro and AHR ligand-induced bone marrow toxicity in vivo.
21                                              Bone marrow toxicity is a dose-limiting side effect of c
22 ,12-dimethylbenz[a]anthracene (DMBA)-induced bone marrow toxicity is p53-dependent in vivo.
23 late-onset CMV disease, viral resistance and bone marrow toxicity limited enthusiasm for longer durat
24 doses to tumors without exceeding kidney and bone marrow toxicity limits.
25                                              Bone marrow toxicity, manifested primarily by anemia and
26                   We therefore conclude that bone marrow toxicity may be mediated by CYP1B1-dependent
27  prior to chemotherapy, the magnitude of the bone marrow toxicity nadir was minimized, even with BSO-
28 oned children, may itself participate in the bone marrow toxicity produced by this metal.
29 used with (131)I-tositumomab results in less bone marrow toxicity than does the weight-based dosing r
30 y, but their usefulness is limited by severe bone marrow toxicity that causes the cumulative depletio
31  represents a promising approach to overcome bone marrow toxicity, the limiting factor for most high-
32                                              Bone marrow toxicity was dose-limiting and dependent on
33 esoporphyrin did not display any significant bone marrow toxicity when used at similar concentrations
34 de phosphate (2-fold) accompanied by greater bone marrow toxicity, whereas the acute toxicity of sodi
35  major limiting factor with this modality is bone marrow toxicity, which arises from the penetrating