ライフサイエンスコーパス: bone marrow toxicity

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1 gBRCA mutations or HRD status, with moderate bone marrow toxicity.

2 r frequencies and resistance to 5-FU-induced bone marrow toxicity.

3 ses beyond those levels which produce severe bone marrow toxicity.

4 locyte colony-stimulating factor to minimize bone marrow toxicity.

5 Ci/m2 of 125I-mAb A33 did not cause bowel or bone marrow toxicity.

6 = 0.009), generally for gastrointestinal or bone marrow toxicity.

7 ality associated with neutropenia and marked bone marrow toxicity.

8 ns to other participants, but none developed bone-marrow toxicity.

9 Cs may be responsible for increased risks of bone marrow toxicity and leukemia.

10 appears generally limited to mild transient bone marrow toxicity and xerostomia because of uptake of

11 Bone-marrow toxicity as a consequence of chronic irradia

12 ty profile, including no genotoxicity and no bone marrow toxicity at the highest evaluated concentrat

13 However, bone marrow toxicity during cyclophosphamide treatment o

14 ations for the use of mouse models to assess bone marrow toxicity for DNA-damaging agents and inhibit

15 ceiving combined MMF and tacrolimus therapy; bone marrow toxicity in 24% of recipients receiving MMF

16 or migration in vitro and AHR ligand-induced bone marrow toxicity in vivo.

17 Bone marrow toxicity is a dose-limiting side effect of c

18 ,12-dimethylbenz[a]anthracene (DMBA)-induced bone marrow toxicity is p53-dependent in vivo.

19 late-onset CMV disease, viral resistance and bone marrow toxicity limited enthusiasm for longer durat

20 doses to tumors without exceeding kidney and bone marrow toxicity limits.

21 Bone marrow toxicity, manifested primarily by anemia and

22 We therefore conclude that bone marrow toxicity may be mediated by CYP1B1-dependent

23 prior to chemotherapy, the magnitude of the bone marrow toxicity nadir was minimized, even with BSO-

24 oned children, may itself participate in the bone marrow toxicity produced by this metal.

25 used with (131)I-tositumomab results in less bone marrow toxicity than does the weight-based dosing r

26 y, but their usefulness is limited by severe bone marrow toxicity that causes the cumulative depletio

27 represents a promising approach to overcome bone marrow toxicity, the limiting factor for most high-

28 Bone marrow toxicity was dose-limiting and dependent on

29 esoporphyrin did not display any significant bone marrow toxicity when used at similar concentrations

30 de phosphate (2-fold) accompanied by greater bone marrow toxicity, whereas the acute toxicity of sodi

31 major limiting factor with this modality is bone marrow toxicity, which arises from the penetrating

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