ライフサイエンスコーパス: tumor bed

1 Gy to regional lymphatics; 54 to 59.4 Gy to tumor bed).

2 the depletion of regulatory T cells from the tumor bed.

3 egib but with an enlarging papule within the tumor bed.

4 activity and altered vascularization in the tumor bed.

5 DCs in the enrichment of Th17-1 cells in the tumor bed.

6 pid neutrophil infiltration into the treated tumor bed.

7 d and neck frequently recurs in the original tumor bed.

8 th extravasation of red blood cells into the tumor bed.

9 on of activated antitumor T cells within the tumor bed.

10 mbination of surgery, followed by PDT of the tumor bed.

11 n and received a dose of > or = 60 Gy to the tumor bed.

12 ause of the presence of methemoglobin in the tumor bed.

13 ly eliminates MDSC in the spleen, blood, and tumor beds.

14 R9(+)CXCR3(+)CD4(+) T lymphocytes into mouse tumor beds.

15 d with pal-prot A and injected directly into tumor beds.

16 = 3 points; less than 10% residual tumor per tumor bed = 1 point; 10% to 50% residual tumor per tumor

17 bed = 1 point; 10% to 50% residual tumor per tumor bed = 2 points; and greater than 50% residual tumo

18 nts; and greater than 50% residual tumor per tumor bed = 3 points.

19 The use of a radiotherapy (RT) boost to the tumor bed after whole-breast RT (WBRT) for ductal carcin

20 ranges that would deliver 95% of the maximum tumor BED, allowing for informed inclusion of clinical c

21 Conformal treatment to the tumor bed allows for significant sparing of critical str

22 rstitial implant to deliver radiation to the tumor bed alone over 4 to 5 days seems to produce 5-year

23 ubstantially protracted retention within the tumor bed and a 36-fold increase in CT contrast 4 h post

24 OT-1 cells identified within the tumor bed and draining lymph nodes of the HSV.4-1BBL-sti

25 elves quickly and extensively throughout the tumor bed and migrate uniquely in juxtaposition to widel

26 is a major obstacle for drug delivery to the tumor bed and plays a crucial role in pancreatic cancer

27 nt time, enables direct visualization of the tumor bed and surrounding critical structures, and costs

28 thereby increasing the effective dose to the tumor bed (and therefore local control) without signific

29 cessary for priming naive T cells within the tumor bed, and demonstrate the importance of DC activati

30 0005) of foci of microvascularity within the tumor bed at 8-T MR imaging.

31 d-dose craniospinal irradiation (CSI) plus a tumor bed boost versus treatments that deliver higher CS

32 Treatment with reduced-dose CSI plus a tumor bed boost was associated with preserved intellectu

33 like antigen-presenting cells (APC) into the tumor bed, but not into lymphoid organs.

34 Radiation therapy (RT) restricted to the tumor bed, by means of an interstitial implant, and last

35 rgeted therapies, radiation delivered to the tumor bed can prompt phenotypic changes in both normal s

36 entages of Ly-6C+ OT-1/GFP in the spleen and tumor bed compared with controls.

37 n of peptide amount and activity for maximal tumor BED, considering the additional constraint of a re

38 Their high secretion of IL9 and IL21 in the tumor bed contributes to their anticancer functions.

39 findings suggest that a DCIS RT boost to the tumor bed could be considered to provide an added increm

40 doses ranged from 23.4 to 39.6 Gy, and total tumor bed doses ranged from 54 to 59.4 Gy.

41 lly improves nano-drug delivery into treated tumor beds due to enhanced vascular permeability.

42 slower, which is consistent with the known "tumor bed effect." For similar size tumors, recurrences

43 y more rapidly than wild-type lymphocytes at tumor beds expressing PD-1 ligand (CD274), and these dif

44 consider the role of an accelerated and more tumor bed-focused course of radiotherapy.

45 red thirty-six (93%) received a boost to the tumor bed for a median total dose of 60.4 Gy.

46 percent of patients received a boost to the tumor bed, for a median total dose of 60.4 Gy.

47 concomitant boost of 0.5 Gy delivered to the tumor bed, for a total dose of 48 Gy to the lumpectomy s

48 ntraoperative tissue biopsies from tumor and tumor bed from 50 patients undergoing surgical resection

49 ural killer T (NKT) cells from the blood and tumor bed in 23 patients with premalignant gammopathy, n

50 type (Langerin(+)), were retained within the tumor bed in 32/32 samples and (b) mature DCs, CD83(+)DC

51 nant breast tumors in 49 patients to tag the tumor bed in anticipation of complete or almost complete

52 problem of preoperative localization of the tumor bed in complete or nearly complete response of bre

53 some reports described their presence in the tumor bed in mice and humans.

54 es) and increased CD8(+) T effector cells in tumor bed in part by modulating TGF-beta1 production.

55 was seen for breast shrinkage, breast edema, tumor bed induration, or pigmentation.

56 luding exposure of the animals to 10% O2 and tumor bed irradiation.

57 kines and costimulatory molecules within the tumor bed may elaborate a more optimal antitumor respons

58 nhance tumor-infiltrating lymphocytes in the tumor bed may substantially augment clinical immunothera

59 First sites of relapse were lung (n = 5), tumor bed (n = 4), and abdomen (n = 2), with one metachr

60 rolling the preferential accumulation in the tumor bed of a peculiar subset of gammadeltaT17 cells di

61 nt NKT cells are detectable in the blood and tumor bed of all cohorts.

62 gnificant squamous cell carcinoma within the tumor bed of locally advanced basal cell carcinoma found

63 e setting of clinical tumor progression, the tumor bed of myeloma patients contains T cells that can

64 y isolated NKT cells from both the blood and tumor bed of patients with progressive disease, but not

65 re seen in the peripheral blood, spleen, and tumor bed of the HSV.4-1BBL-stimulated OT-1/GFP group co

66 The entire tumor beds of the resected specimens were evaluated hist

67 Tumor BED optimization results were calculated and plott

68 The planning target volume was the tumor bed plus a 1-2-cm margin defined at postmastectomy

69 se (NOS) II expression can be induced in the tumor bed, predominantly in host cells that infiltrate a

70 at the delivery of CpG ODN directly into the tumor bed reduces the immunosuppressive activity of mono

71 rovide evidence that driving NK cells to the tumor bed relied on the ability of autophagy-defective t

72 rence, defined as recurrence in the original tumor bed, retroperitoneum, or within the abdominal cavi

73 t (largest focus, 0.3 cm), located in a 3-cm tumor bed showing treatment effect (Figs 1A to 1C).

74 These findings suggest that a tumor bed sterilization approach may be promising for lo

75 el and shows that PDT combined with surgery (tumor bed sterilization) gave significant local control

76 sa (PF) boost (n=51), standard-dose CSR plus tumor bed (TB) boost (n=9), reduced-dose CSR plus PF boo

77 ith areas of low signal intensity within the tumor bed ("tumoral pseudoblush") at MR imaging, were pr

78 lumpectomy followed by RT restricted to the tumor bed using an interstitial implant.

79 (23.4 Gy) followed by 55.8 Gy to the primary tumor bed using three-dimensional conformal technique, a

80 The tumor bed was imaged at computed tomography (CT) in the

81 59.4 Gy were prescribed to the postoperative tumor bed with a 10-mm clinical target volume margin.