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 rapy, in addition to >=90% TR in the primary tumor bed.

3 ologic response between the ILN and the TLND tumor bed.

4 tice is to harvest margins for IFSH from the tumor bed.

5 rom tumors recruit nociceptor neurons to the tumor bed.

6 The boost dose was 55.8 Gy to the tumor bed.

7 bute to increased electrical activity in the tumor bed.

8 intratumoral nerves remain functional at the tumor bed.

9 sal vascular architecture within the treated tumor bed.

10 activity and altered vascularization in the tumor bed.

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

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

13 tory macrophage levels were decreased in the tumor bed.

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

15 pid neutrophil infiltration into the treated tumor bed.

16 ce molecules likely directs axons toward the tumor bed.

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

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

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

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

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

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

23 tions plus 10 Gy in 5 fractions boost to the tumor bed.

24 d l-Arginase activity and IL-10 secretion at tumor beds.

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

26 ne by recruiting CD8+ cytotoxic T cells into tumor beds.

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

28 mmunosuppressive M2-polarized macrophages at tumor beds.

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

30 l: 0.71 +/- 0.21 vs 0.61 +/- 0.21, P < .001; tumor bed: 0.61 +/- 0.17 vs 0.52 +/- 0.17, P = .001) and

31 = 3 points; less than 10% residual tumor per tumor bed = 1 point; 10% to 50% residual tumor per tumor

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

33 l: 1.00 +/- 0.35 vs 1.62 +/- 0.59, P < .001; tumor bed: 2.45 +/- 0.99 vs 2.69 +/- 1.05, P = .03) and

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

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

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

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

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

39 and IgA-producing PCs disseminated into the tumor beds along fibroblastic tracks.

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

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

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

43 was examined by percentage TR in the primary tumor bed and pathologic nodal stage (ypN0) using Kaplan

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

45 ed by tumor cells recruit myeloid cells into tumor bed and reprogram infiltrating myeloid cells into

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

47 but not naive CD4(+) T cells, induced TLS at tumor beds and decreased tumor growth.

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

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

50 0005) of foci of microvascularity within the tumor bed at 8-T MR imaging.

51 al and internal rectal wall contours and the tumor bed at each level and defining eight point-based l

52 wafers releasing BCNU (Gliadel(R)) into the tumor bed at the time of surgical removal of the tumor.

53 thout the use of intravenous contrast of the tumor bed before definitive surgery.

54 (APBI arm) and 50 Gy in 25 fractions with a tumor bed boost (WBI arm) after breast-conserving surger

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

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

57 th 36 Gy craniospinal irradiation plus 54 Gy tumor-bed boost used in ACNS0122.

58 hom intensified treatment strategies such as tumor-bed boost, and possibly regional nodal RT, should

59 as 30.6 Gy whole ventricular field and 54 Gy tumor-bed boost, compared with 36 Gy craniospinal irradi

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

61 over, the MAREMO peptide largely subdues the tumor bed by depleting fibroblasts, repressing tenascin-

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

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

64 zed opportunities for dose escalation to the tumor bed, capabilities that promise to hasten the trans

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

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

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

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

69 ts were grouped by margin assessment method (tumor bed [defect] or resection specimen sampling).

70 tients had significantly larger preoperative tumor bed diameters (difference, 28%; 95% CI, 14%-43%; P

71 ot have significantly different preoperative tumor bed diameters compared with patients with private

72 favorable both during transection and in the tumor bed directly after resection.

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

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

75 en quantified accessible PD-L1 levels in the tumor bed during treatment with anti-PD-1 and anti-PD-L1

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

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

78 ternal and internal rectal wall contours and tumor bed (external: 0.56 +/- 0.25 vs 1.68 +/- 0.56, res

79 ternal and internal rectal wall contours and tumor bed (external: 0.95 +/- 0.03 vs 0.86 +/- 0.04, res

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

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

82 dose deviation to heart, lungs, breasts, and tumor bed for each patient's supine and prone plan.

83 63-Gy simultaneously integrated boost to the tumor bed for patients younger than 60 years.

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

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

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

87 Although tumor bed IFSH is widely used in the management of oral

88 be associated with the inherent inability of tumor bed IFSH margin analysis to accurately account for

89 covalently-bound paclitaxel implanted in the tumor bed, immediately after resection of human cell lin

90 sity of tumor treating fields (TTF) within a tumor bed improves clinical efficacy, but reaching suffi

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

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

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

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

95 is useful in detecting tumor in the primary tumor bed in locally advanced rectal cancer (LARC) after

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

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

98 eased migration of cytotoxic immune cells to tumor beds in xenograft models and patient tumors.

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

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

101 margins, methods for assessment, specimen vs tumor bed margin evaluation, and re-resection of positiv

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

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

104 section histopathology (IFSH) taken from the tumor bed, may have limitations in accuracy.

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

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

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

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

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

110 al blood, normal-appearing brain tissue, and tumor bed of nine treatment-naive patients with GBM.

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

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

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

114 Tumor BED optimization results were calculated and plott

115 or potential tertiary lymphoid structures in tumor beds or surrounding tumor edges.

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

117 nt accumulation of T, B, and plasma cells at tumor beds predicted better survival.

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

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

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

121 "cold" tumors, reduced T cell exhaustion in tumor beds, restricted generation of tumor-associated my

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

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

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

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

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

127 ed accuracy of %RVT calculation when reduced tumor bed (TB) was examined and leverage these results p

128 Tumor or tumor bed tissue was collected whenever possible pre-tre

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

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

131 (23.4 Gy) followed by 55.8 Gy to the primary tumor bed using three-dimensional conformal technique, a

132 ever, the prognostic value of intraoperative tumor bed vs resection specimen sampling is not well def

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

134 ponse (rCR)-defined as no enhancement in the tumor bed-was evaluated for predicting pCR.

135 59.4 Gy were prescribed to the postoperative tumor bed with a 10-mm clinical target volume margin.