ライフサイエンスコーパス: chemoresistant

1 an self-renew and are highly tumorigenic and chemoresistant.

2 ion effects, and patients bearing Mt p53 are chemoresistant.

3 ial to mediate tumor regrowth are relatively chemoresistant.

4 which are frequently radiation-resistant and chemoresistant.

5 ids colonization and renders the tumor cells chemoresistant.

6 with either chemosensitive (50 patients) or chemoresistant (44 patients) relapse, including 22 who f

7 ci at 4092 genes becoming hypermethylated in chemoresistant A2780/cp70 compared with the parental-sen

8 potential importance of WIT-1 methylation in chemoresistant AML.

9 Apaf-1-negative melanomas are invariably chemoresistant and are unable to execute a typical apopt

10 ease progression at 1 year for patients with chemoresistant and chemosensitive disease were 75% and 2

11 -arr1, ARRB1) links Wnt signaling to acquire chemoresistant and EMT phenotype.

12 isolated from ovarian cancer cell lines were chemoresistant and preferentially grew tumors, compared

13 r Notch, but these cells are also relatively chemoresistant and provide trophic support to neuroendoc

14 erexpressed in many human cancers, including chemoresistant and radioresistant breast cancer cells, b

15 herapies may be missing the subpopulation of chemoresistant and radioresistant cancer stem cells (CSC

16 Adult T-cell leukemia (ATL) is a highly chemoresistant and usually fatal T-cell malignancy due t

17 irst 3 years for the chemosensitive relapse, chemoresistant, and induction failure groups were 61%, 4

18 tiple stem cell characteristics, were highly chemoresistant, and were enriched in xenografts residual

19 CK5-positive cells were chemoresistant as determined by fourfold reduced rate of

20 of DNA-PKcs in vivo resensitizes inherently chemoresistant ATM-deficient tumors to genotoxic chemoth

21 timal tri-drug combination in eight distinct chemoresistant bladder cancer cell lines.

22 Malignant gliomas are highly invasive and chemoresistant brain tumors with extremely poor prognosi

23 (TNBC), contributing to the maintenance of a chemoresistant breast cancer stem cell (BCSC) population

24 eatures, and may arise from an earlier, more chemoresistant breast epithelial precursor than basal-li

25 splantation (NMAT) infrequently cures active chemoresistant, bulky, or aggressive B-cell lymphoma (B-

26 Low-grade serous carcinoma of the ovary is chemoresistant but mutations in the MAPK pathway could b

27 PSP94 peptide derivative PCK3145 suppresses chemoresistant cancer cell and tumor growth in vitro and

28 TT and cellular HDAC assays on sensitive and chemoresistant cancer cell lines as well as HDAC profili

29 acious therapeutics against solid tumors and chemoresistant cancer cell lines.

30 e protein, ABCG2, is up-regulated in certain chemoresistant cancer cells and in the mammary gland dur

31 in rapid loss of this prosurvival protein in chemoresistant cancer cells.

32 incurable due to the inability to eradicate chemoresistant cancer stem-like cells (sCSC) that are li

33 lanoma is a highly aggressive and frequently chemoresistant cancer, the incidence of which continues

34 rationally designed therapy for metastatic, chemoresistant cancers and might overcome the problems a

35 In contrast, chemoresistant cancers and normal tissues were poorly pr

36 p53 mutations often occur in aggressive and chemoresistant cancers but are rarely observed in melano

37 have potential therapeutic implications for chemoresistant cancers, especially of brain tumours wher

38 n D1 is observed in many aggressive forms of chemoresistant cancers, these findings provide insight i

39 ts of targeting RAD6 with SMI#9 for managing chemoresistant cancers.

40 lanoma represent biologically aggressive and chemoresistant cancers.

41 grafts to generate paired chemosensitive and chemoresistant cancers.

42 ce that this agent can preferentially target chemoresistant CD133(+) cells with CSC character in SCLC

43 tumours at relapse following chemotherapy or chemoresistant cell lines derived at the time of patient

44 tients, and alternative approaches to target chemoresistant cells are needed.

45 oma bulk populations and indicate that these chemoresistant cells can be specifically targeted via AB

46 restingly, direct delivery of ATP into cross-chemoresistant cells destabilized HIF-1alpha and inhibit

47 d not survive glucose deprivation, while the chemoresistant cells displayed adaptability.

48 These chemoresistant cells exhibited a corresponding upregulat

49 d it represents hematopoietic stem cells and chemoresistant cells from several solid tumors.

50 genotoxic drug treatment favors selection of chemoresistant cells in genetically heterogeneous tumors

51 de evidence that SP is an enriched source of chemoresistant cells in human melanomas, and suggest tha

52 3K activation can lead to the development of chemoresistant cells in prostatic carcinomas through the

53 oxygen species (ROS)-mediated death of even chemoresistant cells independently of p53 status.

54 Chemoresistant cells must consume excess resources to ma

55 MCAM depletion in chemoresistant cells reduced cell proliferation and redu

56 ed that MCAM modulated lactate production in chemoresistant cells that exhibit a distinct metabolic p

57 In tumours, accumulation of chemoresistant cells that express high levels of anti-ap

58 tion, which serves to maintain slow cycling, chemoresistant cells through an IL1beta/IL8/CXCR1 cytoki

59 Inhibition of Akt is required to sensitize chemoresistant cells to CDDP in a p53-dependent manner,

60 e C-terminal GSN fragment (C-GSN) sensitized chemoresistant cells to CDDP, intact GSN and its N-termi

61 y undergoing clinical evaluation, sensitized chemoresistant cells to cisplatin.

62 y proliferate at the expense of the less fit chemoresistant cells.

63 t which is known to favor the development of chemoresistant cells.

64 g also facilitated CDDP-induced apoptosis in chemoresistant cells.

65 Certain chemoresistant colon cancer cells are therefore exquisit

66 displayed a glycolytic phenotype while their chemoresistant counterparts (C200 and PEO4) exhibited a

67 vestigated CSC properties in newly developed chemoresistant CRC cell lines and sought to identify tar

68 Chemoresistant CRC cells are enriched for CSC markers an

69 ore effective therapy should target both the chemoresistant CSCs and the proliferating epithelial cel

70 nt, indicating that paclitaxel enrichment of chemoresistant CSCs is less dependent on microenvironmen

71 scription modulator that is overexpressed in chemoresistant, diffuse large B-cell lymphomas (DLBCLs).

72 eous blocks in both pathways correlated with chemoresistant disease (92% of patients with chemoresist

73 Adverse OS was associated with chemoresistant disease (relative risk [RR], 2.9), more t

74 Resurgence of chemoresistant disease after primary therapy typifies ep

75 ith high-grade NHL, mantle cell lymphoma, or chemoresistant disease had a poor outcome.

76 However, chemoresistant disease is still problematic.

77 ugh their contribution in development of the chemoresistant disease remains elusive.

78 OS were 42% and 55%, whereas for those with chemoresistant disease the PFS and OS were 22% and 29%.

79 chemoresistant disease (92% of patients with chemoresistant disease versus 33% of patients with chemo

80 nitial therapy but is prone to relapses with chemoresistant disease, indicating the need for novel th

81 nal non-operable patients with recurrent and chemoresistant disease.

82 vanced-stage patients relapse and succumb to chemoresistant disease.

83 and that such expression may be a marker of chemoresistant disease.

84 l metastasis and about 50% will relapse with chemoresistant disease.

85 typically followed by recurrence with lethal chemoresistant disease.

86 lethal gynecological cancer, often leads to chemoresistant diseases.

87 VEGF receptors, reduced proliferation of the chemoresistant EOC cells through induction of G2/M cell

88 Investigations in clinical specimens of chemoresistant EOC tissues confirmed increased recruitme

89 potential of dacomitinib in treatment of the chemoresistant EOC.

90 bitors have demonstrated limited activity in chemoresistant EOC.

91 diffuse large B cell lymphoma (ABC-DLBCL), a chemoresistant form of DLBCL.

92 ly chemosensitive, but rapidly relapses in a chemoresistant form with an overall survival of <5%.

93 rgeted therapeutic agents for metastatic and chemoresistant gestational trophoblastic neoplasia.

94 ited the proliferation of chemosensitive and chemoresistant glioma cells but did not display toxicity

95 e, we report higher gelsolin (GSN) levels in chemoresistant gynecological cancer cells compared with

96 In chemoresistant hepatospheres, CD47 was found to be up-re

97 ol with mechanistic rationale against highly chemoresistant human PaC cells.

98 Because NSCLC is highly chemoresistant, it is, usually not treatable.

99 ilostamide, causes profound growth arrest of chemoresistant KM12C colon cancer cells.

100 in a subset of NB cell lines, including the chemoresistant LA-N-6 cell line.

101 ide but in almost every case becomes rapidly chemoresistant, leading to death within 1 year.

102 a promising strategy to target and eliminate chemoresistant leukemic cells.

103 agents) could favor elimination of residual chemoresistant lymphoma cells.

104 as an adjuvant therapy for the treatment of chemoresistant malignancies, and highlight the utility o

105 n hormone therapy resistant (MDA-MB-231) and chemoresistant (MCF-7TN-R) breast cancer cells.

106 s P-gp expression and is associated with the chemoresistant mechanisms of metastatic human breast can

107 cancer cell lines (MDA-MB-231) to study the chemoresistant mechanisms regulated by miRNAs.

108 hich points to the existence of a relatively chemoresistant melanoblast-like cell population residing

109 ed for cytotoxic activity against a panel of chemoresistant melanoma cell lines, and it was found tha

110 nd inducer of cell death in otherwise highly chemoresistant melanoma cells.

111 stigating nanoparticle treatment options for chemoresistant melanomas.

112 or, primary (testicular and mediastinal) and chemoresistant metastatic human GCTs, we show that the p

113 Persistence of chemoresistant minimal residual disease (MRD) plasma cel

114 Multiple chemoresistant models demonstrated suppression of SLFN11

115 rapeutic efficacy in both chemosensitive and chemoresistant models of small cell lung cancer.

116 in several types of cancer cells, including chemoresistant multiple myeloma (MM) cells.

117 ts, but these are short-lived because of the chemoresistant nature of hormone-refractory prostate can

118 e-independent, and likely contributes to the chemoresistant nature of RCCs.

119 Blocking Y5R in chemoresistant NB cells rich in this receptor sensitized

120 gue AN-238 provides an effective therapy for chemoresistant neoplasms such as RCC.

121 d 1 mg/kg/day for 28 days) were evaluated in chemoresistant neuroblastoma-bearing mice and compared w

122 of cancer stem cells markers and sensitized chemoresistant OC cells to carboplatin.

123 ide leverage to treat ovarian cancer that is chemoresistant on the basis of ineffective apoptosis.

124 herefore, it would be beneficial to identify chemoresistant or refractory patients early during thera

125 DM2-overexpressing cancer cells are commonly chemoresistant, our findings suggest that this naturally

126 high abundance from both chemosensitive and chemoresistant ovarian cancer cells via exosomes.

127 C down-regulation in both chemosensitive and chemoresistant ovarian cancer cells.

128 e the therapeutic utility of MePS2 siRNAs in chemoresistant ovarian cancer mouse models via targeting

129 s the PD-L1/PD-1 and CD80/CTLA-4 pathways in chemoresistant ovarian cancer.

130 to prevent the development of recurrent and chemoresistant ovarian cancer.

131 for the development of effective therapy for chemoresistant ovarian cancers.

132 of neoplasms, but particularly in recurrent chemoresistant ovarian carcinomas, suggesting a biologic

133 Lupeol significantly sensitized chemoresistant PaC cells to undergo apoptosis by recombi

134 ucine) as an adjuvant treatment to sensitize chemoresistant pancreatic cancer cells.

135 These miRNAs effectively suppressed chemoresistant patient-derived xenograft growth in vivo,

136 tients in chemosensitive relapse, and 7% for chemoresistant patients.

137 ognostically relevant in MM and may identify chemoresistant PCs in vitro.

138 d be already present at the MRD stage, where chemoresistant PCs show a singular phenotypic signature

139 tor in chemoresistant SCLC cell lines and in chemoresistant PDX compared with matched treatment-naive

140 ment of human ovarian cancer (OVCA), and the chemoresistant phenotype in OVCA cells is associated wit

141 tyrosine kinase activity is required for the chemoresistant phenotype of HER-2/neu-overexpressing NSC

142 NHL B-cell lines, resulting in reverting the chemoresistant phenotype to a sensitive phenotype.

143 the inability of Tie2 activation to induce a chemoresistant phenotype.

144 er cell line PA1 leads to an increase in the chemoresistant phenotype.

145 contribute to the development of a radio- or chemoresistant phenotype.

146 oxicity and thereby may contribute to a more chemoresistant phenotype.

147 ly modified histones, which correlate with a chemoresistant phenotype.

148 pithelial-mesenchymal transition (EMT) and a chemoresistant phenotype.

149 nt survival, effective treatments addressing chemoresistant recurrences are particularly needed.

150 Thus, our results establish a chemoresistant role for RIP1 that maintains inhibitor of

151 iously unexplored therapeutic target in this chemoresistant sarcoma.

152 s a markedly upregulated surface receptor in chemoresistant SCLC cell lines and in chemoresistant PDX

153 nt mutations was found to be associated with chemoresistant secondary lymphomas.

154 inhibited the growth of three of five lethal chemoresistant serous adenocarcinoma PDXa models without

155 strategy poised for testing in patients with chemoresistant serous ovarian cancer.

156 that TPCs can reversibly enter a quiescent, chemoresistant state and thereby underscore the need for

157 pies; however, essentially all progress to a chemoresistant state.

158 el molecular marker for a distinct subset of chemoresistant, stem cell phenotype-expressing tumor cel

159 Intriguingly, three metastatic and chemoresistant subclones, S2-CP9, S2-LM7AA, and S2-013,

160 , suppress proliferation of the less fit but chemoresistant subpopulations.

161 f pluripotency markers (NANOG and POU5F1) in chemoresistant teratomas or transformed carcinomas.

162 DKK4 and NOTCH signaling levels and are more chemoresistant than paired subcutaneous xenografts.

163 ay in TECs and converts naive tumor cells to chemoresistant TSCs, thereby facilitating their invasive

164 rug that, by inhibiting Tim16, may sensitize chemoresistant tumor cell to proapoptotic stimuli.

165 is largely attributed to the development of chemoresistant tumor cells.

166 re generally attributed to subpopulations of chemoresistant tumor cells.

167 cell renal cell cancer (CC-RCC) is a highly chemoresistant tumor characterized by frequent inactivat

168 sophageal adenocarcinoma is a heterogeneous, chemoresistant tumor for which the availability and size

169 ial for STI571 in patients afflicted by this chemoresistant tumor.

170 orubicin and cisplatin chemotherapy, and all chemoresistant tumors adopted a p53-like phenotype after

171 plastic breast cancers (MBC) are aggressive, chemoresistant tumors characterized by lineage plasticit

172 patients bear inoperable, locally advanced, chemoresistant tumors demonstrating the urgent need for

173 evance of these findings to the treatment of chemoresistant tumors in vivo has remained unclear.

174 d the superiority of metronomic protocols in chemoresistant tumors in vivoCancer Res; 77(17); 4723-33

175 lpha, the inhibitor of NF-kappaB, sensitizes chemoresistant tumors to the apoptotic potential of TNFa

176 making it an attractive anticancer agent for chemoresistant tumors with enhanced antiapoptotic activi

177 in tumors are among the most common and most chemoresistant tumors.

178 ncy of p53 mutations observed in this highly chemoresistant tumour type.

179 cer cells, including hormone-independent and chemoresistant types.

180 ncer stem cells (CSC) are hypothesized to be chemoresistant, we investigated CSC properties in newly

181 in the more chemosensitive WERI, but not the chemoresistant Y79 line.