ライフサイエンスコーパス: antitumoral

1 tion-induced cell death, indicating that the antitumoral action of pRb2/p130 can regulate both inhibi

2 rts the utility of LIPU/MB to potentiate the antitumoral activities of doxorubicin and aPD-1 for GBM.

3 ls and on the antioxidant, antimicrobial and antitumoral activities of the yerba mate beverages.

4 olyketide chain of the bengamides upon their antitumoral activities, we targeted the preparation of b

5 rties such as antioxidant, antibacterial and antitumoral activities.

6 cleosides, showing effective antioxidant and antitumoral activities.

7 oglycemic, antioxidant, cardioprotective and antitumoral activities.

8 lass I phosphoinositide-3-kinases, has shown antitumoral activity against estrogen receptor (ER)-posi

9 Inhibitors of ChoKalpha show antitumoral activity and are expected to be introduced s

10 ONC displays antitumoral activity and is in advanced clinical trials

11 e multifunctionality of cell-penetrating and antitumoral activity combined with K(V) channel-inhibiti

12 The nanocarrier revealed enhanced antitumoral activity in animal studies.

13 The compound showed strong antitumoral activity in HER2-mutant or amplified cancers

14 f primary endothelial cells and demonstrated antitumoral activity in mouse models.

15 bination of virotherapy and chemotherapy had antitumoral activity in some chemotherapy-resistant colo

16 tent and nonredundant antiviral activity and antitumoral activity in the mouse; however, their functi

17 nriched green tea drinks and their potential antitumoral activity in vitro were evaluated.

18 Evidence of modest antitumoral activity is suggested.

19 f casein kinase 1 may also contribute to the antitumoral activity of (R)-roscovitine and (S)-CR8.

20 odulation of these heteromers can modify the antitumoral activity of cannabinoids in vivo.

21 nto the mechanisms that modulate the pivotal antitumoral activity of cytotoxic T cells (Tcy) have rec

22 tion, replacing Lys9 or Lys31 eliminates the antitumoral activity of ONC.

23 HNSCC xenografts completely resistant to the antitumoral activity of rapamycin.

24 d functional analogues was demonstrated, and antitumoral activity of this class was determined.

25 FK228 analogues were examined for their antitumoral activity on a variety of human cancer cells

26 lted in a combination of phytochemicals with antitumoral activity with potential for further developm

27 a cytokine with known antiproliferative and antitumoral activity, binds with high affinity to the he

28 ell tumor infiltration and constraines their antitumoral activity, despite expression of activation m

29 ritic cells (IKDCs), which exhibit prominent antitumoral activity, has been subject to debate.

30 ally be proven to have significant localized antitumoral activity, none to date have been shown to in

31 itc genes to enhance both local and systemic antitumoral activity.

32 d because it allows an in situ assessment of antitumoral activity.

33 evented this conversion, promoting sustained antitumoral activity.

34 cardiomyopathy without interfering with its antitumoral activity.

35 portant biological systems, with significant antitumoral activity.

36 We recently identified the antitumoral agent carmofur (4a) as the first nanomolar i

37 m of ruxolitinib, a JAK inhibitor used as an antitumoral agent in cutaneous T-cell lymphomas (CTCL).

38 d thiol peroxidase-like activity) as well as antitumoral agents in bladder carcinoma 5637.

39 se-limiting side effect of a large number of antitumoral agents including paclitaxel (Taxol).

40 ynergistically with several, albeit not all, antitumoral agents.

41 act in a synergistic manner with well-known antitumoral agents.

42 Furthermore, sorafenib has a strong antitumoral and -angiogenic activity in the 5T33MM mouse

43 IL-27 has potent antitumoral and antiosteoclastogenic activities.

44 Here, we investigated the antitumoral and antiosteolytic activities of zoledronic

45 s pipeline to systematically deconvolute the antitumoral and antiviral reactivity and antigenic speci

46 The respective antitumoral and protumoral roles of M1 and M2 tumor-asso

47 activity that would otherwise limit NK cell antitumoral and/or antiinflammatory functions by impairi

48 al, antibacterial, mechanical, fluorescence, antitumoral, and remineralization and regeneration poten

49 The similar antitumoral, antiangiogenic efficacy of systemic overexp

50 We show here the different antitumoral approaches offered by ferrocifen derivatives

51 esulting in recovered cytolytic activity and antitumoral capacity of NK cells and T cells and downmod

52 tal cancer, which paved the way for enhanced antitumoral CD8(+) T-cell immunity and reduced tumorigen

53 s ability to further enhance and prolong the antitumoral cellular immunity.

54 fers high potential for future antiviral and antitumoral chemotherapies.

55 ve wide-spectrum pharmacological strategy in antitumoral chemotherapy, and current research focuses o

56 Plitidepsin is an antitumoral compound safe for treating COVID-19 that tar

57 , antifungal, antimalarial, antifouling, and antitumoral compounds has been described.

58 y NK cells and the subsequent development of antitumoral CTL responses facilitated by 4-1BB-activated

59 to analyze changes in the level of pro- and antitumoral cytokines.

60 Myeloid cells, crucial players in antitumoral defense, are affected by tumor-derived facto

61 aper describes a new class of platinum-based antitumorals differing from cisplatin in several critica

62 case, ferrocenyl group, to function as both antitumoral drug and fluorophore.

63 However, surprisingly, no antitumoral drug has been marketed as a nanocrystal susp

64 r, and its activity may confer resistance to antitumoral drugs such as Taxol.

65 itors that act synergistically with standard antitumoral drugs to prevent cancer cell proliferation.

66 thening the potential of NAMPT inhibitors as antitumoral drugs.

67 alysis, intermediate reaction synthesis, and antitumoral drugs.

68 m calcineurin inhibitors to sirolimus had an antitumoral effect among kidney-transplant recipients wi

69 crophages (MPhi) as the key mediators of the antitumoral effect and demonstrate a strong interdepende

70 chanistically, PAX2 and tamoxifen coexert an antitumoral effect by maintaining high levels of transcr

71 This antitumoral effect correlated with an inhibition of T-AL

72 Disulfiram has demonstrated broad antitumoral effect in several preclinical studies.

73 at the HDAC6 inhibitor AVS100 (SS208) had an antitumoral effect in SM1 melanoma and CT26 colon cancer

74 SN-38's antitumoral effect is 100 to 1000 times more potent than

75 This antitumoral effect is superior to the effect of the corr

76 mTOR signaling in human HCC, as well as the antitumoral effect of a dual-level blockade of the mTOR

77 le electroporation (IRE) and to evaluate the antitumoral effect of IRE, used alone or in combination

78 Further, the antitumoral effect of miR-28 is conserved in a primary m

79 inhibition of the MAPK pathway enhanced the antitumoral effect of mTORC1 inhibition by rapamycin in

80 ferent cancer cell lines, no decrease in the antitumoral effect of paclitaxel was observed.

81 induced apoptosis in vitro, and improved the antitumoral effect of rituximab in xenografted mice.

82 repression of perlecan may represent a novel antitumoral effect of this cytokine through which it eli

83 complete regression of tumor, PMEA had less antitumoral effect than HPMPC, and PMPA had the least.

84 Activation of TLR3 exerts an antitumoral effect through a mechanism of action still p

85 s carry proteins and miRNAs able to exert an antitumoral effect, even within a highly immune-suppress

86 ed for 0.25 to 1.0 mg TM-601 and may have an antitumoral effect.

87 ngiogenesis, resulting in an overall pro- or antitumoral effect.

88 nd type I IFN neutralization prevented TLR7L antitumoral effect.

89 se of SN-38 have demonstrated to enhance its antitumoral effects and reduce the associated systemic t

90 ogether, domatinostat not only exerts direct antitumoral effects but also restores HLA class I surfac

91 We report striking antitumoral effects by a nonlytic viral vector based on

92 Collectively, these data demonstrate potent antitumoral effects by r3LCMV vectors and unveil multipl

93 The mutant virus vSP displayed significant antitumoral effects in an MC38 s.c. tumor model in both

94 age induces pronounced antiproliferative and antitumoral effects in preclinical models.

95 astasis, we examined whether the pro- versus antitumoral effects of CD8+ T cells relate to their Ag s

96 Due to the antitumoral effects of cGAMP, other CDN-based STING agon

97 The antitumoral effects of oncolytic viruses have generally

98 trol of TAM responses that contribute to the antitumoral effects of pharmacologic LXR activation.

99 K1 prevents mTORC1 activation, restoring the antitumoral effects of PI3Kalpha inhibition in resistant

100 The antitumoral effects of r3LCMV were also observed when th

101 ormin (50 mg/kg per day) could influence the antitumoral effects of sorafenib (15 mg/kg per day) in a

102 Both viruses exerted strong antitumoral effects on human hepatocellular carcinoma gr

103 MAPK kinase are implicated in mediating the antitumoral effects resulting from SRPK1 down-regulation

104 ion therapy based on immunosuppressants with antitumoral effects should be preferred.

105 bition of mTORC1/2 exerts antiangiogenic and antitumoral effects that are even more efficacious when

106 in humans many biological actions, including antitumoral effects through the modulation of the farnes

107 Bisphosphonates may also possess important antitumoral effects.

108 ng that multiple pathways contributed to the antitumoral effects.

109 e (6z) that combined both antiangiogenic and antitumoral effects.

110 to be the most active in neuroprotective and antitumoral effects; this sample is especially rich in p

111 that continuous administration improves the antitumoral efficacy of angiogenesis inhibitors, as comp

112 Notably, the antitumoral efficacy of p53 restoration in tumor-bearing

113 ritical role for host-intrinsic IFN-I in the antitumoral efficacy of r3LCMV vectors.

114 The biodistribution and antitumoral efficacy of selected siRNA-loaded LNP-protot

115 To investigate the potential antitumoral efficacy of systemic TSP-2 therapy, we expre

116 vivo, VAI-deleted adenovirus showed superior antitumoral efficacy to wild-type adenovirus in EBV-posi

117 Antitumoral efficacy was documented following intratumor

118 unveil multiple mechanisms underlying their antitumoral efficacy.

119 rcise in a manner that acts to improve their antitumoral efficacy.

120 d allodynia in tumored mice without reducing antitumoral efficacy.

121 ffectively inhibit MMP-2 and MMP-9 with high antitumoral efficacy.

122 immune activating cytokines can deploy their antitumoral function more effectively than systemic admi

123 nstraining carcinogenesis and establishes an antitumoral function of a prototypical oncomiR.

124 sults define a novel mechanism underlying AA antitumoral functions that may serve as a foundation for

125 T cells were found to retain key antitumoral functions under TTFields settings.

126 s via restimulation of pre-existing (memory) antitumoral helper and effector immune cells.

127 L-1alpha, IL-1beta, IL-5, IL-6 and IL-17 and antitumoral IL-2 and IL-12 in tumor-proximal lymph nodes

128 ME) to a more hospitable and hot habitat for antitumoral immune cells, characterized by a decrease in

129 Exploiting antitumoral immune effects could enhance the therapeutic

130 This promoted an antitumoral immune response characterized by a macrophag

131 t TMAB3/3p-hpRNA treatment elicited a potent antitumoral immune response characterized by RIG-I activ

132 unotherapy of GBM explants enables an active antitumoral immune response within the tumor center and

133 P is then sensed by host cells, eliciting an antitumoral immune response.

134 produce IFN and positively contribute to the antitumoral immune response.

135 dition to their established ability to boost antitumoral immune responses, STING agonists can also di

136 lpha-TRT alters the TME and induces systemic antitumoral immune responses, which explains why immune

137 n shows therapeutic potential for increasing antitumoral immune responses.

138 pro-inflammatory tumor microenvironment and antitumoral immune responses.

139 ellular matrix (ECM) inhibition and improved antitumoral immune responses.

140 ard-treated samples, from a protumoral to an antitumoral immune signature.

141 a tree-based survival model to quantify net antitumoral immunity (using ratios of immune effector to

142 he immune cell populations most relevant for antitumoral immunity and allowing us to restrict the use

143 Cs with tumor antigens can elicit productive antitumoral immunity and that enhancements in gene trans

144 ITIM+ FcgammaR, effective anti-idiotypic and antitumoral immunity can be achieved by FcgammaR-targete

145 The antitumoral immunity declined gradually, which led to tu

146 g novel target for modifying T-cell-mediated antitumoral immunity in colorectal cancer.

147 s was shown to foster CD8(+) T-cell-mediated antitumoral immunity in murine colorectal cancer models.

148 rging therapeutic strategies to reinvigorate antitumoral immunity in SLNs.

149 or regression, induced an effective systemic antitumoral immunity in the host and prolonged the media

150 Antitumoral immunity requires organized, spatially nuanc

151 immunogenic cell death (ICD), can propagate antitumoral immunity to augment therapeutic efficacy.

152 ng how complex biological processes, such as antitumoral immunity, occur through concerted actions of

153 tigen-specific inhibitors of T-cell-mediated antitumoral immunity.

154 on and survival, resulting in defective host antitumoral immunity.

155 potentially explaining how some tumors evade antitumoral immunity.

156 r 2'3'-cyclic-GMP-AMP (cGAMP)-STING-mediated antitumoral immunity.

157 oxicity but also triggers otherwise indolent antitumoral immunity.

158 cently developed and promising approaches to antitumoral immunotherapy are being investigated as pote

159 rophages and favored polarization towards an antitumoral M1 phenotype following EphB4-ephrin-B2 inhib

160 Ms from the tumor-permissive M2 phenotype to antitumoral M1 phenotype is an emerging attractive appro

161 crophages but increased the proliferation of antitumoral M1, acting through the SEMA3A receptor neuro

162 e protumoral M2-like MO present in MM toward antitumoral M1-like MO, we tested the pro-M1 cytokine gr

163 ely activated macrophages and an increase in antitumoral macrophages and dendritic cells.

164 This study provides evidence of an antitumoral mechanism of action upon TLR3 activation and

165 of cancer hallmarks and point toward a novel antitumoral mechanism of melatonin in TNBC cells.

166 Here, we provide evidence of a novel antitumoral mechanism of the PUFA arachidonic acid (AA).

167 stage tumor evolution present in humans when antitumoral mechanisms are activated.

168 al clodronate liposomes, which abrogated the antitumoral memory immunity.

169 mTOR, but not calcineurin, inhibition spares antitumoral memory Tc cells by distinctively regulating

170 cterize calvarial marrow as a contributor of antitumoral myeloid antigen-presenting cells (APCs), inc

171 the development of a total synthesis of the antitumoral natural product (+)-pancratistatin; it also

172 represent an innovative strategy to enhance antitumoral NK cell cytotoxicity.

173 tioxidant, anti-inflammatory, antimutagenic, antitumoral or chemopreventive, antiviral, antibacterial

174 ate this essential protein could lead to new antitumoral pharmacological approaches.

175 tumor growth by reprogramming TAMs toward an antitumoral phenotype and increasing their antigen cross

176 Kupffer cells, reprogrammes TAMs towards an antitumoral phenotype and suppresses HCC progression.

177 interfering RNA reprogrammed TAMs toward an antitumoral phenotype, restrained tumor growth and enhan

178 A-NP@R848 could uniquely reprogram TAMs into antitumoral phenotypes, decrease angiogenesis, reprogram

179 nd in the search of new ligands endowed with antitumoral potential and targeting FPPS protein.

180 ed by combining in vitro assays, to test the antitumoral potential on leukemic cells, and a prelimina

181 human cancer cells demonstrating a promising antitumoral profile.

182 Moreover, we also demonstrate that the antitumoral properties of cisplatin were not altered by

183 rthy that an acute septic episode may harbor antitumoral properties under particular circumstances.

184 NK cells, a phenomenon that might impair its antitumoral properties.

185 une encephalitis model, and show a deficient antitumoral response after vaccination.

186 induced a very efficient iNKT cell-dependent antitumoral response in B16 animal model.

187 on of ISR, or silencing of ATF4, rescued the antitumoral response to the tetracyclines.

188 tion suggest a CD4(+) T lymphocyte-dependent antitumoral response, which may be exploited for immunot

189 nontreated tumors, indicative of a systemic antitumoral response.

190 hanced effector function, leading to durable antitumoral response.

191 In particular, antitumoral responses depend on a specialized subset of

192 d immune sensors mediating antimicrobial and antitumoral responses, but recent evidence implicates th

193 Although CD8+ T cells are usually considered antitumoral, several recent studies report that the cell

194 states and can transmit either protumoral or antitumoral signals to glioma cells.

195 saged as a target for combined antiviral and antitumoral strategies against HBV infection and HBV-med

196 argets for the development of more effective antitumoral strategies.

197 n to tumor cells, may represent an efficient antitumoral strategy in certain contexts.

198 l mechanisms involved in complete and proper antitumoral T cell activation have only recently been id

199 increase the frequency/activity of activated antitumoral T cells.

200 In contrast, the antitumoral T-cell response remained largely unchanged.

201 Peripheral antitumoral T-cell responses were detected on alpha-TRT.

202 s exposure (i) reduces the percentage of the antitumoral Th1 subset, inducing a lactate-dependent, SI

203 cancer cells makes it a strategic target for antitumoral therapies, such as compounds that use NTSR1

204 e biomarker of MCC and as a target for novel antitumoral therapies.

205 -treating fields (TTFields) are a localized, antitumoral therapy using alternating electric fields, w

206 an cells, TGF-beta has two opposing actions: antitumoral through pro-apoptotic and cytostatic activit

207 ts have implications for developing clinical antitumoral vaccination regimens in the setting in which