ライフサイエンスコーパス: TAM

1 TAM comprises amphipathic alpha-helices predicted to for

2 TAM concentration in specific tissues (liver, spleen, ly

3 TAM depletion-repletion experiments in a 4T1 mouse model

4 TAM receptors (Tyro-3, Axl, and Mertk) are often correla

5 TAM requires trisomy 21 and truncating mutations in GATA

6 TAM/MU was stable but with yield lower than the grand me

7 TAMs drive T cell inhibition, promote angiogenesis, and

8 TAMs expressed elevated levels of the scavenger receptor

9 TAMs, which include brain-resident microglia and circula

10 bined exome and targeted resequencing of 111 TAM and 141 ML-DS samples with functional analyses.

11 d 'Multifort' (TAM/MU, TY/MU) while in 2018, TAM and 'HM1823' (HM) were grafted on 'Estamino' (TAM/ES

12 nd truncating mutations in GATA1; additional TAM variants are usually not pathogenic.

13 -10)), CCL2/IL13 expression (p<10(-109)) and TAM infiltration (p<10(-96)).

14 n between TC and IM in human lung cancer and TAM associations with overall survival.

15 xploited the coenrichment of alphavbeta3 and TAMs to not only eradicate highly aggressive drug-resist

16 d CD86 and that the fractions of T cells and TAMs that are CTLA-4-positive and CD86-positive, respect

17 n shape both lymphatic endothelial cells and TAMs to synergistically inhibit antitumor immunity and p

18 bitor abundantly produced in tumor cells and TAMs, was reduced in tumor cells of clodronate-treated m

19 that blocking the interplay between GSCs and TAMs by targeting ARS2/MAGL signaling offers a potential

20 ancer, with VEGFR3 expressed on both LVs and TAMs.

21 n murine bone marrow-derived macrophages and TAMs isolated from murine tumors.

22 Here, we explore the properties of MDSCs and TAMs from freshly isolated mouse and human tumors and fi

23 ross tumor types for reprogramming MDSCs and TAMs into antitumorigenic immune cells using a drug that

24 oth a means to identify and target MDSCs and TAMs within the tumor, allowing for delivery of immunomo

25 ecause all solid tumors accumulate MDSCs and TAMs, a general strategy to both identify and reprogram

26 om nonimmunosuppressive subsets of MDSCs and TAMs.

27 on pathway promotes CCL2 transactivation and TAMs infiltration in lung cancer to provide a tumor-prom

28 ation pathway as a promising target for anti-TAMs therapeutic strategies.

29 As TAMs are a dominant immune component in tumors and are n

30 describe recent examples of Nano-TDDS-based TAM modulation, highlighting strategies to overcome in v

31 rpose To understand the relationship between TAM infiltration, tumor vascularization, and correspondi

32 o identified an auto-regulatory loop between TAMs and cancer cells driven by tumor necrosis factor al

33 TNC affects the antitumor function of brain TAM, facilitating the development of novel innate immune

34 We identified a breast TAM signature that is highly enriched in aggressive brea

35 CDDO-methyl ester (CDDO-Me) converts breast TAMs from a tumor-promoting to a tumor-inhibiting activa

36 r phosphorylation by RIPK3, is controlled by TAM kinases.

37 the LXR agonist on other mechanisms used by TAM for the maintenance of an immunosuppressive environm

38 contrast to the pro-tumoural role played by TAMs in glioblastoma, another common brain tumour.

39 lthy tissue was seen but selective uptake by TAMs was seen in 13 different patient samples.

40 age galactose-type lectin (MGL), on CD163(+) TAMs in glioblastoma patient-derived tumor tissues.

41 vival and leads to a higher iNOS(+)/CD206(+) TAM ratio compared to irradiation alone.

42 immunofluorescence staining and a tumor cell-TAM proximity analysis was performed.

43 In immune cells, TAM RTKs can dampen inflammation in favor of homeostatic

44 Consistently, TAMs are considered a major limitation for the efficacy

45 orated ex vivo and correlated with decreased TAM density.

46 chemotaxis of monocytes, thereby decreasing TAMs infiltration, which can be alleviated by CCL2 addit

47 ompetent preclinical mouse model demonstrate TAMs can have a functional role in promoting SHH-MB prog

48 ung cancer, density and topology of distinct TAM phenotypes at the tumor center (TC) versus the invas

49 Hh ligand, and that tumor-derived SHH drives TAM M2 polarization.

50 AHR promotes CCR2 expression, driving TAM recruitment in response to CCL2.

51 gen-specific IgE that recruit and re-educate TAMs towards activated profiles.

52 contrast to strategies designed to eliminate TAMs, these findings suggest that anti-alphavbeta3 repre

53 nd 'HM1823' (HM) were grafted on 'Estamino' (TAM/ES, HM/ES) and 'Multifort' (TAM/MU, HM/MU).

54 on commercial tomato rootstocks 'Estamino' (TAM/ES, TY/ES) and 'Multifort' (TAM/MU, TY/MU) while in

55 n and enhance drug sensitivity by exploiting TAMs to trigger ADCC.

56 at even in a healthy CNS, astrocytes express TAM phagocytic receptors, which were the main astrocytic

57 MARCO-expressing TAM numbers correlated with increased occurrence of regu

58 MARCO-expressing TAMs blocked cytotoxic T-cell and NK-cell activation, in

59 lar, receptors of the tyrosine kinase family TAM (Tyro3, Axl, and MerTK), to maintain self-tolerance.

60 ) signaling in myeloid cells is critical for TAM M2 polarization and tumor growth.

61 These processes were critical for TAM polarization and activity, both in vitro and in vivo

62 omoting TAM M2 polarization, a mechanism for TAM-mediated immunosuppression, and may provide insights

63 MLKL Tyr376 as a direct point of input from TAM kinases into the necroptosis signaling.

64 ia and peripheral macrophages within the GBM-TAM pool, using orthotopically xenografted, immunodefici

65 hat lipids play a crucial role in generating TAMs in the tumor microenvironment (TME).

66 regulation of PD-L1, defining a putative PS->TAM receptor->PD-L1 inhibitory signaling axis in the can

67 These SLAMF7(high)CD38(high) TAMs showed the strongest correlations with exhausted T

68 nd a unique subset of SLAMF7(high)CD38(high) TAMs.

69 MARCO(high) TAMs also significantly accelerate tumor engraftment and

70 MARCO(high) TAMs induce a phenotypic shift towards mesenchymal cellu

71 This study demonstrates how TAM receptors act both as oncogenic tyrosine kinases and

72 what drives M2 polarization of TAMs and how TAMs suppress antitumor immunity within the tumor microe

73 However, TAM blockade failed to decrease tumor progression due to

74 immune therapeutic approach targeting human TAMs immune suppression of NK- and T-cell antitumor acti

75 marked differences among NM, TC-TAM, and IM-TAM.

76 tissue (NM), the TC (TC-TAM), and the IM (IM-TAM) were analyzed with RNA-sequencing (RNA-seq).

77 lls to M2 IM-TAM or lower proximity to M1 IM-TAM were linked with poor survival.

78 and higher proximity of tumor cells to M2 IM-TAM or lower proximity to M1 IM-TAM were linked with poo

79 this study discovers that immunosuppressant TAM kinases are promoters of pro-inflammatory necroptosi

80 hind the acquisition of an immunosuppressive TAM phenotype is not fully clarified.

81 activating ligand for the immunosuppressive TAM family of receptor tyrosine kinases.

82 tates, and the presence of immunosuppressive TAMs at tumors is correlated with decreased survival.

83 D206 and CD115, markers of immunosuppressive TAMs.

84 about the potential role of this pathway in TAM.

85 on peptide, we were able to target miR-21 in TAMs, which decreased tumor growth even under conditions

86 were all found to selectively accumulate in TAMs.

87 KLF4 and suppresses NF-kappaB activation in TAMs.

88 e expression of the ectonucleotidase CD39 in TAMs, which promotes CD8(+) T cell dysfunction by produc

89 of chemotherapy-induced PD-L1 expression in TAMs is warranted to define appropriate patient selectio

90 Moreover, concomitant with a reduction in TAMs the percentage of infiltrating cytotoxic T cells is

91 ated glycans trigger inhibitory signaling in TAMs through glycan-binding receptors.

92 icated that >80% of the injected dose was in TAMs.

93 consequent myeloid-lineage cells, including TAMs, delayed tumor growth.

94 clearly define characteristics of individual TAM populations and suggest that combination therapy wit

95 Anti-inflammatory TAMs (also referred to as M2-polarized) generally suppre

96 The findings suggest that anti-inflammatory TAMs promote tumor-associated angiogenesis and immunosup

97 We found that anti-inflammatory TAMs promoted a metabolic state in breast cancer cells t

98 Anti-inflammatory TAMs secreted the cytokine TGF-beta that, upon engagemen

99 ciated with immune stimulation, and inhibits TAM tumor infiltration, consistent with decreased expres

100 Here, we investigated TAM subtype density and distribution between TC and IM i

101 ear phagocytes from CLM tissues, S-TAM and L-TAM signatures were differentially enriched in individua

102 l area identified small (S-TAM) and large (L-TAM) macrophages that were associated with 5-yr disease-

103 ells with increased infiltration of PD-L1(+) TAMs as well as distant alterations in the bone marrow (

104 In a murine model of CCA, recruited PD-L1+ TAMs facilitated CCA progression.

105 s while also reducing hemosiderin iron-laden TAM accumulation as measured by both iron histology and

106 d immunosuppressive activity of TAM, M1-like TAM differentiation was impaired in the s.c. tumor micro

107 indirectly but selectively sustained M2-like TAM metabolic fitness, mitochondrial integrity, and surv

108 s beta-catenin activation of GSC and M2-like TAM polarization.

109 ritical roles in GSC maintenance and M2-like TAM polarization.

110 ir modulation of lipid metabolism in M2-like TAMs could improve cancer immunotherapy.

111 eath ligand 1 antibody elicited higher local TAM levels and 43% +/- 20 greater therapeutic nanopartic

112 and M2 predominance and juxtaposition of M2 TAM near tumor cells were associated with poor survival.

113 poxia was associated with accumulation of M2 TAM.

114 Palpha pathway while the MN core promotes M2 TAM repolarization, synergistically triggering potent ma

115 ulations in different tumor regions, with M2 TAM predominance, particularly at IM.

116 intain GSCs by an autocrine mechanism and M2 TAMs through a paracrine manner.

117 M1 and M2 TAMs were identified using multiplex immunofluorescence

118 GM-CSF triggered TGFbeta1 expression by M2 TAMs by activating STAT5, NF-kappaB, and/or ERK signalin

119 RISOE cells and polarize them to protumor M2 TAMs.

120 pecially the protumor, immune-suppressive M2 TAMs.

121 rectional interactions with MSCs/CAFs and M2-TAMs.

122 ecreting M2-tumor-associated macrophages (M2-TAMs).

123 Moreover, both MA-TAM master regulators and their target genes are signifi

124 -associated tumor-associated macrophages (MA-TAMs), which drive the malignant phenotypic state of GBM

125 We further demonstrate the origination of MA-TAMs from peripheral blood, as well as their potential a

126 es M1-polarized tumor-associated macrophage (TAM) and CD8 T cell infiltration into subcutaneously imp

127 ion and greater tumor-associated macrophage (TAM) levels.

128 Tumor-associated macrophages (TAM) are highly expressed within the tumor microenvironm

129 Tumor-associated macrophages (TAM) are important tumor-promoting cells.

130 lls (MDSC) and tumor-associated macrophages (TAM) in tumor tissue has been extensively reported.

131 i-inflammatory tumor-associated macrophages (TAM) is associated with worse clinical outcome and resis

132 Tumor-associated macrophages (TAM) promote triple-negative breast cancer (TNBC) progre

133 lls (MDSC) and tumor-associated macrophages (TAM) that inhibit T cells via release of immunosuppressi

134 s of M1 and M2 tumor-associated macrophages (TAM) typify the complexity of macrophage function in can

135 by MHCII(high) tumor-associated macrophages (TAM).

136 ssels (LV) and tumor-associated macrophages (TAM).

137 Tumour-associated microglia/macrophages (TAM) are the most numerous non-neoplastic populations in

138 that TANs and tumor-associated macrophages (TAMs) act in tandem within tumors and contribute both co

139 The roles of tumor-associated macrophages (TAMs) and circulating monocytes in human cancer are poor

140 Tumor-associated macrophages (TAMs) are a complex and heterogeneous population of cell

141 n, we identify tumor-associated macrophages (TAMs) as the primary source of programmed death-ligand 1

142 Tumor-associated macrophages (TAMs) can exist in pro- and anti-inflammatory states.

143 Tumor-associated macrophages (TAMs) can have protumor properties, including suppressin

144 rogramming of tumour-associated macrophages (TAMs) controls tumour growth and anti-tumour immunity.

145 olarization of tumor-associated macrophages (TAMs) correlates with poor outcome for many tumors, so t

146 However, tumor-associated macrophages (TAMs) express cytokines and chemokines that can suppress

147 modulation of tumor associated macrophages (TAMs) from a pro-tumorigenic phenotype (M2) to an anti-t

148 Tumor-associated macrophages (TAMs) have a significant presence in the tumor stroma ac

149 es in the TME, tumor-associated macrophages (TAMs) have gained attention owing to their crucial roles

150 morphology of tumor-associated macrophages (TAMs) in colorectal liver metastasis (CLM) represents a

151 ically targets tumor-associated macrophages (TAMs) in glioblastoma from systemic administration and e

152 of the role of tumor-associated macrophages (TAMs) in the progression of GBMs have demonstrated that

153 ithin the TME, tumor associated macrophages (TAMs) mediate angiogenesis, metastasis, and immunosuppre

154 Tumor associated macrophages (TAMs) play a critical role in biology of various cancers

155 c target, with tumor-associated macrophages (TAMs) playing a critical role in immune suppression.

156 phages such as tumor-associated macrophages (TAMs) promote tumor growth and invasion.

157 lls (GSCs) and tumor-associated macrophages (TAMs) promotes progression of glioblastoma multiforme (G

158 unosuppressive tumor-associated macrophages (TAMs) rather than immunostimulatory dendritic cells (DCs

159 Tumor-associated macrophages (TAMs) recruited from blood monocytes are key in establis

160 Tumor-associated macrophages (TAMs) represent the most abundant hematopoietic cell typ

161 tic cells, the tumor-associated macrophages (TAMs) showed pro-tumoral functions without signature gen

162 Tumor-associated macrophages (TAMs) support tumor growth by suppressing the activity o

163 ey mature into tumor-associated macrophages (TAMs) that promote disease progression through induction

164 oliferation of tumor associated macrophages (TAMs) through multiple mechanisms, partly by reducing th

165 pathway in the tumor-associated macrophages (TAMs) through the TLR2 and MyD88 pathway, and recruits p

166 ells, polarize tumor-associated macrophages (TAMs) to a tumorigenic M2 phenotype.

167 Tumor-associated macrophages (TAMs) usually express an M2 phenotype, which enables the

168 the number of tumor-associated macrophages (TAMs) was not affected by the presence of T cells but di

169 tional states, tumor-associated macrophages (TAMs) were associated with poor prognosis, and we establ

170 and SLAMF7(+) tumor-associated macrophages (TAMs), and a unique subset of SLAMF7(high)CD38(high) TAM

171 expression in tumor- associated macrophages (TAMs), caused a global rewiring of their transcriptional

172 ive target is tumour-associated macrophages (TAMs), which are abundantly present in the Sonic Hedgeho

173 HRS cells and tumor-associated macrophages (TAMs), which associate with PD-1-positive T cells to sup

174 both GSCs and tumor-associated macrophages (TAMs).

175 ent created by tumor-associated macrophages (TAMs).

176 s expressed by tumor-associated macrophages (TAMs).

177 olarization of tumor associated macrophages (TAMs).

178 n inflammatory tumor-associated macrophages (TAMs).

179 accumulate in tumor-associated macrophages (TAMs).

180 ic A-type cyclin TARDY ASYNCHRONOUS MEIOSIS (TAM).

181 tumor-associated macrophages and microglia (TAMs), which are key mediators of immune suppression and

182 that tumor-associated macrophages/microglia (TAMs) can promote tumor progression in the sonic hedgeho

183 actor: the transplantation for Aclf-3 model (TAM) score.

184 ergistic antitumor effects through modifying TAMs in the TME and removing T-cell inhibitory signals,

185 However, most TAM derivatives reported in the literature are based on

186 The typical thoracoabdominal motion (TAM) plot showed the abdomen and rib cage motion in sync

187 'Estamino' (TAM/ES, HM/ES) and 'Multifort' (TAM/MU, HM/MU).

188 'Estamino' (TAM/ES, TY/ES) and 'Multifort' (TAM/MU, TY/MU) while in 2018, TAM and 'HM1823' (HM) were

189 at SLAMF7-SLAMF7 interactions between murine TAMs and CD8(+) T cells induce expression of multiple in

190 dherent hOMCs were transduced with a c-MycER(TAM) gene that enables cell proliferation in the presenc

191 Therefore, c-MycER(TAM)-derived PA5 hOMCs have potential as a regenerative

192 volves from transient abnormal myelopoiesis (TAM), a preleukemic condition in DS newborns.

193 administered intravenously (i.v.) showed no TAM targeting.

194 ve shown that Gas6/PS-mediated activation of TAM receptors on tumor cells leads to subsequent upregul

195 the decreased immunosuppressive activity of TAM, M1-like TAM differentiation was impaired in the s.c

196 ablishing optimal dose and administration of TAM, our study reveals a disparate activity of Cre in di

197 an endogenous metabolic imaging biomarker of TAM infiltration in breast cancer that has high translat

198 In this study, we tested combinations of TAM inhibitors and PD-1 mAbs in a syngeneic orthotopic E

199 actions of the LXR pathway in the control of TAM responses that contribute to the antitumoral effects

200 Here, we assessed dosage and delivery of TAM for activation of Cre in immune cell subsets assesse

201 consensus on the optimal route and dosage of TAM administration in vivo.

202 spatial distribution, and gene expression of TAM phenotypes as prognostic factors for overall surviva

203 ent (TME), we observed distinct functions of TAM as oncogenic kinases, as well as inhibitory immune r

204 r results reveal the marked heterogeneity of TAM populations in different tumor regions, with M2 TAM

205 Importantly, both knockout and inhibition of TAM kinases protect mice from systemic inflammatory resp

206 ation therapy did not show greater levels of TAM or DDNP (P = .82).

207 Serum levels of TAM peaked 1 week after initiating treatment then slowly

208 ) and different doses, we found that 3 mg of TAM administered orally for five consecutive days provid

209 nografts in vivo and decreased the number of TAM.

210 Spatial profiling of TAM iron deposit infiltration defined regions of maximal

211 cterization can serve as a simple readout of TAM diversity with strong prognostic significance.

212 Here, we identify an unexpected role of TAM kinases as promoters of necroptosis, a pro-inflammat

213 Pharmacologic or genetic targeting of TAM kinases results in a potent inhibition of necroptoti

214 d modulate the immunosuppressive activity of TAMs.

215 While density of TAMs did not correlate with survival of CLM patients, th

216 use model of SHH-MB, we found the density of TAMs is higher in the ~50% of tumors that progress to le

217 tion of macrophage recruitment, depletion of TAMs, reprograming of TAMs, and blocking of the CD47-SIR

218 olism in the differentiation and function of TAMs and suggests targeting TAM fatty acid oxidation as

219 production, differentiation, and function of TAMs; however, the discovery of selective CSF1R inhibito

220 CCR2 expression and altered infiltration of TAMs and CTLs as evidenced by immunohistochemical and fl

221 thway significantly inhibits infiltration of TAMs, leading to the suppression of lung cancer metastas

222 Finally, dual inhibition of TAMs and G-MDSCs potentiated ICB.

223 focus our discussion on current knowledge of TAMs, and describe recent examples of Nano-TDDS-based TA

224 tanding the contributions and limitations of TAMs in SCC progression.

225 recruitment, polarization, and metabolism of TAMs during tumor progression.

226 Density and morphological metrics of TAMs were measured and correlated with clinicopathologic

227 caveolin-2 deficient bone marrow (origin of TAMs) suppresses tumor growth and increases numbers of M

228 However, what drives M2 polarization of TAMs and how TAMs suppress antitumor immunity within the

229 erizes the global transcriptional profile of TAMs driving mesenchymal GBM pathogenesis, providing pot

230 ruitment, depletion of TAMs, reprograming of TAMs, and blocking of the CD47-SIRPalpha pathway, are di

231 , we report an unexpected beneficial role of TAMs in SHH medulloblastoma.

232 immunosuppressive, tumor-supporting state of TAMs and reprogram them to a phenotype that induces anti

233 is expressed on a specific subpopulation of TAMs in the tumor.

234 urther found that HRS cells, and a subset of TAMs, are positive for the CTLA-4 ligand CD86 and that t

235 Significantly, PLX5622 reduces a subset of TAMs, prolongs mouse survival, and reduces the volume of

236 ted delivery improves phenotype switching of TAMs from pro- towards anti-tumor expression in vitro.

237 exhibited its effects via direct actions on TAM RTKs expressed on intratumoral macrophages and dendr

238 rylmethyl radicals, the so-called trityl- or TAM-radicals, are stable and do survive over longer time

239 , we used a reversibly switchable p53 (p53ER(TAM)) mouse allele to generate Eu-Myc-driven lymphomas i

240 ells with CRISPR-engineered switchable p53ER(TAM) alleles responded to p53 reactivation when CDKN2A/p

241 monotherapeutic administration of either pan-TAM kinase inhibitor (BMS-777607) or anti-PD-1 mAb thera

242 ecule RXDX-106 as a selective and potent pan-TAM RTK inhibitor with slow dissociation kinetics and si

243 The pan-TAM small-molecule kinase inhibitor RXDX-106 activates b

244 eby tumor-bearing mice were treated with pan-TAM kinase inhibitor (BMS-777607) or anti-PD-1 alone or

245 .) mediated the activation of PC-Treg and PC-TAM interaction pathways, which induced the immunosuppre

246 growth and increases numbers of M1-polarized TAMs in wild type mice.

247 from M2-polarized TAMs into the M1-polarized TAMs.

248 effect is skewing the TAMs from M2-polarized TAMs into the M1-polarized TAMs.

249 ial growth factor A blockade for prohibiting TAM infiltration, especially against BMDMs.

250 The authors found that c-Maf promoted TAMs' immunosuppressive activity, governed their metabol

251 ical role for tumor-derived SHH in promoting TAM M2 polarization, a mechanism for TAM-mediated immuno

252 vation domain in the middle of the proteins (TAM) synergizes with a C-terminal one (TAC).

253 the differentiation and function of protumor TAMs in the TME.

254 n factor as a master regulator of protumoral TAM polarization.

255 scape of NSCLC in the presence of protumoral TAMs expressing the macrophage receptor with collagenous

256 ising immunotherapeutic approach to redirect TAMs to serve as tumor killers for late-stage or drug-re

257 CDDO-Me remodels the breast TME, redirecting TAM activation and T cell tumor infiltration in vivo.

258 ctor 1 receptor (CSF1R) inhibitor, to reduce TAM density.

259 en proposed as a potential therapy to reduce TAMs, especially the protumor, immune-suppressive M2 TAM

260 Clodronate significantly reduced TAMs and splenic macrophages, resulting in reduced SCC v

261 ion and transcription of genes that regulate TAM generation and function.

262 Here, three major strategies for regulating TAMs are highlighted, emphasizing the role of biomateria

263 f IL37 in lung cancer cell lines repolarized TAMs, resulting in recovered cytolytic activity and anti

264 olarizing transcription factors to reprogram TAMs without causing systemic toxicity.

265 Results TAM levels were higher in orthotopic thyroid tumors comp

266 patients, the cell area identified small (S-TAM) and large (L-TAM) macrophages that were associated

267 f mononuclear phagocytes from CLM tissues, S-TAM and L-TAM signatures were differentially enriched in

268 To stop TAM-mediated immunosuppression, we use a novel treatment

269 ts GSC maintenance, reduces tumor-supportive TAMs (M2), and potently inhibits GBM growth.

270 les in maintaining GSCs and tumor-supportive TAMs in GBM, indicating that targeting Wnt/beta-catenin-

271 the levels of circulating GM-CSF, suppressed TAM recruitment, and decreased the levels of circulating

272 Tamoxifen (TAM) inducible Cre recombinase system is an essential to

273 reERT2) IL-4Ralpha(-/lox) mice, a tamoxifen (TAM)-inducible IL-4Ralpha knockdown model to investigate

274 estrogen deprivation (LTED) with tamoxifen (TAM) or aromatase inhibitors leads to endocrine-resistan

275 drug delivery nanoparticle (DDNP) to target TAM, and an antibody-neutralizing colony stimulating fac

276 The ability to selectively target TAMs opens the door to targeted immunotherapy for ovaria

277 and function of TAMs and suggests targeting TAM fatty acid oxidation as a potential therapeutic moda

278 s and other therapeutic strategies targeting TAMs.

279 Notably, lower density of M1 TC-TAM and higher proximity of tumor cells to M2 IM-TAM or

280 q identified marked differences among NM, TC-TAM, and IM-TAM.

281 om adjacent nontumor tissue (NM), the TC (TC-TAM), and the IM (IM-TAM) were analyzed with RNA-sequenc

282 Here, we show that TAM accumulation in human and mouse tumors correlates wi

283 We demonstrate that TAMs are composed of 2 morphologically distinct cell typ

284 e progression of GBMs have demonstrated that TAMs are significant contributors to tumor growth, invas

285 The TAM score can help stratify posttransplant survival and

286 Expression of the TAM (TYRO3, AXL, MER) family of receptor tyrosine kinase

287 eptor P2Y12, and the tyrosine kinases of the TAM family Mer tyrosine kinase (MerTK)/Axl.

288 CDDO-Me treatment redirects the TAM transcriptional profile, inducing signaling pathways

289 The overall effect is skewing the TAMs from M2-polarized TAMs into the M1-polarized TAMs.

290 We now report the location of this TAM as well as the pleiotropic mechanism of action of an

291 Tumor cell proximity to TAM was linked with tumor cell survival and hypoxia was

292 atients with advanced BC after resistance to TAM and aromatase inhibitors develops.

293 thymocytes had a notably higher response to TAM.

294 intratumoral monocyte differentiation toward TAMs and away from DCs via suppression of DC-promoting t

295 After comparing two TAM delivery methods (intraperitoneal versus oral gavage

296 7, genotypes were non-grafted 'TAMU Hot Ty' (TAM) and 'Tycoon' (TY) and each grafted on commercial to

297 In many tumor types, TAMs contribute toward tumor malignancy and are therefor

298 PET/CT imaging and autoradiography, whereas TAM burden was determined using immunofluorescence.

299 e highest total and marketable yields, while TAM/ES was very unstable for yields across test environm

300 ed a unique ApoE G-MDSC subset enriched with TAM blockade; further analysis of a human scRNA-Seq data