ライフサイエンスコーパス: tumor

1 YCN independence in an initially MYCN-driven tumor.

2 ACC is a rare but aggressive tumor.

3 ly correlates with the aggressiveness of the tumor.

4 Two expert radiologists segmented each tumor.

5 nment components and biomarkers throughout a tumor.

6 for somatic BRCA1/2 mutations of the primary tumor.

7 nical SOCE/Ca(2+)-induced apoptosis in other tumors.

8 ation therapy are at risk for subsequent CNS tumors.

9 immunotherapy than corresponding mesenchymal tumors.

10 es of patients suffering from adrenocortical tumors.

11 o major genomic subtypes of primary stage Ta tumors.

12 ccurred in all four tumors or in all stage 4 tumors.

13 the spatial layout typically found in human tumors.

14 T levels were increased in androgen-deprived tumors.

15 tance mechanisms to sensitize ICBT-resistant tumors.

16 s as a potential treatment for MYC-dependent tumors.

17 d apoptotic bodies and exosomes derived from tumors.

18 superior antitumor efficacy on various solid tumors.

19 and in six SCLC patient-derived CTC explant tumors.

20 ils were missing for a proportion of excised tumors.

21 utic approaches are needed to target dormant tumors.

22 ontrol in the rituximab-resistant A20-huCD20 tumors.

23 cyclic peptide preferentially accumulates in tumor (2 h after injection) and is rapidly cleared from

24 f cholinesterase, bilirubin, type of primary tumor, age at radioembolization, hepatic tumor burden, p

25 These tumors also frequently displayed ERG gene fusions involv

26 in 5,724 subjects with at least one invasive tumor and 1,943 subjects with in situ tumors only.

27 the most common and deadliest type of brain tumor and contains a population of self-renewing, highly

28 injected FAM-labeled UNO (FAM-UNO) homed to tumor and sentinel lymph node MEMs in different cancer m

29 d drug combinations simultaneously in living tumors and across a diverse immunocompetent patient popu

30 lue for dissecting cellular heterogeneity in tumors and analyzing single circulating tumor cells.

31 ngle-cell RNA-seq from 11 primary colorectal tumors and matched normal mucosa.

32 ry of therapeutic nucleic acids within brain tumors and provide a promising new delivery platform for

33 tagonist blocked granulocyte infiltration of tumors and showed strong anti-tumor effects.

34 regulator of neutrophil recruitment to colon tumors and that it is essential in shaping the protumori

35 transcriptional heterogeneity in colorectal tumors and their microenvironments using single-cell RNA

36 erpreting the off-target efficacy of TKIs in tumors and to envisaging strategies aimed at facilitatin

37 ulation and tolerogenic activity of MDSCs in tumors, and inhibited the expression of immunosuppressiv

38 se (6-[(18)F]FDG) was studied in EMT6 cells, tumors, and muscle and correlated to GLUT1 and GLUT5 exp

39 have been obtained mostly in neuroendocrine tumors, and only limited data are available for cancer t

40 in 11% and/or overexpressed in 15% of breast tumors, and overexpression of MYST3 correlated with wors

41 pproach for the treatment of prostate cancer tumors, and possibly other carcinomas where Sef is downr

42 success has yet to be extrapolated to solid tumors, and the reasons for this are being actively inve

43 e attempted to find the associations between tumor angiogenesis and radiomic imaging features from PE

44 hts into the inhibitory effect of SFN on HCC tumor angiogenesis as well as tumor growth, and indicate

45 Immune checkpoint therapies target tumor antigen-specific T cells, but less is known about

46 nce between (18)F-FDHT and (18)F-FES PET and tumor AR and ER expression measured immunohistochemicall

47 biomarkers for the pancreatic neuroendocrine tumors are needed.

48 Tumors arising from centrosome amplification exhibit fre

49 ere, we demonstrated that human SS and mouse tumors arising from SS18-SSX expression in the embryonic

50 t-fit procedure, designed to yield simulated tumors as close as possible to the observed ones, vary b

51 s melanoma are used to extract a snapshot of tumor-associated alteration in the serum.

52 TORC1 versus mTORC2 in cancer, their role in tumor-associated blood vessels and tumor immunity, and p

53 t and therapeutic resistance are linked with tumor-associated macrophage (TAM) and myeloid-derived su

54 Here, we investigate the roles of tumor-associated signals in regulating endothelial cell

55 Treatment of WAP-Int3 tumor bearing mice with an IKK inhibitor resulted in tum

56 er efficacy of cisplatin and radiotherapy in tumor-bearing mice.

57 significantly prolongs the survival of brain tumor-bearing mice.

58 el prognostic biomarker to predict high-risk tumors before they metastasize.

59 del of MLL-AF9-driven leukemogenesis reduced tumor burden and prolonged host survival.

60 in a statistically significant difference in tumor burden or survival distributions compared to treat

61 ary tumor, age at radioembolization, hepatic tumor burden, presence of extrahepatic disease, and sex.

62 han targeting private events in reducing the tumor burden.

63 it striking single-agent activity in certain tumors, but the mechanisms accounting for hypersensitivi

64 However, radioresistance in irradiated tumors can also develop, resulting in relapse.

65 Hypoxic stress has a strong impact on tumor cell biology.

66 echanism underlying the effect of ILT3.Fc on tumor cell growth involves inhibition of the p70S6K sign

67 ent via a multistep process including direct tumor cell lysis, induction of cytotoxic or apoptosis-se

68 egulate immune function or cell adhesion and tumor cell metastasis.

69 To test the non-tumor cell microenvironment role of RAGE, we performed s

70 ckdown significantly decreased IL-6-mediated tumor cell migration, tumorsphere formation and ALDH-pos

71 lso reveals the impact of such cross-talk on tumor cell phenotypes that are critical for cancer initi

72 ion and resulted in more compactly clustered tumor-cell colonies in coculture with PC3 cells, which m

73 was evaluated and compared with circulating tumor cells (CellSearch).

74 expression was also observed in circulating tumor cells (CTC) during prostate cancer metastasis.

75 urther increased uPA expression in TSC2-null tumor cells and immortalized TSC2-null angiomyolipoma ce

76 e found that NRP1 shRNA expressing KRAS (mt) tumor cells caused increased cell viability by decreasin

77 developed to isolate individual circulating tumor cells from blood, these devices are ineffective at

78 TRAIL-R suppression in tumor cells impaired CCL2 production and diminished both

79 elopment and the potential of SOCS1-silenced tumor cells in raising an effective anti-melanoma immune

80 e of HIF-1 In addition, LOX was expressed by tumor cells in the bone marrow from colorectal cancer pa

81 ion augmented CAR T cell mediated killing of tumor cells in vitro and enhanced clearance of PD-L1+ tu

82 Although the role of 5-LO in tumor cells is beginning to emerge, with the notion that

83 e arrest, leaving a significant reservoir of tumor cells that may acquire or exhibit resistance.

84 mRNA expression predicts the sensitivity of tumor cells to cytotoxic treatments can play an importan

85 fined as nuclear staining in more than 5% of tumor cells).

86 essing migratory and stem-like properties of tumor cells, also inhibit endothelial phenotypes of brea

87 hese cells have reduced cytotoxicity against tumor cells, and mice with NFATc1-deficient T cells are

88 However, following intravenous injection of tumor cells, mice lacking PITPalpha develop fewer lung m

89 eduction of fibrin formation surrounding the tumor cells, rendering the metastases susceptible to muc

90 IL) expressing PD-1 can recognize autologous tumor cells, suggesting that cells derived from PD-1(+)

91 plified in osimertinib-resistant EGFR-mutant tumor cells, the effects of which were overcome by combi

92 stress activates protein kinase D1 (PKD1) in tumor cells, we investigated the effect of excitotoxicit

93 ses interleukin (IL)-33 released from breast tumor cells, which is crucial for the induction of IL-13

94 fferently to excess centrosomes than do most tumor cells-they undergo senescence in vascular sprouts

95 y in tumors and analyzing single circulating tumor cells.

96 PGBD5-induced DNA rearrangements in rhabdoid tumor cells.

97 llowed by lethal regrowth of more aggressive tumor cells.

98 mTORC2 kinase activity and invasion in colon tumor cells.

99 Optic gliomas are brain tumors characterized by slow growth, progressive loss of

100 Tumors contain hostile inflammatory signals generated by

101 The three stage 4 tumors contained mutations in genes encoding protein pro

102 CD20-IL-21 therapy resulted in a significant tumor control in the rituximab-resistant A20-huCD20 tumo

103 This agrees well with the calculated tumor control probability.

104 treatment would be associated with effective tumor control upon treatment with anti-PD-L1 therapy.

105 with substantial reduction in the number of tumor cytotoxic T lymphocytes.

106 nificantly increases the plasma abundance of tumor-derived microRNA rapidly after treatment.

107 anti-apoptotic BCL-2 proteins contributes to tumor development and resistance to therapy by suppressi

108 Tumor development and therapeutic resistance are linked

109 Since acidosis is a hallmark of tumor development, progression, and aggressiveness, the

110 ence in primary cells, an initial barrier to tumor development.

111 in targeting cancer cells and metastases for tumor diagnosis, imaging, and therapy.

112 Conclusion Maximum tumor diameter demonstrates superior performance relativ

113 0.81; 95% CI, 0.56-1.18; P = .273) or whose tumors did have KRAS mutations (adjusted RR, 0.59; 95% C

114 any cause or from cancer for patients whose tumors did not contain KRAS mutations (adjusted RR, 0.81

115 Elevated MPV was associated with tumor differentiation (p < 0.001).

116 ugh macrophages were more potent in uptaking tumor DNA, increase of DNA sensing by blocking the inter

117 Neurofibromas are benign peripheral nerve tumors driven by NF1 loss in Schwann cells (SCs).

118 n significant activity, particularly against tumors driven by the estrogen receptor (ER).

119 Adaptive therapy, using patient-specific tumor dynamics to inform on/off treatment cycles, suppre

120 nfiltration of tumors and showed strong anti-tumor effects.

121 Previous studies suggest that peripheral tumors elicit central pro-inflammatory cytokine producti

122 umor size and invasiveness and could lead to tumor eradication.

123 Glioblastoma (GBM) tumors exhibit potentially actionable genetic alteration

124 The relationship to histologic tumor extent needs to be further analyzed.

125 r hyperplasia (FNH) is a common benign liver tumor for which conservative management is indicated.

126 onally affected multiple times in individual tumors for 11 of 12 single-cell sequencing data sets fro

127 yet the sequence of alterations that promote tumor formation are incompletely understood.

128 binding significantly accelerated colorectal tumor formation while having no discernable effect on sm

129 essential to retinoblastoma cell growth and tumor formation, and ectopic MYCN partially reversed the

130 e polyomavirus oncogene most responsible for tumor formation.

131 ng no discernable effect on small intestinal tumor formation.

132 m November 2013 through May 2017, along with tumor-free liver tissues (control tissues) and periphera

133 e show that a high LOX expression in primary tumors from patients with colorectal cancer was associat

134 promise of future widespread resequencing of tumor genomes in providing new insights into the contrib

135 There was some evidence of heterogeneity by tumor grade ( P = .02), with an increased risk for low-i

136 tagenes also have predictive value regarding tumor grade and patient outcomes.

137 genes, and knockdown of circCCDC66 inhibited tumor growth and cancer invasion in xenograft and orthot

138 PUMA, which induces anoikis to suppress PDAC tumor growth and metastasis.

139 t provides an improved theoretical basis for tumor growth control and may also find utility in therap

140 is required for oncogenic transcription and tumor growth in non-small-cell lung cancer (NSCLC).

141 eam genes and promote cell proliferation and tumor growth in vivo Taken together, our findings reveal

142 Moreover, tumor growth is accelerated, not only in tristetraprolin

143 microparticles (MPs), supported accelerated tumor growth which was halted by PMP transfusion.

144 CTX014 decreased tumor growth, affected the accumulation and tolerogenic

145 of SFN on HCC tumor angiogenesis as well as tumor growth, and indicate that SFN has potential for th

146 cells decreased B16-F10 metastasis and s.c. tumor growth, and this was IFN-gamma dependent.

147 ges and reduces CD8+ T cells to promote lung tumor growth.

148 n and diminished both lung MDSC presence and tumor growth.

149 reduced AR and AR-V7 levels to mitigate CRPC tumor growth.

150 Early anatomic imaging may show that a tumor has increased in size, but this could represent ps

151 (2,201 v 2,558 patient cases; 2,278 v 2,659 tumors), HER2 positivity remained constant (15.7% v 15.5

152 d and compared with the visual assessment of tumor heterogeneity.

153 ne system can mount T cell responses against tumors; however, the antigen specificities of tumor-infi

154 allenges in accurate control of large volume tumor hyperthermia for longer duration (>30min.).

155 hese findings suggest that multiple distinct tumor immune microenvironments co-exist within a single

156 r role in tumor-associated blood vessels and tumor immunity, and provide an update on mTOR inhibitors

157 as a probe to identify Thy-1(+) CAF-enriched tumors in a compendium of 1,586 lung adenocarcinomas, th

158 bservation alone strategy for low-risk Wilms tumor incorporating both clinical features and biomarker

159 yme in the kynurenine pathway which augments tumor-induced immune tolerance.

160 Recent studies have found that tumor-infiltrating lymphocytes (TIL) expressing PD-1 can

161 umors; however, the antigen specificities of tumor-infiltrating lymphocytes (TILs) are not well under

162 r by remotely supplying a distinct subset of tumor-infiltrating SiglecF(high) neutrophils, which exhi

163 on of several derepressed miR-155 targets in tumor-infiltrating, miR-155-deficient CD8(+) T cells, su

164 extension of lifespan, cardioprotection, and tumor inhibition.

165 Genetic depletion of p62 robustly inhibited tumor-initiating frequencies, as well as growth rates of

166 differing outcomes-loss of p53 promotes both tumor initiation and progression; loss of Arf promotes t

167 ioma stem cells (GSCs), which contributes to tumor initiation and treatment resistance.

168 The analysis of invading leader cells at the tumor invasion front is of significant interest as these

169 hroughput genomic and molecular profiling of tumors is emerging as an important clinical approach.

170 Cancer cell invasion from primary tumors is mediated by a complex interplay between cellul

171 ression of Arf in tumor stromal cells, as in tumor keratinocytes themselves, contributes to suppressi

172 These tumors lack deregulation of APC/beta-catenin signaling c

173 environment, which dynamically modulates the tumor landscape.

174 do not experience uniform uptake throughout tumors, leading to sub-lethal cell killing that can impa

175 ed oHSV alone, effectively tracks metastatic tumor lesions and significantly prolongs the survival of

176 The median SUVmax of 94 tumor lesions was 7.3 (range, 1.6-59.5).

177 In individual tumors, levels of MMP2 and MMP13 correlated more closely

178 A low but significant target expression in tumor, lung, and stomach was confirmed by immunohistoche

179 he patients (88.7% of cases were in adults), tumors (mainly ganglioglioma) in 23.6%, and malformation

180 function by recognizing the highly expressed tumor marker CD133, which is located on the surface of l

181 luating the role of pretreatment circulating tumor markers as predictors of prognosis in chemotherapy

182 h bilateral involvement (n = 27 of 55; 47%), tumor masses (n = 27 of 36; 75%), and involvement of the

183 othesized therapeutic response is related to tumor metabolic phenotype, and that altering tumor metab

184 tumor metabolic phenotype, and that altering tumor metabolism could change therapeutic outcome.

185 s yields high resolution 3D maps of multiple tumor microenvironment components and biomarkers through

186 R2 rapidly formed tumors outside the primary tumor microenvironment in nude mice, exhibited signature

187 to its products, the function of 5-LO in the tumor microenvironment remains unclear.

188 acrophages are prominent immune cells in the tumor microenvironment that exert potent effects on canc

189 D8(+) dendritic cells were identified in the tumor microenvironment.

190 We investigated a size-controlled, dual tumor-mitochondria-targeted theranostic nanoplatform (Po

191 deficient LNCaP prostate carcinoma xenograft tumor model.

192 henomenon in an aggressive MCF10-CA1a breast tumor model.

193 findings in vitro and in vivo in two murine tumor models, in primary human breast and lung cancer ce

194 T-cell activation and antitumor activity in tumor models.

195 The tumor necrosis factor (TNF) family ligand ectodysplasin

196 Dysregulation of tumor necrosis factor (TNF) receptor signaling is a key

197 nzyme-linked immunosorbent assays quantified tumor necrosis factor (TNF), interleukin (IL)-12, and IL

198 levels of inflammatory cytokines, including tumor necrosis factor (TNF).

199 nfluenza A (H5N1) virus induce expression of tumor necrosis factor alpha, interleukin-6, and interleu

200 including the long-sought-after nephrin and tumor necrosis factor genes.

201 We examined the role of tumor necrosis factor receptor-associated factor 2 (Traf

202 B cells, which produced elevated amounts of tumor necrosis factor-alpha (TNFalpha) that contributed

203 y proteins (inducible nitric oxide synthase, tumor necrosis factor-alpha, and interleukin 6).

204 Serum tumor necrosis factor-alpha, interleukins, hemogram, and

205 er than agonists in detecting neuroendocrine tumors (NETs).

206 M exposure, and amount of exercise, affected tumor number and size.

207 vasive tumor and 1,943 subjects with in situ tumors only.

208 ce orthotopically implanted with gliosarcoma tumors or glioma stem-like cells, respectively.

209 No single mutation occurred in all four tumors or in all stage 4 tumors.

210 E-cadherin, CD24, and VEGFR2 rapidly formed tumors outside the primary tumor microenvironment in nud

211 12 patients were available for assessment of tumor overlap.

212 ls.SIGNIFICANCE STATEMENT By comparing brain tumor patients to healthy children, we establish that ch

213 were employed for both in vitro and in vivo tumor phenotyping to identify the tumorigenicity of the

214 enes involved in oxidative stress responses, tumor progression and chemoresistance.

215 the colorectal tumor stroma associates with tumor progression and reduced survival time of patients

216 iation and progression; loss of Arf promotes tumor progression but not initiation.

217 gs indicate that R-ketorolac treatment slows tumor progression in an aggressive model of breast cance

218 is that plays important roles in metabolism, tumor progression, viral replication, and skin barrier f

219 have different effects on cell behavior with tumor progression.

220 mary transforming proteins in HPV that drive tumor progression.

221 is beginning to emerge, with the notion that tumor-promoting functions are attributed to its products

222 cytic) M-MDSC infiltration, which results in tumor radioresistance.

223 evaluated biometrics for prediction of local tumor recurrence after renal cell carcinoma ablation.

224 Tumor recurrence remains the main reason for breast canc

225 ficantly higher than those in other abnormal tumor regions (P < .001 and P = .008 for contrast-enhanc

226 ber 1994 and October 1995 in one of six SEER tumor registries and who completed a 15-year follow-up s

227 Eliminating PEPD causes cell death and tumor regression due to p53 activation.

228 e now produced a compound that shows durable tumor regression in a lymphoma xenograft model.

229 aring mice with an IKK inhibitor resulted in tumor regression.

230 The tumors represented in the patient cohort were mainly gas

231 (TNFalpha) that contributed to the increased tumor resistance to BRAF inhibitors.

232 y small size, SN-NPM possessed superior long tumor retention time (>5days) and much higher accumulati

233 n patterns across tumor types and individual tumor samples.

234 es superior performance relative to existing tumor scoring systems and other evaluated biometrics for

235 Although polyoma virus middle T-driven tumors showed altered primary and metastatic profiles in

236 g mice carrying orthotopic breast MDA-MB-231 tumors showed that the cyclic peptide preferentially acc

237 K-Ras-beta-catenin tumors showed up-regulation of beta-catenin targets like

238 oma, including the gastroesophageal junction tumors (Siewert I), were randomized between open and MI

239 inum-refractory disease, mediastinal primary tumor site, nonseminoma histology, intermediate- or poor

240 already approved by the FDA, can reduce both tumor size and invasiveness and could lead to tumor erad

241 herapy outcomes was provided by pretreatment tumor size and the underlying immune recruitment dynamic

242 cell death both in vitro and in vivo through tumor-specific (1) O2 generation and subsequent ROS medi

243 One-hundred fifty-one tumor specimens stained positive for podoplanin (33 high

244 Tumor specimens were collected from Baptist Cancer Cente

245 ogist is critical for patient management for tumor staging and assessing treatment response.

246 ost-LT surveillance, provide a framework for tumor staging and risk stratification, and select candid

247 ed expression is associated with an advanced tumor state and a poor prognosis.

248 coculture with PC3 cells, which might boost tumor stem-like properties.

249 of EGFR in myeloid cells from the colorectal tumor stroma associates with tumor progression and reduc

250 Intriguingly, increased expression of Arf in tumor stromal cells, as in tumor keratinocytes themselve

251 ide clinical candidates for reactivating the tumor suppression function of p53 in cancer by dual targ

252 those p53-inducible genes most critical for tumor suppression remain elusive.

253 s growing understanding of the oncogenic and tumor suppressive functions of JARID1 proteins, which ar

254 In summary, ARID1A has context-dependent tumor-suppressive and oncogenic roles in cancer.

255 Here we report a tumor-suppressive mode of action for growth-differentiat

256 ted factor 2 (EAF2) is an androgen-regulated tumor suppressor and its intracellular localization can

257 The multispecific transcription factor and tumor suppressor FOXO3 is an important mediator of apopt

258 These latter findings support a tumor suppressor function for KIND1, and identify c-Jun

259 ead to the replacement of single, functional tumor suppressor genes by the mutant alleles.

260 pression and increased expression of several tumor suppressor genes, including Src homology region 2

261 ependent growth in the context of concurrent tumor suppressor loss.

262 18 gene has been proposed to act either as a tumor suppressor or as an oncogene in different human ca

263 Loss of the tumor suppressor p53 (encoded by TP53) provides cancer c

264 We found induction of tumor suppressor protein, p53, and apoptosis with suppre

265 p53 tumor suppressor responds to various cellular stresses a

266 The tumor suppressor serine/threonine kinase 11 (LKB1/STK11)

267 owed that Mig-6 has an important function of tumor suppressor via inhibition of STAT3 phosphorylation

268 Comutated, myeloid tumor-suppressor genes contribute to phenotypic variabil

269 acquired with careful attention to protocol, tumor SUV has a within-subject coefficient of variation

270 Tumor targeting results were quantitatively similar at 7

271 ime (>5days) and much higher accumulation in tumors than in normal organs, as shown by near-infrared

272 after BCM-PTX injection further improved the tumor therapeutic effect and elongated the survival time

273 tember 2014 who had preoperative CT data and tumor tissue available was studied.

274 between 4 antibodies revealed regression for tumor tissue cores (R2 = 0.42-0.91) and cell line cores

275 Conclusion Mechanical tumor tissue disruption with pulsed focused ultrasound-i

276 The first patient's tumor tissue was investigated for secretin and VIP.

277 d HLA class-I expression was observed in MCC tumor tissues and MCC cell lines.

278 ated ( approximately 70 times) in colorectal tumor tissues compared with their normal pairs.

279 similar at 72 and 144 h after injection, but tumor-to-blood-pool SUV ratios increased with time after

280 In addition, tumor-to-liver contrast was superior in the parametric K

281 fter initiation of pulsed focused ultrasound tumor treatment, and these increases persisted for 3 hou

282 immune checkpoint expression patterns across tumor types and individual tumor samples.

283 Dose- and time-dependent tumor uptake was studied in nude BALB/c mice bearing a s

284 rived suppressor cell (MDSC) infiltration in tumors via chemokine axis.

285 and reveals unexpected mechanisms mediating tumor viability and invasion, including potassium channe

286 DNA tumor viruses such as Kaposi's sarcoma-associated herpes

287 ET/CT combined with baseline total metabolic tumor volume (TMTV) could detect early relapse or refrac

288 Location of pelvic tumor was the major inferior disease-specific prognostic

289 e response to PD-1 blockade in a mesenchymal tumor, we identified PTEN mutations and reduced expressi

290 imals with subcutaneous R3230 adenocarcinoma tumors were allocated to RFA or sham treatment with or w

291 The primary tumors were breast cancer (92 patients, 426 scans), non-

292 Head and neck tumors were independently associated with a higher numbe

293 Finally, epithelial tumors were more susceptible to elimination by immunothe

294 All tumors were treated in a single procedure using the 4C o

295 , especially those with HER2 and ER negative tumors, who will receive one of the widely-accepted chem

296 DiD-NCM had similar high-level uptake in tumor with DiD-BCM within the first 3days, its accumulat

297 ies, as well as growth rates of BCSC-derived tumor xenografts in immunodeficient mice.

298 ls in vitro and enhanced clearance of PD-L1+ tumor xenografts in vivo.

299 aving observed complete eradication of solid tumor xenografts, we conclude that targeted alpha-therap

300 ditive reduction in the growth of MDA-MB-231 tumor xenografts.

301 metastasis of intravenous and intraprostatic tumor xenografts.