ライフサイエンスコーパス: teratoma

1 tumors that contain a variety of cell types (teratomas).

2 One 14-year-old girl had an ovarian teratoma.

3 ans, the most common teratoma is the ovarian teratoma.

4 etal regeneration without the formation of a teratoma.

5 available had tumours, most commonly ovarian teratoma.

6 s reported for the presence of viable GCT or teratoma.

7 ody encephalitis was associated with ovarian teratoma.

8 of 90% choriocarcinoma, 9% seminoma, and 1% teratoma.

9 carcinoid, parotid pleomorphic adenoma, and teratoma.

10 tibody positivity had evidence of an ovarian teratoma.

11 although Dmrt1 mutant females do not develop teratomas.

12 essed pluripotent cell markers and generated teratomas.

13 ll transplantation was safe and did not form teratomas.

14 ansgene are highly susceptible to developing teratomas.

15 ility is limited by their propensity to form teratomas.

16 g force in the initiation and progression of teratomas.

17 ression were observed in a small fraction of teratomas.

18 tended passage, and have the ability to form teratomas.

19 formation of neural tube-like structures in teratomas.

20 d inhibits angiogenesis and proliferation in teratomas.

21 e infarcted mouse heart without formation of teratomas.

22 lly develop, resulted in a high incidence of teratomas.

23 rentiated into cardiac cells without forming teratomas.

24 he capacity to differentiate in vitro and in teratomas.

25 ontractile function without the formation of teratomas.

26 e embryonic germ layers both in vitro and in teratomas.

27 yonic or pluripotent stem cells, do not form teratomas.

28 ophages do not develop abnormal pathology or teratomas.

29 , transplanted hiEndoPCs do not give rise to teratomas.

30 ined even after in vivo differentiation into teratomas.

31 nce after prolonged culture and did not form teratomas.

32 ES-derived cell transplantation and risk of teratomas.

33 differentiated TKO embryoid bodies (EBs) and teratomas.

34 NA profile and development in the context of teratomas.

35 is rarely described in patients with ovarian teratomas.

36 ), and secondary somatic-type malignancy +/- teratoma (20%).

37 Of the 269 patients with viable GCT or teratoma, 20 to 86 (7% to 32%) patients had evidence of

38 omyoma, 25 fibroma, 14 myxoma, 6 vascular, 4 teratoma, 3 lipoma, and 15 other.

39 at was removed (5/8) than in those without a teratoma (4/23; p = 0.03).

40 , viable nonteratomatous germ cell tumor +/- teratoma (41%), and secondary somatic-type malignancy +/

41 SGCT with immature teratoma or NSGCT without teratoma (5-year CIDD rate, 38.1%, 19.9%, and 17.4%, res

42 We propose that the teratoma, a recognized standard for validating pluripote

43 Vhl(2B/2B) teratomas additionally displayed a growth advantage over

44 ated derivatives pose cancer risk by forming teratomas after transplantation.

45 with teratoma than those with NSGCT without teratoma and seminoma (5-year CIDD rate, 27.4%, 17.4%, a

46 The patient was found to have an ovarian teratoma and serum and cerebrospinal fluid NMDAR antibod

47 Despite resection of the teratoma and treatment with immunosuppressive therapy, t

48 ild-type iPSCs and support the generation of teratomas and chimeric mice.

49 The SSCiPSC were able to form teratomas and generated chimeras with a higher skin chim

50 the cell cycle in G0/G1 and differentiate in teratomas and in culture.

51 ng of the biology of spontaneously occurring teratomas and related tumors in humans can help to guide

52 at)/+, P53-/- male mice developed testicular teratomas and survived an average of 65 days, whereas no

53 59693 was stronger for nonseminomas, and for teratomas and teratocarcinomas in particular (N = 58; CT

54 Tumours, usually ovarian teratoma, and herpes simplex encephalitis are known trig

55 oung age (teenager to young adult), systemic teratoma, and high response to treatment characterize th

56 into bona fide endothelial cells within the teratoma, and that these ES-derived endothelial cells fo

57 e the capability to form embryoid bodies and teratomas, and can differentiate into all three germ lay

58 ns poorly, form small, poorly differentiated teratomas, and cannot generate chimeric mice.

59 express endogenous pluripotency genes, form teratomas, and contribute to multiple tissues, including

60 that expressed pluripotency markers, formed teratomas, and contributed to cell types of all germ lay

61 Taken together, teratomas are a promising platform for modeling multi-li

62 Teratomas are a unique class of tumors composed of ecto-

63 Ovarian teratomas are frequently described in patients with N-me

64 ey may originate anywhere along the midline, teratomas are most commonly found in sacrococcygeal, gon

65 Teratomas are rare neoplasms composed of tissue elements

66 nderstanding why a minority of patients with teratomas are seen with autoimmune encephalitis may impr

67 Dnd1(Ter/Ter) mutant mice, where testicular teratomas arise only on the 129/SvJ genetic background.

68 to derivatives of the three germ layers in a teratoma assay, and are karyotypically normal.

69 ents as well as a detailed comparison to the teratoma assay.

70 In vitro, in vivo, and teratoma assays demonstrated that either a directly sort

71 ferentiation and proliferation using in vivo teratoma assays in nonobese diabetic mice with severe co

72 cells gave rise to all three germ layers in teratoma assays, though sex-specific differences could b

73 ion potential in embryoid body formation and teratoma assays.

74 not in 39 controls, reliably distinguishing teratomas associated with NMDAR encephalitis (P < .001).

75 e management of NMDAR encephalitis and other teratoma-associated autoimmune diseases.

76 Among 249 patients with teratoma-associated encephalitis, 211 had N-methyl-D-asp

77 Patients found to have teratoma at PC-RPLND have a 10-year probability of freed

78 le germ cells also generated fully developed teratomas at a high rate.

79 and imaging studies were performed in human teratoma-bearing mice for up to 48 h after injection.

80 tumor that expresses NMDAR (usually ovarian teratoma), but in male patients and children the presenc

81 Allogeneic ES cells also caused cardiac teratomas, but these were immunologically rejected after

82 emales on a mixed background did not develop teratomas, but were fertile and produced viable off-spri

83 FIF is differentiated from the teratoma by the presence of vertebral column often with

84 at concern, as reflected in the formation of teratomas by transplanted pluripotent cells.

85 Additionally, we demonstrated that teratomas can be sculpted molecularly via microRNA (miRN

86 CRISPR-Cas9 knockout screens, we showed that teratomas can enable simultaneous assaying of the effect

87 hFc inhibited autocrine wnt signaling in the teratoma cell lines PA-1, NTera-2, Tera-2, and NCCIT.

88 l types across all 3 germ layers, that inter-teratoma cell type heterogeneity is comparable with orga

89 fied by gene expression analysis of cultured teratoma cells, were also modulated in the tumor xenogra

90 ents with signs of demyelination had ovarian teratoma compared with 18 of 50 anti-NMDAR controls (p50

91 served in patients who had NSGCT with mature teratoma compared with those with either NSGCT with imma

92 in28, and SSEA4), and can differentiate into teratomas composed of the three germ layers.

93 The ability of Pofut2 mutant embryos to form teratomas comprised of tissues from all three germ layer

94 ES cells remained pluripotent and generated teratomas consisting of the three germ layers.

95 Cardiac teratomas contained no more cardiomyocytes than hind-lim

96 ltured under differentiating conditions, and teratomas containing tissues of ectoderm, mesoderm, and

97 patients with teratoma than in those without teratoma (CSF 395 vs 110, difference 285 [134-437], p=0.

98 Here we review the features of teratomas derived experimentally from human pluripotent

99 number of genes frequently overexpressed in teratomas derived from EiPSCs, and several such gene pro

100 owth, and MIF inhibition effectively reduced teratoma development after ESC transplantation.

101 the microenvironment on stem cell growth and teratoma development using undifferentiated ESCs.

102 stringent control of retinal detachment and teratoma development will be necessary before initiation

103 environment that supported the initiation of teratoma development.

104 Teratoma did not express miR-371a-3p.

105 Abnormal neurons within teratomas distinguish cases with NMDAR encephalitis from

106 ixed background Dnd1(Ter/Ter) mutants, where teratomas do not typically develop, resulted in a high i

107 rns of relapse with different outcomes: pure teratoma, early viable NS relapse (< 2 years), and late

108 testicular germ-cell tumours (such as benign teratoma, epidermoid cyst and malignant yolk-sac tumours

109 All histologic subgroups, except teratoma, express this marker.

110 demonstrated that allogenic CP hESC-derived teratomas, fibroblasts, and cardiomyocytes are immune pr

111 es (93.2%) were benign (rhabdomyoma, myxoma, teratoma, fibroma, and hemangioma).

112 ase recurrence, 10 (33%) had recurrence with teratoma, five (17%) had recurrence with teratoma with m

113 versus 129-Chr19(MOLF/Ei)), and resistant to teratoma formation (FVB), we found that germ cell prolif

114 tency, such as pluripotency gene expression, teratoma formation and contribution to chimeras.

115 Lack of teratoma formation and evidence of long-term myoblast en

116 l and genetic integrity were demonstrated by teratoma formation and normal karyotype, respectively.

117 Teratoma formation assays were performed, and tumors wer

118 iPSCs and canine embryonic stem cells; (iii) teratoma formation assays; and (iv) karyotyping for geno

119 inhibited proliferation, clonogenicity, and teratoma formation by Lu-iPSCs, and diminished clonogeni

120 luripotent stem cells (hESCs and hiPSCs), is teratoma formation by residual undifferentiated cells.

121 c retained pluripotency, differentiation and teratoma formation capabilities.

122 mECM preparations also completely inhibited teratoma formation from ESC inoculations.

123 ed hESCs to immune-deficient mice results in teratoma formation from hESCs irradiated at all doses, d

124 this issue of Blood use a novel strategy of teratoma formation from human induced pluripotent stem c

125 n a heterogeneous population and can prevent teratoma formation in an in vivo tumorigenicity assay.

126 The risk of teratoma formation in iVPCs is also reduced in compariso

127 s normal differentiation in vitro and benign teratoma formation in vivo of the HMGA1-derived iPSCs.

128 rentiated hPSCs >10(6)-fold, thus preventing teratoma formation in vivo.

129 germ cell loss and protects from testicular teratoma formation on a mixed genetic background.

130 Cs), however, this can only be monitored via teratoma formation or in vitro differentiation, as ethic

131 ffects of stem cells without the problems of teratoma formation or limited cell engraftment and viabi

132 erns for PSCs related to their potential for teratoma formation or neural overgrowth.

133 schemic mouse retina and limb, and they lack teratoma formation potential.

134 E12.5, E13.5 and E14.5, immediately prior to teratoma formation, and correlated this information with

135 ly differentiated into Schwann cells with no teratoma formation, and they secreted higher concentrati

136 (ED) origins with normal karyotype, verified teratoma formation, pluripotency biomarkers, and tri-lin

137 of embryoid body (EB) differentiation, like teratoma formation, signifies a spontaneous differentiat

138 iPSC injection resulted in teratoma formation, whereas iPSC-EV injection was safe.

139 tiation of ESCs can help prevent the risk of teratoma formation, yet proliferating neural progenitors

140 poietic stem/progenitor cells (HSPCs) during teratoma formation.

141 tion, colony expansion, cryopreservation and teratoma formation.

142 fective in folliculogenesis and conducive to teratoma formation.

143 ll types derived of all 3 germ layers during teratoma formation.

144 an initial treatment aborts embryoid body or teratoma formation.

145 rm cells but not in Sertoli cells to prevent teratoma formation.

146 ltimately lose all PGCs with no incidence of teratoma formation.

147 get genes, whose missexpression may underlie teratoma formation.

148 hosphatase and aquaporin-1 for 7 mo, without teratoma formation.

149 and could cause other complications such as teratoma formation.

150 yocardial infarction without any evidence of teratoma formation.

151 cting single cells, and effectively prevents teratoma formation.

152 ach was demonstrated by the lack of tumor or teratoma formation.

153 rom pluripotency, both in culture and during teratoma formation.

154 5 and two additional PSMs completely removed teratoma-formation potential from incompletely different

155 ctivated cell sorting (FACS) greatly reduced teratoma-formation potential of heterogeneously differen

156 uman immune system, we demonstrate that most teratomas formed by autologous integration-free hiPSCs e

157 In addition, the majority of teratomas formed by B6 EiPSCs were immunogenic in B6 mic

158 Global gene expression analysis of teratomas formed by B6 ESCs and EiPSCs revealed a number

159 In contrast to B6 ESCs, teratomas formed by B6 ViPSCs were mostly immune-rejecte

160 X6 expression was significantly decreased in teratomas formed by TET1-deficient hESCs.

161 be characterized, methods to purge residual teratoma-forming cells from differentiated populations m

162 To ensure complete removal of teratoma-forming cells, we identified additional pluripo

163 uencing (RNA-seq) of 179,632 cells across 23 teratomas from 4 cell lines, we found that teratomas rep

164 Reactive changes were present in teratomas from controls, including ferruginated neurons

165 in vivo, inducing transcriptionally distinct teratomas from which pluripotent cells can be recovered.

166 f partially reprogrammed iPSC cases (6 of 14 teratomas) generated major dysplasia and malignant tumor

167 ectopically localized Tuj1(+) cells in RB-KO teratomas grown in vivo Taken together, these results id

168 m ESCs specifically reduced angiogenesis and teratoma growth, and MIF inhibition effectively reduced

169 ity is comparable with organoid systems, and teratoma gut and brain cell types correspond well to sim

170 ssion in a human embryonic stem cell-derived teratoma (hESCT) tumor model previously shown to have hu

171 embryonal, 10% yolk sac tumor, and 5% mature teratoma histologies.

172 splantation of Pax3-induced cells results in teratomas, however, indicating the presence of residual

173 ure teratoma in 178 patients (85%), immature teratoma in 15 patients (7%), and teratoma with malignan

174 PC-RPLND pathology revealed mature teratoma in 178 patients (85%), immature teratoma in 15

175 female), and tumor association (43%; ovarian teratoma in all cases) were similar to the population at

176 Presence of teratoma in ORCH and PC-RPLND specimens was not a progno

177 years (range, 13-71 years); 689 patients had teratoma in ORCH specimen, and 535 did not.

178 2 groups according to presence or absence of teratoma in ORCH specimen.

179 Presence of teratoma in patients with metastatic testicular germ cel

180 PC-RPLND; 5-year PFS for patients with pure teratoma in PC-RPLND specimen versus necrosis only was 6

181 urvival outcomes of patients with or without teratoma in primary tumor and postchemotherapy retroperi

182 a of the ovary (six mature) and one a mature teratoma in the mediastinum; five of five tumors examine

183 patients will harbor either viable cancer or teratoma in the retroperitoneum.

184 initial PC-RPLND and were found to have only teratoma in the retroperitoneum.

185 logeneic ESCs from 129/SvJ mice fail to form teratomas in B6 mice due to rapid rejection by recipient

186 nbred C57BL/6 (B6) mice can efficiently form teratomas in B6 mice without any evident immune rejectio

187 They form well-differentiated teratomas in immune-compromised mice that secrete human

188 gene expression and in the capacity to form teratomas in immune-deficient mice.

189 s their capability to self-renew and to form teratomas in immunodeficient mice.

190 to the diagnosis, management and outcome of teratomas in infants and children.

191 ES cells also formed teratomas in infarcted hearts, indicating injury-related

192 y form embryoid bodies in tissue culture and teratomas in mice.

193 d mouse ES cells consistently formed cardiac teratomas in nude or immunocompetent syngeneic mice.

194 ontrast to wild-type cells, did not generate teratomas in the host brains, leading to strongly enhanc

195 ey maintain their pluripotency markers, form teratomas in vivo, and differentiate into all three germ

196 logy, expressed pluripotency markers, formed teratomas in vivo, had a normal karyotype, retained and

197 differentiation yet fail to efficiently form teratomas in vivo, whereas DeltaPsi(m)H cells behave in

198 They differentiate in vitro and form teratomas in vivo.

199 have lost pluripotency genes and do not form teratomas in vivo.

200 entiate to all three germ layers and to form teratomas in vivo.

201 s also generate embryoid bodies in vitro and teratomas in vivo.

202 ormal karyotype in vitro, as well as develop teratomas in vivo.

203 ng iPSCs formed embryoid bodies in vitro and teratomas in vivo.

204 he presence of teratoma, particularly mature teratoma, in an NSGCT primary tumor is associated with a

205 Using mouse strains with low versus high teratoma incidence (129 versus 129-Chr19(MOLF/Ei)), and

206 Stra8-deficient mice had an 88% decrease in teratoma incidence, providing direct evidence that prema

207 , expressed all pluripotency markers, formed teratomas indistinguishable from those of mESCs, and und

208 In susceptible strains, where teratomas initiate around E15.5-E17.5, many mutant germ

209 In the 129 family of inbred strains of mice, teratomas initiate around embryonic day (E) 13.5 during

210 iotic switch in XY germ cells contributes to teratoma initiation.

211 In humans, the most common teratoma is the ovarian teratoma.

212 The traditional method for grading immature teratomas is challenged by a new classification.

213 of primary location, definitive therapy for teratomas is complete surgical resection.

214 The presence of a tumour (usually an ovarian teratoma) is dependent on age, sex, and ethnicity, being

215 ldren with mature teratoma (MT) and immature teratoma (IT) to assist future treatment plans.

216 s of the pancreas (focal fatty infiltration, teratoma, liposarcoma).

217 ved neurons and various tissues derived from teratomas manifested cell-type specific respiratory chai

218 Malignant transformation of mature teratomas may be predicted by preoperative squamous cell

219 l imaging helps in differentiating it from a teratoma, meconium peritonitis and abdominal ectopic pre

220 Endothelial differentiation in the ES teratoma model allows gene-targeting methods to be used

221 n vitro Moreover, trisomic stem cells formed teratomas more efficiently, from which undifferentiated

222 factors for relapse of children with mature teratoma (MT) and immature teratoma (IT) to assist futur

223 a (n = 9), thrombus (n = 4), myxoma (n = 3), teratoma (n = 2), and paraganglioma, pericardial cyst, P

224 tic cysts (n = 5; two endometriomas); mature teratoma (n = 3); hydrosalpinx (n = 2); fibroma (n = 1);

225 (n = 10), other cancers (n = 5), and ovarian teratoma (n = 8); 3 additional patients without detectab

226 Pathology included necrosis only (25%), teratoma +/- necrosis (20%), viable nonteratomatous germ

227 The histologic finding of teratoma occurs in approximately 40% of all postchemothe

228 Eleven patients had teratoma of the ovary (six mature) and one a mature tera

229 We evaluated the long-term impact of teratoma on survival in patients with NSGCT.

230 ermoid cysts, one patient had sacrococcygeal teratoma, one patient had a cystadenofibroma (partial bo

231 efinite NMDAR-Ab encephalitis (eight ovarian teratomas, one Hodgkin's lymphoma), 18 (32.1%) a Possibl

232 The same mutation also leads to testicular teratomas only on the 129Sv/J background.

233 The lack of teratoma or any ectopic tissue formation in the implante

234 d with those with either NSGCT with immature teratoma or NSGCT without teratoma (5-year CIDD rate, 38

235 ven that at least 7% to 32% of men will have teratoma or viable GCT outside the boundaries of a modif

236 The potential for the formation of teratomas or other neoplasms is a major safety roadblock

237 markers (NANOG and POU5F1) in chemoresistant teratomas or transformed carcinomas.

238 No teratomas or tumors were found in any of the animals (n=

239 OR = 1.16; 95% CI: 1.04, 1.29), particularly teratomas (OR = 1.26; 95% CI: 1.12, 1.41); and retinobla

240 Genetically, Tgkd teratomas originate from mature oocytes that have comple

241 ve completed meiosis I, suggesting that Tgkd teratomas originate from these trapped oocytes.

242 Differentiated Vhl(2B/2B)-derived teratomas overexpressed joint HIF targets Vegf and EglN3

243 Similarly, HSPCs can be isolated from teratoma parenchyma and reconstitute a human immune syst

244 The presence of teratoma, particularly mature teratoma, in an NSGCT prim

245 ) had either viable germ cell tumor (GCT) or teratoma present in the RPLND specimen.

246 , pregnancy association, presence of ovarian teratoma, prior herpes simplex virus encephalitis, and i

247 d pathology of these spontaneously occurring teratomas provide important clues for preclinical safety

248 3 teratomas from 4 cell lines, we found that teratomas reproducibly contain approximately 20 cell typ

249 ere closely related to immune infiltrates in teratomas resected from 4 of 4 cases.

250 Atypical neurons were seen within teratomas resected from 4 of 5 cases but not in 39 contr

251 dysplastic) CNS neuronal elements in ovarian teratomas resected from cases vs controls, as well as ch

252 em neuronal elements were detected in 4 of 5 teratomas resected from cases with NMDAR encephalitis an

253 Testicular teratomas result from anomalies in germ cell development

254 lost oriP/EBNA-1 episomal vectors, generated teratomas, retained donor identity, and differentiated i

255 alable approach to efficiently eliminate the teratoma risk associated with hESCs without apparent neg

256 tural organization, functional benefits, and teratoma risk of engineered heart muscle (EHM) in a chro

257 tained no more cardiomyocytes than hind-limb teratomas, suggesting lack of guided differentiation.

258 yed a growth advantage over Vhl(-/-)-derived teratomas, suggestive of a tight connection between pert

259 ination gene DMRT1, which has been linked to teratoma susceptibility in mice.

260 consistent with previous genetic mapping of teratoma susceptibility loci to the region containing Gf

261 lar dysgenesis, pluripotency regulation, and teratoma susceptibility that is highly sensitive to gene

262 DNF coreceptors Gfra1 and Ret for effects on teratoma susceptibility.

263 induction of differentiation, associate with teratoma susceptibility.

264 tural variation in Dmrt1 activity can confer teratoma susceptibility.

265 igenesis, respectively, were co-expressed in teratoma-susceptible germ cells and tumor stem cells, su

266 cid 8 (Stra8), were prematurely expressed in teratoma-susceptible germ cells and, in rare instances,

267 oma (EC) and its differentiated derivatives, teratoma (TE), yolk sac tumor (YST), and choriocarcinoma

268 were higher in patients with poor outcome or teratoma than in patients with good outcome or no tumour

269 [2369-9885], p=0.0025), and in patients with teratoma than in those without teratoma (CSF 395 vs 110,

270 was observed in patients who had NSGCT with teratoma than those with NSGCT without teratoma and semi

271 curred more frequently in patients who had a teratoma that was removed (5/8) than in those without a

272 ion of bone matrix, without the formation of teratomas that is consistently observed when undifferent

273 hey most closely resemble spontaneous benign teratomas that occur early in both mouse and human life.

274 has any study assessed their ability to form teratomas, the definitive test of pluripotency.

275 institution undergoing initial PC-RPLND for teratoma to determine their clinical outcome.

276 n which human iPS cells differentiate within teratomas to derive functional myeloid and lymphoid cell

277 ations into preclinical models has generated teratomas (tumors arising from undifferentiated hPSCs),

278 ce results in a >90% incidence of testicular teratomas, tumors consisting cells of multiple germ laye

279 (MGCs) fail to enter G1/G0 and instead form teratomas: tumors containing many embryonic cell types.

280 1.9% (95% CI, 57.1% to 66.2%) for those with teratoma versus 63.1% (95% CI, 58.0% to 67.8%) for those

281 Ovarian teratoma was most common and was predicted best when bot

282 An element of teratoma was present in 82 NSGCT primary tumors (42%).

283 The presence of a fetiform teratoma was suspected and surgery revealed an encapsula

284 The frequency of ovarian teratomas was 56% in women >18 years old, 31% in girls <

285 and NANOG promoters and differentiation into teratomas, we determined that only one colony type repre

286 evel and histology for a metastatic immature teratoma were prognostic of a worsened outcome.

287 s of pathologic stage II and retroperitoneal teratoma were unaffected.

288 concentrations during pregnancy, and ALL and teratomas were associated with traffic density near the

289 to 12 to 15 weeks after transplantation, no teratomas were detected.

290 Three additional teratomas were diagnosed at index CT only.

291 Formalin-fixed, paraffin-embedded ovarian teratomas were examined for the presence of CNS tissue a

292 Cystic structures, but no teratomas, were observed in NT-ES-beta-cell grafts.

293 hed that ES cells will spontaneously develop teratomas when grown within immunocompromised mouse host

294 N-betaCat), P53-/- mice developed testicular teratomas, whereas only 10% of the non-Tg(DeltaN-betaCat

295 in, loss of Dmrt1 causes a high incidence of teratomas, whereas these tumors do not form in Dmrt1 mut

296 , immature teratoma in 15 patients (7%), and teratoma with malignant transformation in 17 patients (8

297 ith teratoma, five (17%) had recurrence with teratoma with malignant transformation, and 15 (50%) had

298 ll lymphoma, breast cancer, liposarcoma, and teratoma with reversible neutropenia as the main toxic e

299 haracteristic epigenetic changes, and formed teratomas with all three germ layers.

300 enetic states similar to ES cells and formed teratomas with three germ layers in nonobese diabetic/se