ライフサイエンスコーパス: teratoma

1 ion of viable disease (GCT other than mature teratoma).

2 roid cancer) and not treated in one (ovarian teratoma).

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

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

5 etal regeneration without the formation of a teratoma.

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

7 available had tumours, most commonly ovarian teratoma.

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

9 carcinoid, parotid pleomorphic adenoma, and teratoma.

10 tibody positivity had evidence of an ovarian teratoma.

11 etic abnormalities similar to the metastatic teratoma.

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

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 d inhibits angiogenesis and proliferation in teratomas.

20 e infarcted mouse heart without formation of teratomas.

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

22 rentiated into cardiac cells without forming teratomas.

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

24 ophages do not develop abnormal pathology or teratomas.

25 , transplanted hiEndoPCs do not give rise to teratomas.

26 he capacity to differentiate in vitro and in teratomas.

27 ontractile function without the formation of teratomas.

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

29 ctable model for studying the development of teratomas.

30 requency, B lineage lymphomas, sarcomas, and teratomas.

31 e formation of intracardiac and extracardiac teratomas.

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

33 intrinsic chemotherapy resistance of mature teratomas.

34 ined even after in vivo differentiation into teratomas.

35 nce after prolonged culture and did not form teratomas.

36 ES-derived cell transplantation and risk of teratomas.

37 differentiated TKO embryoid bodies (EBs) and teratomas.

38 NA profile and development in the context of teratomas.

39 is rarely described in patients with ovarian teratomas.

40 although Dmrt1 mutant females do not develop teratomas.

41 essed pluripotent cell markers and generated teratomas.

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

43 cantly affecting the rate of retroperitoneal teratoma (21% v 22%, respectively; P = .89) or pathologi

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

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

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

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

48 cordant allelic loss patterns between mature teratoma and all of the other germ cell tumor components

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

50 Concordant genetic alterations observed in teratoma and stroma suggest that both are derived from t

51 ammatory abnormalities and systemic tumours (teratoma and thymoma), and they do not develop SIADH-lik

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

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

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

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

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

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

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

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

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

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

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

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

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

65 ves of all three germ layers in vitro and in teratomas, and showed germ line transmission.

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

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

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

69 Teratomas are rare neoplasms composed of tissue elements

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

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

72 All 16 patients had mature teratoma as one component of their mixed germ cell tumor

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

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

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

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

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

78 ion potential in embryoid body formation and teratoma assays.

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

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

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

82 loss in the epithelial cells of the adjacent teratoma at all nine DNA loci studied.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 Cardiac teratomas contained no more cardiomyocytes than hind-lim

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

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

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

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

102 Compared with controls, s.c. teratomas derived from knock-in embryonic stem cells wer

103 we observed increased microvessel density in teratomas derived from Vhl(-/-) as well as VHL(Y112H), V

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

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

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

107 environment that supported the initiation of teratoma development.

108 Abnormal neurons within teratomas distinguish cases with NMDAR encephalitis from

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

110 rentially expressed genes were identified in teratomas (EGR1 and MMP7), yolk sac tumors (PTPN13 and F

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

112 Surprisingly, teratomas expressing the VHL(Y112H) mutant protein displ

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

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

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

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

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

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

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

120 Teratoma formation assays were performed, and tumors wer

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

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

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

124 c retained pluripotency, differentiation and teratoma formation capabilities.

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

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

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

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

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

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

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

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

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

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

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

136 However, the risk of teratoma formation would need to be eliminated before ES

137 minates residual, pluripotent EBCs, prevents teratoma formation, and enriches the EBCs for cells that

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

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

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

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

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

143 tion, colony expansion, cryopreservation and teratoma formation.

144 fective in folliculogenesis and conducive to teratoma formation.

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

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

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

148 get genes, whose missexpression may underlie teratoma formation.

149 cting single cells, and effectively prevents teratoma formation.

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

151 weeks, but the rescue failed due to immature teratoma formation.

152 was accompanied with only a low incidence of teratoma formation.

153 has been observed only in culture or during teratoma formation.

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

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

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

157 yocardial infarction without any evidence of teratoma formation.

158 5 and two additional PSMs completely removed teratoma-formation potential from incompletely different

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ealed germ cell cancer in 53.5% of patients, teratoma in 34.2% of patients, and fibrosis in 12.2% of

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

177 stromal cells adjacent to metastatic mature teratoma in postchemotherapy lymph node specimens freque

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

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

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

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

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

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

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

185 e embryonic stem cells were used to generate teratomas in immunocompromised mice, allowing independen

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

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

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

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

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

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

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

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

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

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

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

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

198 They differentiate in vitro and form teratomas in vivo.

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

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

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

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

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

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

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

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

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

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

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

210 The formation of stem cell-derived tumors (teratomas) is observed when engrafting undifferentiated

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

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

213 nt cells to avoid the generation of multiple teratomas, longevity of the graft, and possible immunolo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 ients (30%) with nonseminoma had findings of teratoma or viable GCT at postchemotherapy surgery.

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

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

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

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

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

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

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

237 tral hypoventilation associated with ovarian teratoma (OT) and cerebrospinal fluid (CSF) inflammatory

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

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

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

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

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

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

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

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

246 Testicular teratomas result from anomalies in germ cell development

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

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

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

250 (CDH, n=13), and resection of sacrococcygeal teratoma (SCT, n=4).

251 were seen in 10 of 14 tumors in which mature teratoma showed loss of heterozygosity.

252 the stroma that was not seen in the matching teratoma specimens.

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

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

255 ression and 22% incidence of retroperitoneal teratoma supports RPLND as the preferred primary interve

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

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

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

259 tural variation in Dmrt1 activity can confer teratoma susceptibility.

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

261 induction of differentiation, associate with teratoma susceptibility.

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

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

264 rther divided into embryonal carcinoma (EC), teratoma (T), yolk sac tumor (YS), and choriocarcinoma (

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

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

267 [2369-9885], p=0.0025), and in patients with teratoma than in those without teratoma (CSF 395 vs 110,

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

269 However, untreated cells formed numerous teratomas that contained derivatives of endoderm, mesode

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

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

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

273 ed and removed in four patients (mediastinal teratoma, thymoma, thymic carcinoma and thyroid cancer)

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

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

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

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

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

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

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

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

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

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

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

285 Three additional teratomas were diagnosed at index CT only.

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

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

288 on of ganciclovir (50 mg/kg) did not develop teratomas when compared with control animals (n=4) treat

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

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

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

292 lymph nodes that contained metastatic mature teratoma with "fibrosis" to determine the reactive or ne

293 rs (GCT), 12 had malignant transformation of teratoma with elements of non-GCT, and nine had both GCT

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

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

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

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

298 d into severe combined immunodeficient mice, teratomas with derivatives from all three embryonic germ

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

300 ommonly been studied in tissue culture or in teratomas, yet these methods have stopped short of demon