ライフサイエンスコーパス: myc gene

1 se, TNF and TGFbeta signaling, Hif1alpha and Myc genes).

2 ed at promoter-proximal pause sites of the c-myc gene.

3 pproximately 820-bp promoter region of the c-myc gene.

4 es within approximately 1,400 bp 5' to the c-myc gene.

5 with the promoter region of the endogenous c-myc gene.

6 ld greater than that of a known MAR in the c-myc gene.

7 ress the transcriptional elongation of the c-myc gene.

8 stoma gene product and upregulation of the c-myc gene.

9 ivity at the Ig switch region and off-target Myc gene.

10 activating expression of the translocated c-myc gene.

11 ssed in cells carrying extra copies of the N-myc gene.

12 ar upstream element (FUSE) upstream of the c-myc gene.

13 imidine sequence in the P2 promoter of the c-myc gene.

14 tic increase in ERalpha recruitment to the c-Myc gene.

15 r more sites within 2.4 kb upstream of the c-myc gene.

16 t in the transcriptional activation of the c-MYC gene.

17 ion at the first exon/intron border of the c-myc gene.

18 es induced by the top2(S740W) in the human c-myc gene.

19 o restriction fragments from the germ-line c-myc gene.

20 s the expression pattern of the endogenous N-myc gene.

21 gain of chromosome 15, which contains the c-myc gene.

22 rich strand from the promoter of the human c-MYC gene.

23 s a transcriptional repressor of the human c-myc gene.

24 n factors for optimal transcription of the c-Myc gene.

25 druplex formation within the intron of the N-myc gene.

26 t," a few hundred kilobases telomeric to the Myc gene.

27 erences in expression or function of a given MYC gene.

28 was not dependent upon transcription of the Myc gene.

29 ls even as cells show amplification of the N-myc gene.

30 e E-responsive promoter regions of pS2 and c-myc genes.

31 ssion, including expression of the socs3 and myc genes.

32 liferation via repression of cyclin D1 and c-myc genes.

33 ls with chromosomally integrated amplified N-myc genes.

34 naturally metastatic cells with amplified N-myc genes.

35 stage-specific activation of translocated c-myc genes.

36 ivating the transcription of cyclin D1 and c-Myc genes.

37 e and in the promoter regions of bcl-2 and c-myc genes.

38 aled common insertions in either notch1 or c-myc genes.

39 uroblastoma selects for cells that amplify N-myc genes.

40 nRNP) K is a transcription factor for the c- myc gene, a proto-oncogene critical for the regulation o

41 tal translocation region by insertion of a c-myc gene about 50 kb from the IgH intron enhancer in a y

42 Herein, aspects of c-myc gene activation and the function of the c-Myc protei

43 Mutation of the cell cycle regulator N-myc gene also leads to an apparently identical phenotype

44 ble antibodies have facilitated the study of MYC gene alterations and protein expression in large ser

45 MYC gene alterations have been identified in other matur

46 MYC gene alterations in large B-cell lymphomas are frequ

47 ed Myc expression in cancers can result from MYC gene amplification and translocation but also from a

48 Although MYC gene amplification and translocations have been obse

49 The data implicate L-MYC gene amplification and/or overexpression in human Ov

50 myc gene amplification has been identified in many large

51 may be a better prognostic indicator than N-myc gene amplification in neuroblastoma.

52 equently in human B lymphoid tumors, while N-myc gene amplification is frequent in human neuroblastom

53 expression of c-Myc mRNA, caused either by c-myc gene amplification or by enhanced signaling via STAT

54 Among 11 SCLC cell lines with L-myc gene amplification, four were found to have alterati

55 he XRCC4/p53-deficient MBs have high-level N-myc gene amplification, often intrachromosomally in the

56 to induce transcription of the endogenous c-myc gene and cell entry into S phase.

57 regulate the expression of the endogenous c-myc gene and is a potent activator of the c-myc promoter

58 outlines the nature and regulation of the c-myc gene and of c-Myc and presents the systems and condi

59 e chromosomal translocations involving the c-myc gene and one of the Ig loci.

60 rks diverge from an origin 5' to the human c-myc gene and that a 2.4-kb core fragment of the origin d

61 lex that binds to the MIF-1 element in the c-myc gene and the major histocompatibility complex class

62 Focal CNAs affecting the MYC gene and the PTEN gene were observed only in a minor

63 und to co-localize at the promoters of the c-myc gene and the RPPH1 sRNA in vivo.

64 phoma (BL) cell lines carry a translocated c-myc gene and, in 60-80% of cases, exhibit mutations in t

65 e a transcriptional block on the Cox-2 and c-myc genes and that this block may be a potential target

66 region of the progesterone-regulated avian c-myc gene, and nuclear matrix-like attachment sites flank

67 g defects, lower levels of REF1/Aly at the c-myc gene, and nuclear retention of bulk HeLa poly(A)+ RN

68 chromosome 8q24), the map location of the c-Myc gene, and six of the tumors exhibited copy number lo

69 ains after proviral integration within the c-myc gene, and subsequent expansion of Myc-overexpressing

70 kens after proviral integration within the c-Myc gene, and subsequent expansion of Myc-overexpressing

71 Deletion mutations were introduced into myc genes, and the levels of their mRNAs were compared w

72 the regulation or expression level of the c-myc gene are among the most common found in human and an

73 locations of the coding exons of the human c-myc gene are consistent features of human Burkitt lympho

74 ic morphology and overexpress the cellular c-MYC gene are highly aggressive and carry a very poor pro

75 h the physically linked cad and endogenous N-myc genes are coamplified.

76 The HER2 (ERBB2) and MYC genes are commonly amplified in breast cancer, yet l

77 lyses revealed that both the mouse and human Myc genes are direct transcriptional targets of N1(IC) a

78 nd tamoxifen at ER alpha-regulated pS2 and c-myc genes are in part mediated by HER-2/neu.

79 ocations juxtaposing immunoglobulin (Ig) and MYC genes are the hallmarks of human Burkitt lymphoma (B

80 The MYC genes are the most frequently activated oncogenes in

81 Although the structure and expression of Myc genes are well characterized, the function and bioch

82 f RNA transcripts detected fusion of the HPV/Myc genes, arising from apparent microhomologous recombi

83 ulation of B-cell survival and confirm the c-myc gene as one of the downstream targets of A-myb in th

84 d levels of acetylated histone H3 within the MYC gene associated with reduced levels of MYC protein a

85 elial regression through the repression of c-myc gene at the chromatin level.

86 The precise mechanism of myc gene autoregulation is unknown.

87 t lymphomas (BL) and murine plasmacytomas, c-myc genes become juxtaposed to immunoglobulin heavy-chai

88 The c-myc gene becomes transcriptionally activated as a conseq

89 , located in the 5'-flanking region of the c-myc gene, between nucleotides -1406 and -1387 (relative

90 HPV-16 genome was integrated adjacent to the Myc gene, both of which were amplified 40-fold.

91 istal K79 methylation-marked enhancer in the MYC gene bound by AR and DOT1L not present in AR-negativ

92 hancers (WREs) located in close proximity to MYC gene boundaries.

93 a cell lines that do not have an amplified c-myc gene but differ in their p53 status, high c-myc leve

94 contrast, lack structural alterations in the MYC gene, but have deregulated Myc protein due to the ac

95 prostate tumors have amplifications of the c-Myc gene, but the precise role of c-Myc in prostate canc

96 id gene itself as well as in the bcl-6 and c-myc genes, but not in the p53 gene, consistent with aber

97 s the MYC promoter and thereby activates the MYC gene by a beta-catenin/transcription factor 4 (TCF4)

98 sible mechanism for transactivation of the c-myc gene by mutant p53 is proposed.

99 ng c-Myc activity due to disruption of the c-myc gene by targeted homologous recombination are defect

100 involves direct promoter targeting of the c-myc gene by the complexes.

101 It is well established that Ha-ras and c-myc genes collaborate in promoting transformation, tumor

102 s downregulate expression of the amplified N-myc gene, concurrent with the arrest of cell proliferati

103 All v-myc genes contain point mutations which seem to confer a

104 Moreover, inappropriate expression of c-myc genes contributes to the development of many types o

105 o BL develop in mice bearing a mutated human MYC gene controlled by a reconstructed Ig lambda locus e

106 FDG signature was similarly associated with MYC gene copy gain, increased MYC transcript levels, and

107 ate that modulating HuD expression affects N-myc gene copy number as well as expression.

108 Thus, N-myc gene copy number is modulated by alteration of HuD e

109 N-myc gene copy numbers and transcription rates are simila

110 a frequently lethal childhood tumor in which MYC gene deregulation, commonly as MYCN amplification, p

111 f the chromosomal translocation leading to c-myc gene deregulation, remains unclear.

112 Here we show that the Drosophila Myc gene diminutive is an X-linked numerator.

113 , we showed that T3 directly activated the c-Myc gene during metamorphosis in the intestine via bindi

114 ers in either orientation, 5" and 3", of the myc gene elevated reporter activity from 2- to 160-fold,

115 cruitment of androgen receptor (AR) to the c-Myc gene enhancer and induced H3K9 demethylation, increa

116 1,25D inhibited MYC gene expression and accelerated its protein turnover

117 neuroendocrine differentiation, increased L-myc gene expression and decreased c-myc gene expression.

118 er, MLLT1-mutant tumours show an increase in MYC gene expression and HOX dysregulation.

119 iption, mediated by a rapid suppression of c-myc gene expression and its binding to KOR promoters, an

120 Aberrant MYC gene expression by the Wnt/beta-catenin pathway is i

121 Both anaplasia and increased c-myc gene expression have been shown to be negative progn

122 nts (95%), DNA index (ploidy) in 18 (90%), N-myc gene expression in 14 (70%), and cytogenetic analysi

123 trate that the suppressive effect of OM on c-myc gene expression in H3922 cells occurs at the transcr

124 y of TFOs designed to act as repressors of c-myc gene expression in human leukemia and lymphoma cells

125 mily, we determined the normal patterns of L-myc gene expression in the developing mouse by RNA in si

126 Aberrant myc gene expression in transgenic mice is correlated wit

127 fic molecules and discuss their effects on c-MYC gene expression in vitro and in vivo.

128 Deregulated c-myc gene expression is associated with many human and an

129 C-myc gene expression is greater in the undamaged carotid

130 Therefore, post-transcriptional control of N-myc gene expression must differ between these cell types

131 NOTCH2 and c-MYC gene expression positively correlated with AR expres

132 which alters immunoglobulin mu (Igmu) and c-myc gene expression, RTA did not affect Igmu and c-myc e

133 ons in endothelin-induced c-fos, c-jun, or c-myc gene expression, suggesting either that the inhibito

134 ivity and the effect of these compounds on c-MYC gene expression, we have demonstrated, using a cellu

135 estigate mechanisms of regulation of human N-myc gene expression, we observed that N-myc promoter-chl

136 ene, mediated by a rapid downregulation of c-myc gene expression.

137 etylcholinesterase activity, and decreased N-myc gene expression.

138 e to bind to NF-kappaB elements and induce c-myc gene expression.

139 pression of beta-interferon (IFN-beta) and c-myc gene expression.

140 ited IGF-I-dependent changes of GAP-43 and c-myc gene expression.

141 on is not a major factor in the control of L-myc gene expression.

142 reased L-myc gene expression and decreased c-myc gene expression.

143 he H4R3me2a mark, and the complex promotes c-MYC gene expression.

144 Es accompanies transcriptional activation of MYC gene expression.

145 MYC also elevated let-7a miRNA and decreased Myc gene expression.

146 Tbx20 led to increased Tbx2 and decreased N-myc gene expression.

147 s multiple biosynthetic routes and induces c-MYC gene expression.

148 alterations affecting proto-oncogenes of the myc gene family are frequently detected in human lung ca

149 e basis for the evolutionary conservation of myc gene family has remained unclear.

150 Therefore, the myc gene family must have evolved, to a large extent, to

151 h DNA oligonucleotide originating from the N-myc gene folds into G-quadruplex structures in the prese

152 The targeted knockout of the c-myc gene from rat fibroblasts leads to a stable defect i

153 in 73% of animals, either the c-myc or the N-myc genes had been disrupted and deregulated.

154 The c-myc gene has been implicated in multiple cellular proces

155 region of mutant p53 responsiveness in the c-myc gene has been mapped to the 3' end of exon 1; (iii)

156 gged with an immunoreactive epitope from the myc gene has been used to map the position of the glycos

157 n certain types of Burkitt's lymphoma, the c-myc gene has undergone translocation to the S regions as

158 MYC genes have both essential roles during normal develo

159 berrations (e.g., translocations) in a given MYC gene in a particular tumor progenitor cell type.

160 le in the deregulation of the translocated c-myc gene in Burkitt's lymphoma and suggest that interfer

161 The deregulation of expression of the c-myc gene in Burkitt's lymphoma results from the transloc

162 f the frequent mutations that occur in the c-myc gene in Burkitt's lymphomas.

163 gest aberrant translational control of the c-myc gene in cell lines derived from patients with MM, wh

164 The origin of replication of the c-myc gene in HeLa cells was previously identified at low

165 cancer drugs within a 683-bp region of the c-myc gene in human CEM leukemia cells.

166 rther reinforces the important role of the c-Myc gene in KSHV lytic replication and latency.

167 e differentiation program shutting off the c-Myc gene in large pre-B cells.

168 , we demonstrated an essential role of the c-myc gene in promoting cell survival of WEHI 231 cells in

169 the promoter and downstream regions of the c-myc gene in response to estrogen.

170 he transfected promoter and the endogenous N-myc gene in single-copy, but not amplified lines.

171 ks, which moved through this region of the c-myc gene in the 5' to 3' direction, were specifically ar

172 tiation of DNA replication upstream of the c-MYC gene in the HeLa cell cycle.

173 Enhanced expression of the amplified N-myc gene in the tumor cells may be associated with poor

174 the PNNs and tumors, and amplification of C-MYC gene in the tumors were confirmed by Southern blot a

175 uitment within the regulatory regions of the Myc gene in tumor cells of the compound mice.

176 uence (CCCTCCCCA; CT-element) of the human c-myc gene in vitro.

177 ta-cat promotes H3K4 trimethylation at the c-Myc gene in vivo.

178 site was detected in the first exon of the c-myc gene in VM-26-treated cells.

179 Deletion of both c-Myc genes in B cells led to severely impaired proliferat

180 attern of deregulated expression of linked c-myc genes in BL and plasmacytoma cell lines.

181 crease in histone acetylation along linked c-myc genes in Raji BL cells.

182 eview evidence implicating each of the above MYC genes in specific neoplastic diseases and have attem

183 melting of specific cis elements of active c-myc genes in vivo suggested that transcriptionally assoc

184 t the activity of a cellular oncogene, the c-MYC gene, in addition to inactivation of the tumor suppr

185 mal human fibroblasts with one copy of the c-myc gene inactivated by targeted homologous recombinatio

186 fine numerous biological activities of the c-myc gene, including transformation, immortalization, blo

187 Ba/F3 cell proliferation, suggesting that c-Myc gene induction is required for IFN-gamma-mediated ce

188 bursal lymphoma in chickens after proviral c-myc gene integration, while the HB-1 retrovirus carries

189 By inserting an intact mouse Myc gene into the mouse genome, proximal to the Ig enhan

190 target gene of c-Myb and activation of the c-myc gene is a necessary event in Myb-mediated transforma

191 Amplification of the N-myc gene is a significant adverse prognostic factor in n

192 The Myc gene is a universal oncogene that promotes aggressiv

193 ar run-on analyses, we determined that the N-myc gene is actively transcribed in all cell types exami

194 not clear if activation of the endogenous c-myc gene is an apoptotic signal after toxicant exposure.

195 sporadic TNBC patients, amplification of the MYC gene is correlated with increased expression of the

196 differential functional expression of the c-myc gene is discussed.

197 The c-myc gene is frequently deregulated and overexpressed in

198 Expression of the c-myc gene is frequently dysregulated in malignant tumors

199 Transgenic mice in which the myc gene is juxtaposed to an immunoglobulin enhancer (E(

200 The N-myc gene is overexpressed due to genomic amplification i

201 Although the c-myc gene is overexpressed in approximately 70% of human

202 hermore, we and others have shown that the c-myc gene is potently transactivated by A-Myb in several

203 Transcription of the c-myc gene is repressed by Blimp-1 during B-cell different

204 tion that the deregulated expression of each MYC gene is reproducibly associated with only certain na

205 The expression of the Myc gene is synergistically regulated by KLF1 and KLF2,

206 sequence and expression of the endogenous c-myc gene is the same in resistant and susceptible birds,

207 The c-myc gene is translocated to one of the immunoglobulin ge

208 ression, transforming function of retroviral myc genes is restricted to avian cells, and that of retr

209 The MYCC (c-MYC) gene is amplified in 30-60% of human ovarian cancer

210 binding site, conserved in mouse and human c-myc genes, is found immediately downstream of the major

211 ion including feedback autoregulation of the MYC gene itself.

212 Furthermore, c-myc gene knockout fibroblasts are refractory to transfor

213 A cis element of the human c-myc gene, known to be melted in vivo, and its associated

214 smid containing the promoter region of the c-myc gene linked to a reporter gene.

215 methodology, we have established that the c-myc gene, located at 8q21, exhibited amplification of 87

216 serting a single-copy histidine-tagged mouse Myc gene, Myc(His), into the mouse Ig heavy-chain Calpha

217 The human N-myc gene normally is expressed in only a subset of fetal

218 The prototypic v-Myc gene of MC29 virus differs from avian c-Myc by a ser

219 HN2, and only detectable in the amplified c-myc gene of the Colo320HSR cell line.

220 slinks were not detectable in the N-ras or c-myc genes of LS174T, J6 or U937 cells treated with HN2,

221 suggesting that the amplification for the c-myc gene on 8q was relatively specific, and this was con

222 g array of biological activities makes the c-myc gene one of the most intriguing oncogenes and presen

223 a possesses two functionally interchangeable MYC genes, one in females and one in males.

224 r in tumors harboring either the wild-type c-Myc gene or the NCR allele.

225 show that a single extra copy of either the Myc gene or the region encompassing Pvt1, Ccdc26 and Gsd

226 e stably transfected C2C12 cells with mutant myc genes or chimeric genes in which various myc sequenc

227 The transcriptional effects of deregulated myc gene overexpression are implicated in tumorigenesis

228 is was identified as an early consequence of myc gene overexpression in two models of retroviral lymp

229 s may block Myc function by repressing the c-myc gene P2 promoter, as well as by antagonizing Myc-dep

230 These data indicate that c-Myc gene plays an important role in mediating CD437-indu

231 le-stranded far upstream element of active c-myc genes, possesses potent transcription activation and

232 Segments of the human c-myc gene possessing non-B structure in vivo located with

233 v-abl and frequently harbored a rearranged c-myc gene, probably as a result of chromosome translocati

234 The c-myc gene produces an oncogenic transcription factor that

235 tone deacetylase 1 and 2 to the endogenous c-myc gene promoter and the subsequent deacetylation of it

236 n can bind to the cis-element of the human c-myc gene promoter and to the gene promoter of STZ/ZAT10,

237 ulates the transcriptional activity of the c-myc gene promoter by dissociating the active form of NF-

238 Both TIP30 and CIA are recruited to the c-myc gene promoter by liganded ERalpha in the second tran

239 ith high affinity a specific region at the c-MYC gene promoter characterized by parallel G-quadruplex

240 the identification of the first dual BCL2/c-MYC gene promoter G-quadruplex ligand.

241 binding site (acceptor site) for PR in the c-myc gene promoter is composed of RBF dimers bound to a s

242 he TDRD3-TOP3B complex is recruited to the c-MYC gene promoter primarily by the H4R3me2a mark, and th

243 the expression of c-myc by binding to the c-myc gene promoter.

244 ssociated region (MAR) of the Pg-regulated c-myc gene promoter.

245 ubtype of Notch-independent T-ALLs that bear Myc gene rearrangements and Pten mutations.

246 ted Burkitt or Burkitt-like morphology and c-myc gene rearrangements and, therefore, appeared to be B

247 BCL6, immunoglobulin heavy chain (IGH), and MYC gene rearrangements in a large PCNSL cohort treated

248 onstrated in 3 other cases (19%), although c-myc gene rearrangements were not seen by Southern blotti

249 lymphoma, and all 12 cases studied lacked c-myc gene rearrangements.

250 gets of AFF4/SEC, and SEC recruitment to the MYC gene regulates its expression in different cancer ce

251 recruitment of beta-catenin and AR on the c-Myc gene regulatory locus in the tumor tissues expressin

252 ver half a megabase of DNA upstream of their Myc gene removed still thrive in the absence of stress.

253 ing to the specific promoter region of the c-Myc gene, resulting in drastic suppression of c-Myc expr

254 In mice, complete disruption of the N-myc gene results in fetal death on the first day of rena

255 hose whose tumors had amplification of the N-myc gene (RR = 0.26; P = .112; EFS, 67% v 0%).

256 The c-myc gene's regulatory sequences were normal in those cel

257 g that dispersion and amplification of the c-MYC gene sequences occurred after and was most likely tr

258 ly patients whose tumors have an amplified c-myc gene show improved disease-free and overall survival

259 The c- and N- myc genes showed three general classes of sequence conse

260 ry closely related to the structure of the c-myc gene single-strand binding proteins (MSSPs).

261 tes in the promoters of both the c-myb and c-myc genes, suggesting that c-myb and c-myc may be among

262 However, the complexity and diversity of Myc gene targets has confounded attempts at identifying

263 kilobase pair region upstream of the human c-myc gene that contains 86 CpGs.

264 tivity and suppresses promoter activity of c-MYC gene that contains G-quadruplex DNA forming sequence

265 L-3 and IFN-gamma induce expression of the c-Myc gene that is not dependent on the Stat1 activity.

266 atopoietic tumor cell lines having altered c-myc genes, the c-Myc S proteins are constitutively expre

267 imidine-rich DNA sequence upstream of the c -myc gene to activate its expression.

268 a is characterized by translocation of the c-MYC gene to an immunoglobulin enhancer region, resulting

269 diester TFOs directed to four sites in the c-myc gene to inhibit gene expression and proliferation of

270 cting homopyrimidine tract upstream of the c-myc gene to which the well-characterized transcription f

271 novel cAMP-dependent increase in renin and c-myc gene transcription by binding as a monomer to a uniq

272 monstrate the rapid and potent abrogation of MYC gene transcription by representative small molecule

273 ibitor p27 which was an indirect effect of c-myc gene transcription control by Ada3.

274 ium nitroprusside (SNP), rapidly represses c-myc gene transcription in a protein synthesis-independen

275 paB and AhR resulting in the activation of c-myc gene transcription in breast cancer cells.

276 ed as a DNA-binding protein that regulates c-Myc gene transcription through binding to the far upstre

277 ctor activity, which regulates the rate of c-myc gene transcription, to determine whether the increas

278 ced histone H3 acetylation and activation of MYC gene transcription.

279 s a cAMP-responsive regulator of renin and c-myc gene transcriptions by the interaction with a specif

280 er transplantation of human NSCs cloned by v-myc gene transfer, HB1.F3 cells, is a feasible therapeut

281 s transcribed from two similarly constructed myc genes transiently cotransfected into proliferating C

282 se results implicate H-DNA-induced DSBs in c-myc gene translocations in diseases such as Burkitt's ly

283 to chromosomal translocations that bring the MYC gene under the control of a super-enhancer.

284 nesis in a transgenic model expressing the c-myc gene under the MMTV-LTR promoter.

285 C/Grb2/MAPK and STAT6 pathways and through c-myc gene up-regulation.

286 In vitro binding to the c-myc gene was abolished after deletion of the N-terminal

287 a 280-base pair region in intron 1 of the c-myc gene was explored.

288 Whereas overexpression of the c-myc gene was found to promote apoptosis in fibroblasts,

289 ng fluorescence in situ hybridization, the c-myc gene was localized to hamster chromosome 6qb.

290 sis showed that the induction of egr-1 and c-myc genes was associated with a transient recruitment of

291 d to suppress polymerase elongation on the c-myc gene, we employed the chromatin immunoprecipitation

292 utations of the 5' noncoding region of the c-myc gene were demonstrated in 3 other cases (19%), altho

293 TBLV insertions near the c-myc gene were detectable in 2 of 30 tumors tested, where

294 lated E2F sites derived from the c-myb and c-myc genes whereas both E2F1 and E2F3 fail to transactiva

295 Two other v-Myc genes which carry a mutation at thr-61 (avian MH2) o

296 IRF4) directly regulates expression of the c-Myc gene, which is not only associated with various B ce

297 catenin/TCF4-mediated transcription of the c-myc gene, which was caused by GLIPR1-mediated redistribu

298 Histone hyperacetylation of control c-myc genes, which was induced by the deacetylase inhibito

299 l evidence implicates amplification of the N-myc gene with aggressive tumor growth and poor outcome i

300 ults in the decreased levels of GATA-1 and c-myc genes, with an accompanying induction of apoptosis.