ライフサイエンスコーパス: seminoma

1 of 21 patients, P < .001 when compared with seminomas).

2 carcinoma, one renal cell carcinoma, and one seminoma.

3 in PC evaluation of residual masses in bulky seminoma.

4 disease, multiple myeloma, brain cancer, and seminoma.

5 activity of VeIP in patients with recurrent seminoma.

6 rvical or anal invasive cancer) and possibly seminoma.

7 low inguinal orchiectomy in clinical stage I seminoma.

8 ta exist on its efficacy in early metastatic seminoma.

9 help discover potential therapy targets for seminoma.

10 67 patients who underwent RPLND for RP-only seminoma.

11 A and Plk1, that is down regulated in human seminoma.

12 r CSI nonseminoma and within 3 years for CSI seminoma.

13 ar invasion-negative CSI nonseminoma and CSI seminoma.

14 for relapse in patients treated for advanced seminoma.

15 -170) were associated with decreased risk of seminoma.

16 roups were associated with decreased risk of seminoma.

17 ons may be inversely associated with risk of seminoma.

18 to radiotherapy in the treatment of stage I seminoma.

19 tomography in evaluating residual lesions in seminoma.

20 type showed higher levels of expression than seminomas.

21 nt from sample to sample, especially for the seminomas.

22 n nonseminomas, but only 0.08% methylated in seminomas.

23 prevalent mechanism of immune disruption in seminomas.

24 CFIm25, which is downregulated in the human seminomas.

25 ion we found to be abolished in 96% of human seminomas.

26 rnatives to adjuvant radiotherapy in stage I seminomas.

27 luripotency between embryonal carcinomas and seminomas.

28 velopment and is observed in the majority of seminomas.

29 d spectrum of KIT mutations in 54 testicular seminomas, 1 ovarian dysgerminoma and 37 non-seminomatou

30 oma (4.5-fold), brain cancer (3.5-fold), and seminoma (2.9-fold) were raised and increasing significa

31 Fourteen seminomas (25.9%) contained exon 17 point mutations incl

32 a than those with NSGCT without teratoma and seminoma (5-year CIDD rate, 27.4%, 17.4%, and 10.3%, res

33 rage of 12p genes) expression profiles of 17 seminomas, 84 nonseminoma GCTs, and 5 normal testis samp

34 er orchiectomy for CSI nonseminoma (90%)/CSI seminoma (92%).

35 levels are high in carcinoma in situ and in seminoma, a tumor derived from carcinoma in situ but sti

36 ximately 50% of patients with recurrent pure seminoma achieve durable CR with conventional or high-do

37 mic mast cell disorders, as well as cases of seminoma, acute myelogenous leukemia (AML), and gastroin

38 uding gastrointestinal stromal tumor (GIST), seminoma, acute myelogenous leukemia (AML), and mastocyt

39 in the management of early-stage testicular seminoma after inguinal orchiectomy.

40 tudy population comprised 2804 patients with seminoma and 2386 with nonseminoma.

41 GCT population encompassed 359 patients with seminoma and 257 with nonseminoma; 371 had clinical stag

42 ere disease-free, and 26 of 35 patients with seminoma and 90 of 149 patients with nonseminomatous ger

43 urative potential in patients with recurrent seminoma and appears to produce a higher CR rate and mor

44 BRE1A/B and dimethylated H3K79 in testicular seminoma and in the premalignant lesion in situ carcinom

45 lar germ cell tumours (TGCT), which comprise seminoma and non-seminoma subtypes, are the most common

46 pathological types of testicular cancer are seminoma and non-seminomatous germ-cell cancer.

47 l of the genotypes were associated with both seminoma and nonseminoma TGCT subtypes.

48 and, separately, with each histologic type (seminoma and nonseminoma).

49 t is shed on the different familial risks of seminoma and nonseminoma.

50 Trends were examined separately for seminoma and nonseminoma.

51 tumors (GCTs) and are applicable toward both seminoma and nonseminoma.

52 fferences in COS and CDFS were noted between seminoma and nonseminoma; patients >/= 40 years old had

53 etermined, in part, by a distinction between seminoma and nonseminomatous GCT (NSGCT).

54 with KIT inhibitors are GIST, mastocytosis, seminoma and possibly some cases of AML.

55 ostorchiectomy hCG and LDH for patients with seminoma and preorchiectomy elevations.

56 y key gene expression programs share between seminoma and primordial germ cells, and further characte

57 genase had sensitivities of less than 50% in seminoma and slightly higher sensitivities in nonseminom

58 hemotherapy is better than radiation even in seminoma and that seminoma is more chemosensitive than n

59 ve of seven achieving PR-negative status had seminoma and therefore did not undergo postchemotherapy

60 One patient with CSI seminoma and two patients with CSI nonseminoma died beca

61 methylation was detected in four of 10 (40%) seminomas and 15 of 18 (83%) nonseminoma TGCT (NSTGCT) c

62 herapy for patients who have metastastic non-seminomas and a good prognosis, and alternatives to adju

63 f the 12p11-p12 amplicon in human testicular seminomas and an ovarian carcinoma cell line using an ex

64 n normal spermatogenesis and is expressed in seminomas and dysgerminomas, a subset of human germ cell

65 ling in undifferentiated human GCTs, such as seminomas and embryonal carcinoma, but not in normal tes

66 l tumors, acute myeloid leukemia, testicular seminomas and mastocytosis.

67 as a biomarker in particular for testicular seminomas and might be causally related to the disease.

68 nagement trials, and high cure rates in both seminomas and non-seminomas have enabled a framework of

69 e significant epigenetic differences between seminomas and nonseminomas by restriction landmark genom

70 inical differences between the two subtypes, seminomas and nonseminomas, remains unclear.

71 cell tumors (GCTs) comprise distinct groups: seminomas and nonseminomas, which include pluripotent em

72 ors of adolescents and adults (TGCTs), i.e., seminomas and nonseminomas.

73 (GCTs) comprise two major histologic groups: seminomas and nonseminomas.

74 GCTs are categorized as seminomas and nonseminomatous GCTs (NSGCTs) based on the

75 al genotype, distinguishing nonseminoma from seminomas and other human tumors, may be associated with

76 ells in 73% of testicular germ-cell tumours (seminomas and teratomas), expressed hTR consistent with

77 arcinoma composed of 90% choriocarcinoma, 9% seminoma, and 1% teratoma.

78 cinoma, choriocarcinoma, yolk sac carcinoma, seminoma, and teratoma with malignant transformation to

79 ancer (choriocarcinoma, embryonal carcinoma, seminoma, and/or yolk sac tumor).

80 ch as SCLC, gastrointestinal stromal tumors, seminomas, and leukemias.

81 r deletion was more strongly associated with seminoma (aOR 3.0; 95% CI 1.6-5.4; P = .0004) than with

82 Most patients with advanced seminoma are cured with standard first-line programs of

83 ART recommendations for stage I seminoma are declining.

84 lly found in AML, systemic mastocytosis, and seminoma are insensitive to imatinib mesylate (IC50 > 5-

85 KLHL11-IgG and seminoma are the most common serological and cancer asso

86 Two of three extragonadal seminomas are continuously disease-free.

87 Optimal treatment strategies for early-stage seminomas are evolving toward surveillance versus chemot

88 Furthermore, we demonstrate that seminomas are more highly hypomethylated than nonseminom

89 in as a key factor able to affect testicular seminoma behavior, highlighting leptin receptor as a pot

90 ficacy of radiation for stage I and stage II seminoma, but another study adds to the evidence that ad

91 iotherapy is effective treatment for stage I seminoma, but is associated with a risk of late non-germ

92 y contribute to tumorigenesis in a subset of seminomas, but are not involved in NSGCT.

93 ther nine candidate genes were methylated in seminomas, but MGMT (44%), APC (29%) and FHIT (29%) were

94 lysis showed complete separation of YSTs and seminomas by global gene expression profiles and identif

95 er adjuvant carboplatin for clinical stage I seminoma can be successfully treated with a cisplatin-ba

96 CS II seminoma can be treated with surgery to avoid rigors of

97 Adjuvant radiation therapy (ART) for stage I seminoma can cause adverse late effects and alternative

98 NSCLC), renal cell carcinoma (RCC), sarcoma, seminoma, cancer of unknown primary origin, or other tum

99 Human seminoma cell line TCam-2 also expressed leptin along wi

100 nal examination using seminoma samples and a seminoma cell line.

101 was significantly higher in human testicular seminoma compared with normal adult testis.

102 s methylated for RASSF1A and MGMT, while the seminoma component was methylated only for RASSF1A.

103 APC and CDH13 promoter methylation, but the seminoma component was unmethylated for all genes analys

104 Optimal treatment strategies for early-stage seminomas continue to evolve toward surveillance versus

105 lity, intratubular germ cell neoplasias, and seminoma development.

106 Patients with clinical stage I seminoma diagnosed from January 2013 to December 2018 we

107 acute lymphoblastic leukaemia and testicular seminoma, differ from the common adult cancers in origin

108 ortant in the pathogenesis of neoplasms with seminoma differentiation.

109 y key pathways and genes that may facilitate seminoma disseminating beyond the seminiferous tubules.

110 n the phosphotransferase domain in tumors of seminoma/dysgerminoma differentiation.

111 logical subtypes included immature teratoma, seminoma, embryonal carcinoma, yolk sac tumor, and chori

112 Both patients with viable seminoma found at surgery died of disease.

113 Of men diagnosed with stage I seminoma from 1990 through 2004, 3,125 were identified u

114 Patients who underwent primary RPLND for seminoma from 2014 to 2021 were identified.

115 n postorchiectomy for early-stage testicular seminoma generates 39% more medical costs per patient ov

116 ir potential involvement in human testicular seminoma growth and progression remains unexplored.

117 apy, as a standard treatment for early-stage seminoma, has been declining due both to the efficacy of

118 A small minority of patients with pure seminoma have resistant tumors and require salvage chemo

119 nd high cure rates in both seminomas and non-seminomas have enabled a framework of effective cancer t

120 increased FGF4 expression especially in non-seminomas having EC components.

121 genomic alterations of early and late stage seminoma identified CNVs that correlate with progression

122 eurologic syndrome preceded the diagnosis of seminoma in 9 of the 13 patients.

123 l cell in one), nine (5.8%) of 155 with LTM (seminoma in six, mixed germ cell in one, Leydig cell in

124 esent in three (8%) of 40 patients with CTM (seminoma in two, embryonal cell in one), nine (5.8%) of

125 in two), and three (0.3%) of 884 with no TM (seminoma in two, other in one).

126 nce increased by 100%, with the incidence of seminoma increasing twice as much (124.4%) as the incide

127 Surgery in early metastatic seminoma is a prospective phase II single-arm, multi-ins

128 Survival in stage I seminoma is almost 100%.

129 ter than radiation even in seminoma and that seminoma is more chemosensitive than nonseminoma, a rene

130 Seminoma is the most common malignant solid tumor in 14

131 r Network guidelines, clinical stage (CS) II seminoma is treated with radiotherapy or chemotherapy.

132 atients, 1,139 CSI nonseminoma and 1,344 CSI seminoma managed with active surveillance, with the majo

133 es from different tumor entities (leiomyoma, seminoma, mantle cell lymphoma, melanoma, breast cancer,

134 erstanding of the basic biologic features of seminoma may lead to improvements in the management of t

135 produce a multi-omics atlas of in situ human seminoma microenvironment, which could help discover pot

136 atric GCT, yolk sac tumor (YST; n = 18), and seminoma (n = 9).

137 association was testicular/extra-testicular seminoma (n=13, 50%). Hearing impairment (bilateral, 62%

138 rtal (type II) malignant GCTs may present as seminoma, non-seminoma or mixed histologies.

139 MMP7), yolk sac tumors (PTPN13 and FN1), and seminomas (NR6A1, DPPA4, and IRX1).

140 nto two main subtypes, seminoma (SE) and non-seminoma (NSE), but their molecular distinctions remain

141 rm cell tumors (TGCT): seminoma (SE) and non-seminoma (NSE).

142 of testicular germ cell tumors, known as non-seminomas, often contain differentiated cells representa

143 malignant GCTs may present as seminoma, non-seminoma or mixed histologies.

144 ng markers to guide or monitor treatment for seminoma or to detect relapse in those treated for stage

145 en, are categorized histologically as either seminomas or nonseminomas/mixed germ cell tumors.

146 r ovaries, where they are termed germinomas, seminomas, or dysgerminomas, respectively.

147 ficantly higher FRR for nonseminoma than for seminoma (P = 0.06).

148 0.006), nonseminoma (P(trend) = 0.007), and seminoma (P(trend) = 0.05).

149 , our results obtained from mouse models and seminoma patients demonstrated the opposite.

150 221 (19%) CSI-nonseminoma and 173 (13%) CSI-seminoma patients.

151 A 37-year-old man with a history of seminoma presented with vertigo, ataxia, and diplopia.

152 After orchidectomy, most patients with seminoma receive adjuvant radiotherapy as standard of ca

153 d tomography scan/tumor-markers in 87%/3% of seminoma recurrences, in 48%/38% of lymphovascular invas

154 mately 20% of patients with clinical stage I seminoma relapse.

155 90% of CSI-nonseminoma and 99% of CSI-seminoma relapses exhibited International Germ Cell Coll

156 One seminoma-related death occurred after radiotherapy and n

157 articularly those of germ cell origin, i.e., seminomas, relative to normal testis control, nonseminom

158 rapy residual mass in patients with advanced seminoma remain controversial.

159 Comparison of embryonal carcinoma with seminomas revealed relative overexpression of several st

160 pe, there was a suggestion of a reduction in seminoma risk associated with the highest concentrations

161 criptomics) and functional examination using seminoma samples and a seminoma cell line.

162 In all, 61% NSTGCT components but no seminoma samples demonstrated promoter methylation at tw

163 oma cell samples and more distantly with the seminoma samples.

164 GCTs) are classified into two main subtypes, seminoma (SE) and non-seminoma (NSE), but their molecula

165 types of testicular germ cell tumors (TGCT): seminoma (SE) and non-seminoma (NSE).

166 but diverge phenotypically and clinically as seminoma (SE) and nonseminoma (NSE), the latter includin

167 From 20 seminomas (SEM), 14 non-seminomatous germ cell tumors (N

168 cularly in seminoma, the question of whether seminoma should be treated with different chemotherapy s

169 Seminomas show almost no CpG island methylation, in cont

170 PFS and OS in metastatic seminoma significantly improved in our modern series com

171 ours (TGCT), which comprise seminoma and non-seminoma subtypes, are the most common cancers in young

172 f imprinting occurs frequently in testicular seminomas, suggesting an important role for FAM50B in sp

173 and 71 percent, respectively, of a panel of seminomas tested.

174 e most closely linked to cannabis use is non-seminoma testicular cancer.

175 xpression was detected in four spermatocytic seminomas-testicular tumors that most likely originate f

176 The Trial of Imaging and Surveillance in Seminoma Testis (TRISST) assessed whether magnetic reson

177 tent with the embryonic hPGCs and a germline seminoma that share a CD38 cell-surface marker, which co

178 g GCC chemotherapy response, particularly in seminoma, the question of whether seminoma should be tre

179 currences after primary RPLND for CS IIA/IIB seminoma to determine if various clinical factors could

180 genetic events characterize progression from seminoma to NSTGCTs.

181 but relies on data of only 660 patients with seminoma treated between 1975 and 1990.

182 Data on 2,451 men with metastatic seminoma treated with cisplatin- and etoposide-based fir

183 Long-term survivors of seminoma treated with post-orchiectomy XRT are at signif

184 roaches of radiotherapy with chemotherapy in seminoma treatment.

185 howed that LDFI treatment markedly decreased seminoma tumor growth.

186 These findings advance our knowledge of seminoma tumorigenesis and produce a multi-omics atlas o

187 was found in 12 out of 19 sampled testicular seminomas-tumors originating from embryonic germ cells w

188 rm cell tumors and the changing incidence of seminoma versus nonseminoma in the population.

189 ins (1.5 [1.1-2.2]) consequent on a risk for seminomas was high (3.2 [1.6-6.5]; p = 0.001).

190 ccurrence of HRAS mutations in spermatocytic seminoma, we proposed that activating HRAS mutations bec

191 d loss of heterozygosity (LOH) in 25 primary seminomas, we confirmed several previously reported geno

192 One hundred four patients with advanced seminoma were assessed.

193 es directly associated with the diagnosis of seminoma were included in the analysis.

194 en patients with progressive, advanced, pure seminoma were treated with salvage chemotherapy.

195 The pediatric seminomas were significantly enriched for genes associat

196 d overexpression in embryonal carcinomas and seminomas, which included the known stem cell genes NANO

197 lvage chemotherapy in patients with advanced seminoma who experience disease progression after receiv

198 Patients with advanced seminoma who have normal radiographs or residual masses

199 pective review of 24 patients with recurrent seminoma who were treated at Indiana University with VeI

200 idence yielded, 33-year-old men with stage I seminoma who were undergoing CT surveillance were projec

201 e studied morphologically were found to have seminoma with atypia.

202 RPLND is a treatment option for testicular seminoma with clinically low-volume retroperitoneal lymp

203 RPLND as first-line treatment for testicular seminoma with clinically low-volume retroperitoneal lymp

204 ipants had undergone orchiectomy for stage I seminoma with no adjuvant therapy planned.

205 tumor cell lysates, was largely confined to seminomas with a genomic KIT mutation.

206 D-L1-negative yolk sac tissue, dysgerminomas/seminomas with high PD-L1 expression are associated with

207 t originate from the same precursor cells as seminomas yet have lost their germ cell characteristics.

208 ular cancer of various histologies including seminomas, yolk sac tumors, and malignant teratomas.