ライフサイエンスコーパス: seminoma

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

2 low inguinal orchiectomy in clinical stage I seminoma.

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

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

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

6 in PC evaluation of residual masses in bulky seminoma.

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

8 activity of VeIP in patients with recurrent seminoma.

9 rvical or anal invasive cancer) and possibly seminoma.

10 ar invasion-negative CSI nonseminoma and CSI seminoma.

11 for relapse in patients treated for advanced seminoma.

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

13 roups were associated with decreased risk of seminoma.

14 ons may be inversely associated with risk of seminoma.

15 to radiotherapy in the treatment of stage I seminoma.

16 tomography in evaluating residual lesions in seminoma.

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

18 CFIm25, which is downregulated in the human seminomas.

19 rnatives to adjuvant radiotherapy in stage I seminomas.

20 luripotency between embryonal carcinomas and seminomas.

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

22 velopment and is observed in the majority of seminomas.

23 type showed higher levels of expression than seminomas.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 Trends were examined separately for seminoma and nonseminoma.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 ART recommendations for stage I seminoma are declining.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 ortant in the pathogenesis of neoplasms with seminoma differentiation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 0.006), nonseminoma (P(trend) = 0.007), and seminoma (P(trend) = 0.05).

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

113 221 (19%) CSI-nonseminoma and 173 (13%) CSI-seminoma patients.

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

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

116 90% of CSI-nonseminoma and 99% of CSI-seminoma relapses exhibited International Germ Cell Coll

117 One seminoma-related death occurred after radiotherapy and n

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

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

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

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

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

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

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

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

126 Seminomas show almost no CpG island methylation, in cont

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

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

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

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

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

132 genetic events characterize progression from seminoma to NSTGCTs.

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

134 roaches of radiotherapy with chemotherapy in seminoma treatment.

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

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

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

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

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

140 One hundred four patients with advanced seminoma were assessed.

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

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

143 The pediatric seminomas were significantly enriched for genes associat

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

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

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

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

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

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

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

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

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