ライフサイエンスコーパス: papilloma virus

1 mortalized with the E6 and E7 genes of human papilloma virus.

2 ntified as an important target for the Human Papilloma Virus.

3 ds 85-115 of the E4 protein of type 75 human papilloma virus.

4 naling such as v-src, BCR/ABL, and E6 of the papilloma virus.

5 thway since ME180 is infected with the human papilloma virus.

6 tegies against oncogenesis mediated by human papilloma virus.

7 reasing percentage are associated with human papilloma virus.

8 such as the vaccines for influenza and human papilloma virus.

9 us, adeno-associated virus type 2, and human papilloma virus.

10 l end of the E6 protein from high-risk Human Papilloma Virus.

11 e to elimination of foreskin harboring human papilloma virus.

12 es are available against rotavirus and human papilloma virus.

13 patitis B virus, hepatitis C virus and human papilloma virus.

14 virus 16 copies/cell, and SiHa, 1 to 2 human papilloma virus 16 copies/cell) and two negative cell li

15 viral gene content (CaSki, 200 to 600 human papilloma virus 16 copies/cell, and SiHa, 1 to 2 human p

16 HPECs are immortalized using human papilloma virus 16 E6 and/or E7 as molecular tools to in

17 including the SV40 large T antigen and human papilloma virus 16 E6-antigen.

18 Expression of the human papilloma virus 16 E7 protein (which inactivates all mem

19 ycle checkpoints (for example, E7 from human papilloma virus 16, and cyclin D1), deregulate Myc trans

20 Human papilloma virus-16 (HPV-16) associated oropharyngeal can

21 strains were produced that secrete the human papilloma virus-16 (HPV-16) E7 protein expressed in HPV-

22 with a retroviral vector encoding the human papilloma virus 18 E6 gene, which inactivates endogenous

23 T-cell chemotaxis in a model of stable human papilloma virus-18 infection.

24 Two capsid virus-like particles, human papilloma virus (55 nm, approximately 20,000 kDa) and No

25 fect of Prdx6, which was observed in a human papilloma virus 8-induced and a chemically induced tumor

26 Infection of influenza or human papilloma virus 9-mer peptide-pulsed DCs from different

27 aluate temporal trends and the role of human papilloma virus and to determine the academic training a

28 therapeutic vaccine candidates against human papilloma viruses and melanoma have been developed recen

29 tion (CRT), associated with anogenital human papilloma virus, and often appears in HIV infection.

30 High-risk human papilloma viruses are known to be associated with cervic

31 ad and neck squamous cell cancer, both human papilloma virus-associated and human papilloma virus-neg

32 f renewed importance in the context of human papilloma virus-associated disease, in which young patie

33 ces the effect of radiation therapy in human papilloma virus-associated oropharyngeal SCC, we hypothe

34 ces the effect of radiation therapy in human papilloma virus-associated oropharyngeal squamous cell c

35 the metallothionein 1 promoter in the bovine papilloma virus-based expression vector drove the highes

36 induces G-to-A or C-to-T mutations in human papilloma virus cervical cell lines and genital warts.

37 NBF solutions were also evaluated for human papilloma virus content using DNA ISH.

38 ed protein (E6AP; as classified in the human papilloma virus context) is an E3 ligase that has an imp

39 erface is reminiscent of that seen in bovine papilloma virus E1 protein.

40 mer d(GACCGCGGTC), containing half the human papilloma virus E2 binding site, has been solved from tw

41 sette, whose expression is controlled by the papilloma virus E2 protein.

42 ranscription of the genes encoding the human papilloma virus E6 and E7 proteins and is over-expressed

43 d by wt-p53 but not by mutant p53, and human papilloma virus E6 inhibited the p53-dependent activatio

44 Inactivation of p53, by the human papilloma virus E6 oncoprotein, does not prevent PTEN-in

45 , ubiquitinates p53 in the presence of human papilloma virus E6 protein, while Nedd-4 does not.

46 n be abrogated by the co-expression of human papilloma virus E6 protein.

47 Elimination of p53 by expression of human papilloma virus E6 resulted in an inability to down-regu

48 The human papilloma virus E6-associated protein (E6AP) functions a

49 hibition in melanoma, colon cancer and human papilloma virus-E6/E7 tumour models.

50 ntly inactivated by the binding of the human papilloma virus E7 oncoprotein in cervical cancer.

51 in affects the antitumor efficacy of a human papilloma virus E7 peptide vaccine (CyaA-E7) capable of

52 or the growthpromoting activity of the human papilloma virus E7 protein.

53 mouse embryonic fibroblasts but not in human papilloma virus-E7 expressing fibroblasts.

54 he only cell type directly infected by human papilloma virus, express functional gammac and its co-re

55 Human papilloma virus has shown differential levels of prevale

56 est women for the causative agent, the human papilloma virus, has emerged as a potential screening to

57 Vaccines against rotavirus and human papilloma virus have entered clinical use.

58 cy virus, human T cell leukemia virus, human papilloma virus, hepatitis B and C viruses, herpes simpl

59 he other group 1 carcinogens including human papilloma virus, hepatitis C virus, and Helicobacter pyl

60 he other Group 1 carcinogens including human papilloma virus, hepatitis C virus, and Helicobacter pyl

61 Risk factors, including human papilloma virus, HIV, and the practice of circumcision h

62 al diseases such as hepatitis B virus, human papilloma virus, HIV, or chronic hepatitis C.

63 ve focused on its association with the human papilloma virus; however, there have also been several s

64 a peptide from the clinically-relevant human papilloma virus (HPV) 16 E7 oncoprotein induces cytotoxi

65 Identifying human papilloma virus (HPV) and human immunodeficiency virus (

66 ents whose lesions tested positive for human papilloma virus (HPV) and/or who endorsed a history of c

67 High-risk types of human papilloma virus (HPV) are increasingly associated with o

68 Human papilloma virus (HPV) causes focal infections of epithel

69 d with vemurafenib for the presence of human papilloma virus (HPV) DNA and identified 13% to be posit

70 The prevalence of human papilloma virus (HPV) DNA in different histological subt

71 We assayed for the presence of human papilloma virus (HPV) DNA in serum and/or peripheral blo

72 The E6 and E7 oncoproteins of human papilloma virus (HPV) drive the majority of genital canc

73 ppressor pathways are disrupted by the human papilloma virus (HPV) E6 and E7 oncoproteins, because E6

74 es and identified protein partners for human papilloma virus (HPV) E6 proteins.

75 Loss of p16(INK4A) or the presence of human papilloma virus (HPV) E6/E7 oncogene products not only p

76 Recently, the human papilloma virus (HPV) has been implicated in the rising

77 ical cancer has elucidated the role of human papilloma virus (HPV) in the pathogenesis of cervical ca

78 nomas (OPSCC) that are associated with human papilloma virus (HPV) infection carry a more favorable p

79 licated estrogenic exposure as well as human papilloma virus (HPV) infection in cervical carcinogenes

80 confirmed by a study on the effects of human papilloma virus (HPV) infection to the EC's response to

81 In a longitudinal study of human papilloma virus (HPV) infection, female adolescents aged

82 case-control datasets (samples either Human Papilloma Virus (HPV) positive or negative).

83 In women, naturally induced anti-human papilloma virus (HPV) serum antibodies are a likely mark

84 E6/E7 oncogenes of high-risk human papilloma virus (HPV) subtypes are essential for the dev

85 Specific human papilloma virus (HPV) types appear to be necessary etiol

86 ted with approximately 13 carcinogenic human papilloma virus (HPV) types in a broader group that caus

87 Despite preventive human papilloma virus (HPV) vaccination efforts, cervical canc

88 cussed include influenza, hepatitis B, human papilloma virus (HPV), human T-cell lymphotrophic virus

89 virus (HBV), hepatitis C virus (HCV), human papilloma virus (HPV), human T-cell lymphotropic virus (

90 99% of cervical cancers are caused by human papilloma virus (HPV), measurement of HPV (HPV test) was

91 DNA of human papilloma virus (HPV), the major etiological agent of ce

92 Human papilloma virus (HPV)-16 DNA was hybridized to probes th

93 We have shown that the human papilloma virus (HPV)-16 E7 gene is sufficient to induce

94 -3a differentially regulates different human papilloma virus (HPV)-16 variants that are associated wi

95 of normal oral epithelial cells and a human papilloma virus (HPV)-immortalized oral epithelial cell

96 In the TC-1 mouse allograft model of human papilloma virus (HPV)-induced cancer, a single administr

97 Human papilloma virus (HPV)-like particles (VLPs) have been us

98 the vulva is diverse and includes both human papilloma virus (HPV)-positive and HPV-negative pathways

99 Purpose The incidence of human papilloma virus (HPV)-positive oropharyngeal cancers has

100 articularly higher among patients with human papilloma virus (HPV)-positive tumors.

101 positive patients followed closely for human papilloma virus (HPV)-related anal neoplasia after trans

102 mor induction by pathogenic strains of human papilloma virus (HPV).

103 to tobacco, alcohol and infection with human papilloma virus (HPV).

104 d transcription of oncogenes, HIV, and human papilloma virus (HPV).

105 ith solar radiation exposure, HIV, and human papilloma virus (HPV).

106 lines in which p53 was inactivated by human papilloma virus (HPV)16E6 protein or by a dominant-negat

107 tion and screening recommendations for human papilloma virus (HPV); and appropriate testing for HIV a

108 in (LAMP-1) to the cytoplasmic/nuclear human papilloma virus (HPV-16) E7 antigen, creating a chimera

109 controlling tumors induced by type 16 human papilloma virus (HPV-16).

110 Over the past 20 years, high-risk human papilloma-virus (HPV) infection has been established as

111 association with high-risk subtypes of human papilloma virus (HPV16 and HPV18).

112 The impact of human papilloma virus (HPV16) E7 proteins and retinoblastoma (

113 High-risk human papilloma viruses (HPVs) have been recognized as importa

114 gical role of infection with high-risk human papilloma viruses (HPVs) in cervical carcinomas is well

115 d to infection with high-risk types of human papilloma viruses (HPVs).

116 al. (2014) demonstrate that high-risk human papilloma viruses (hrHPVs) attenuate the magnitude of re

117 cytokine expression and the absence of human papilloma virus in aggressive tumors.

118 ytokine expression and the presence of human papilloma virus in chemoradiation-sensitive basaloid tum

119 mal viruses--e.g., simian virus 40 or bovine papilloma virus--in which the initiator protein, T antig

120 lls transfected with the E6 protein of human papilloma virus (inactivating p53).

121 tumours induced by 'high-risk' mucosal human papilloma viruses, including human cervical carcinoma an

122 DNA methylation changes in relation to human papilloma virus infection and age.

123 s typically associated with anogenital human papilloma virus infection.

124 n the protein-protein interaction network of papilloma virus infection.

125 Cervical cancer is associated with human papilloma virus infection.

126 comprising susceptibility to cutaneous human papilloma virus infections and associated nonmelanoma sk

127 , a long-term risk of severe cutaneous human papilloma virus infections persists, possibly related to

128 al-kidney-cancer-associated breakpoint and a papilloma virus integration site.

129 Sexual transmission of human papilloma virus is a leading risk factor for cervical ca

130 that loss of p53 through mutation, or human papilloma virus-mediated inhibition, prevents recruitmen

131 h human papilloma virus-associated and human papilloma virus-negative tumors.

132 The human papilloma virus oncogene 16E6 induces telomerase activit

133 ns in the pocket and by binding of the human papilloma virus oncoprotein E7.

134 ntigen of SV40 virus, by E6 protein of human papilloma virus, or by genetic deletion led to the same

135 organs or any history of herpes virus, human papilloma virus, or human immunodeficiency virus infecti

136 p-regulated DEK protein levels in both human papilloma virus-positive hyperplastic murine skin and a

137 Human papilloma virus presence does not seem to be required fo

138 mental, and sexual health (including a human papilloma virus programme), an investment of US$4.6 per

139 Inactivation of pocket proteins with human papilloma virus protein E7 partially, but not completely

140 though a recent study also showed that human papilloma virus-reactive T cells can induce complete reg

141 Funding for human papilloma virus-related projects gradually rose, from 3.

142 cers, a malignancy associated with oncogenic papilloma viruses, remain a major disease burden in the

143 ty against herpes simplex virus (HSV), human papilloma virus, respiratory syncytial virus (RSV), deng

144 the E6 and E7 transforming proteins of human papilloma virus serotype 16 was necessary to establish l

145 human immunodeficiency virus (HIV) and human papilloma virus; several cancers, including follicular l

146 Human papilloma virus status was not found to be associated wi

147 Peptides from papilloma virus strains containing the motif VHFFK induc

148 Despite infection with high-risk human papilloma virus subtypes, which is a major etiological f

149 These guidelines incorporate human papilloma virus testing based on a multicenter trial doc

150 ppropriate methods of incorporation of human papilloma virus testing into the screening protocols.

151 r, and MIS inhibits the growth of both human papilloma virus-transformed and non-human papilloma viru

152 an papilloma virus-transformed and non-human papilloma virus-transformed cervical cell lines, with a

153 ternary complex comprising full-length human papilloma virus type 16 (HPV-16) E6, the LxxLL motif of

154 R2 is able to induce the expression of human papilloma virus type 16 (HPV-16) genes via binding to a

155 is able to activate expression of the human papilloma virus type 16 (HPV-16) upstream regulatory reg

156 E7 is the main transforming protein of human papilloma virus type 16 (HPV16) which is implicated in t

157 Inhibition of wild-type p53, by either human papilloma virus type 16 E6 or a dominant-negative p53, r

158 ental cultures with viral oncoproteins human papilloma virus type 16 E6/E7 with and without hTERT, an

159 which binds pRB), or both E6 and E7 of human papilloma virus type 16.

160 me 8q24.21 at which integration of the human papilloma virus type 18 (HPV-18) genome occurred and tha

161 c, mutant type 5 adenovirus (Ad5), and human papilloma virus type 18.

162 A peptide from human papilloma virus type 40 (HPV 40) containing VHFFR, and o

163 nkage of CRT to a model tumor antigen, human papilloma virus type-16 (HPV-16) E7, for the development

164 nced adjuvant activity, such as in the human papilloma virus vaccine Cervarix(R).

165 or the expression of the E6 protein of human papilloma virus, were treated with exogenous ceramide, t