ライフサイエンスコーパス: papilloma

1 with a lesion that resembled a conjunctival papilloma.

2 It may resemble conjunctival squamous papilloma.

3 of the tumor suppressor PTEN causes squamous papillomas.

4 eased the number of mutant Hras-induced skin papillomas.

5 compared with high indices in dysplasias and papillomas.

6 tinocytes, which are precursor cells to skin papillomas.

7 promoter in normal-appearing skin and benign papillomas.

8 er promotes the malignant conversion of skin papillomas.

9 ha mutations were detected in carcinomas and papillomas.

10 radecanoylphorbol-13-acetate (TPA) developed papillomas.

11 se conditions, CD34KO mice failed to develop papillomas.

12 pontaneous skin tumors, mainly squamous cell papillomas.

13 bserved in carcinomas compared with those in papillomas.

14 ropapillomas, and one (17%) of six sclerotic papillomas.

15 ed cells, usually originating in intraductal papillomas.

16 nitrite levels were also decreased by BRB in papillomas.

17 ally induced mouse cSCCs, compared to benign papillomas.

18 th calreticulin can rapidly clear persistent papillomas.

19 with neoplasia, and 71% of lesions arose in papillomas.

20 neoplasia (classic) and seven arising within papillomas.

21 ly half of the mice also developed cutaneous papillomas.

22 (High Mobility Group Box 1) in wound-induced papillomas.

23 o the development of chemically induced skin papillomas.

24 ency of malignancy was one (3%) of 38 benign papillomas, 10 (67%) of 15 atypical papillomas, two (50%

25 were identified by FCM as squamous (2 benign papillomas, 2 grade 2 conjunctival intraepithelial neopl

26 or multiplicity and malignant progression of papillomas after chemical skin carcinogenesis were signi

27 ed cytokines were also reduced in transgenic papillomas, although the dermal macrophages themselves d

28 In skin papilloma and squamous cell carcinoma (SCC), levels of P

29 We report resemblance to conjunctival papilloma and the result of vital staining with 0.05% To

30 Ikkalpha+/- mice developed 2 times more papillomas and 11 times more carcinomas than did Ikkalph

31 nogen-treated skin led to the development of papillomas and aggressive SCC.

32 ires augmentation of signal output, which in papillomas and angiosarcomas is achieved via increased H

33 These mice developed papillomas and angiosarcomas, which were associated with

34 its expression was maintained in transgenic papillomas and cancer.

35 ne, and this mutation was identified in most papillomas and carcinomas although several papillomas an

36 alpha expression promotes the development of papillomas and carcinomas and that the integrity of the

37 t papillomas and carcinomas although several papillomas and carcinomas in K14-LMP1 and K14-LMP1/LMP2A

38 osis virus type 1 (BPCV1) is associated with papillomas and carcinomas in the endangered marsupial th

39 The development of papillomas and carcinomas was determined in the tumor in

40 RasGRP1 transgenic mice develop spontaneous papillomas and cutaneous squamous cell carcinomas, some

41 V vaccination for treatment of oral squamous papillomas and cutaneous verruca vulgaris.

42 The mice developed fewer papillomas and had systemic hair loss.

43 ical agent of anogenital warts and laryngeal papillomas and has been included in both the quadrivalen

44 Whereas H-Ras(G12V) elicited papillomas and hematopoietic tumors, K-Ras(G12V) induced

45 ical agent of anogenital warts and laryngeal papillomas and is included in the 4-valent and 9-valent

46 reases protein levels of Pdcd4 in mouse skin papillomas and keratinocytes as well as in human HEK293

47 nstrate that wounding induces benign tumors (papillomas and keratoacanthomas) in InvEE mice.

48 cyclin D2 results in an increased number of papillomas and malignant progression.

49 Some of the Ikkalpha+/- papillomas and most Ikkalpha+/- carcinomas lost the rema

50 re resistant to the development of both skin papillomas and squamous cell carcinoma (SCC) elicited by

51 one had no effect, whereas TPA alone induced papillomas and squamous cell carcinomas (SCC).

52 ion causes a dramatic reduction in classical papillomas and squamous cell carcinomas (SCCs), but the

53 RasGRP1) are prone to developing spontaneous papillomas and squamous cell carcinomas, suggesting a ro

54 a-ras mutations with dramatic development of papillomas and squamous cell carcinomas.

55 train produces both transient and persistent papillomas and that vaccination of the mice with a DNA e

56 s ( approximately 15%); and (iii) no visible papillomas and viral clearance ( approximately 65%).

57 We find that, in viral warts (papillomas) and HPV gene-induced epidermal tumors, AKT a

58 with conjunctival nevi, 19 with conjunctival papilloma, and 2 with conjunctival-reactive lymphoid hyp

59 y carcinoma, 3 lobular carcinoma, 1 invasive papilloma, and 4 sentinel lymph nodes).

60 Biopsy showed squamous cell papilloma, and DNA sequencing revealed HPV-32.

61 intraepithelial neoplasias, promoting facial papillomas, and derepressing Wnt signaling.

62 xpression in regions of the skin epithelium, papillomas, and squamous cell carcinomas.

63 s/fos-Delta5PTEN(flx) hyperplasia, cysts and papillomas, and while malignant conversion required p53

64 Transgenic papillomas appeared earlier and were more numerous (6 +/

65 clinical outcomes: (i) persistent (>2-month) papillomas ( approximately 20%); (ii) transient papillom

66 garis lesions (warts) and oral squamous cell papillomas are common lesions caused by human papillomav

67 Conjunctival papillomas are larger and more likely to be multiple in

68 seven percent were found to have intraductal papilloma as the source of discharge, with fibrocystic d

69 apsids, efficiently induced the outgrowth of papillomas as early as 3 weeks after application to abra

70 with malignancy (67%), diagnosis of atypical papilloma at core biopsy should prompt excision for defi

71 inical features and outcomes of conjunctival papilloma based on age at initial examination.

72 Papillomas bearing the mutation showed increased Erk act

73 lymphangiogenesis is greatly accelerated in papilloma-bearing p19/Arf- or p53-deficient mice, which

74 umors converted from exophytic to endophytic papillomas before progressing to carcinomas.

75 A comparison of conjunctival papillomas between age groups revealed significant diffe

76 otocol described here, a highly reproducible papilloma burden is expected within 10-20 weeks with pro

77 We report the case of recurrent oral papillomas caused by HPV-32 with complete resolution aft

78 Finally, overexpression of Stat3C in a papilloma cell line led to enhanced cell migration and e

79 he change in tumor multiplicity, SP-1 murine papilloma cell lines that were generated to stably expre

80 milarly suppress tumor formation by adjacent papilloma cells.

81 squamous cell carcinoma (SCC) but not benign papilloma clonal lineages and with independently induced

82 feration, epidermal hyperplasia and onset of papillomas compared with wild-type counterparts.

83 ting a permissive K14.ROCK(er)/HK1.ras(1205) papilloma context (wound-promoted/NF-kappaB(+)/p53(-)/p2

84 laboratory mouse strain in which persistent papillomas could be established.

85 Mek1 knockout mice had smaller papillomas, delayed tumor onset, and half the tumor burd

86 , and 10% of mutant mice develop spontaneous papillomas, demonstrating the role of Fgfr2b in post-nat

87 A-C/EBP expression after papilloma development caused the papillomas to regress w

88 ases in both the incidence and prevalence of papilloma development compared with the WT ATF2 mice.

89 as and Myc in vitro and significantly blocks papilloma development in vivo in a carcinogen-induced sk

90 ice with TPA alone was sufficient to trigger papilloma development with a shorter latency and an appr

91 ns cooperatively with mutant Hras to promote papilloma development, although the effect is relatively

92 This protocol induces skin papilloma development, causing a selection of cells bear

93 competes with apoptosis during initiation of papilloma development.

94 Benign papilloma diagnosed at core biopsy is infrequently (3%)

95 Previously persistent papillomas disappeared within 2 months after the final v

96 The papillomas displayed a normal cytokeratin pattern but ex

97 g in a dramatic increase in the formation of papillomas during epidermal carcinogenesis.

98 14-CreER(tam)/LSL-K-ras(G12D) mice developed papillomas exclusively in the oral mucosa within 1 month

99 uPAR genetic deficiency decreased papilloma formation and accelerated keratinocyte differe

100 igenesis, Par3 deficiency results in reduced papilloma formation and growth.

101 -null mice showed a significant reduction in papilloma formation compared with wild-type mice.

102 ormation, suggesting that the suppression of papilloma formation has a p53-dependent mechanism.

103 with an early role in tumorigenesis, murine papilloma formation in a classical chemical carcinogenes

104 ity to mutant Harvey-Ras (HRas(Q61L))-driven papilloma formation in the 7,12-Dimethylbenz[a]anthracen

105 This down-regulation occurs before papilloma formation or tumorigenesis and leads to cutane

106 pinB2 abrogates the increased sensitivity to papilloma formation seen on DUSP5 deletion.

107 tocol, PKD1-deficient mice were resistant to papilloma formation when compared with control littermat

108 al carcinogenesis, both transgenes increased papilloma formation, but only the T188Ibeta1 transgene s

109 eterozygous for p53 were more susceptible to papilloma formation, suggesting that the suppression of

110 ioned as a weak tumor promoter and increased papilloma formation.

111 e expressing LMP2A did not induce or promote papilloma formation.

112 re partially resistant to chemically induced papilloma formation.

113 hat one Mek1 allele is sufficient for normal papilloma formation.

114 MBA/PMA 2-stage carcinogenesis model of skin papilloma formation.

115 h cooperated with H-Ras mutations to promote papilloma formation.

116 tiation and promotion are required steps for papilloma formation.

117 n exposure strongly suppressed benign tumor (papilloma) formation, and that the few, small lesions th

118 In marked contrast, papillomas formed normally in Chk1 hemizygous skin but s

119 of apoptotic cells in DMBA-treated skin and papillomas from osteopontin-null versus WT mice.

120 Here, we show that benign pre-metastatic papillomas from wild-type mice trigger lymphangiogenesis

121 llomas) was compared with high-risk atypical papilloma group.

122 both DMBA and TPA to induce large numbers of papillomas had a higher incidence and earlier onset of c

123 exposure, as well as coinfection with human papilloma, hepatitis B, hepatitis C and Epstein-Barr vir

124 normal human oral keratinocytes (NHOKs) and papilloma-immortalized human oral keratinocyte (HOK16B)

125 showed no residual lesion in 10, intraductal papilloma in 14, intraductal papillomatosis in two, papi

126 VSV-based CRPV vaccination cured all of the papillomas in 5 of 30 rabbits.

127 mavirus 1 (MmuPV1/MusPV1) induces persistent papillomas in immunodeficient mice but not in common lab

128 ces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 loss and novel NF-kappa

129 er levels in areas of fibrocystic change and papillomas, in all benign breast disease lesions, and in

130 mice showed a marked decrease both in tumor/papilloma incidence and multiplicity compared with WT mi

131 man RDEB-cSCC, whereas wild-type mice formed papillomas, indicating that the aggressiveness of RDEB-c

132 Furthermore, papillomas induced by CRPV genomic DNA deficient for L2

133 ted rabbits from CRPV challenge but not from papillomas induced by cutaneous challenge with CRPV geno

134 12V) allele copy number was increased in all papillomas induced by TPA.

135 ed rapid induction of gene expression during papilloma induction and during wound healing.

136 Conjunctival papilloma is a benign epithelial tumor occurring in both

137 Frequent recurrence of laryngeal papillomas is a consequence of long-term persistence of

138 Inverted sinonasal papilloma (ISP) is a locally aggressive neoplasm associa

139 -foot skin reaction, hair changes, verrucous papillomas, keratoacanthomas, and squamous cell carcinom

140 h classic epidermal tumors such as verrucous papillomas, keratoacanthomas, and squamous cell carcinom

141 jor cytokeratin derangements in the squamous papillomas may be of ancillary diagnostic value for lesi

142 nancy were benign papilloma (n=1), sclerotic papilloma (n=1), micropapilloma (n=2), and atypical papi

143 dings associated with malignancy were benign papilloma (n=1), sclerotic papilloma (n=1), micropapillo

144 ma (n=1), micropapilloma (n=2), and atypical papilloma (n=10).

145 agnoses of benign papilloma (n=38), atypical papilloma (n=15), sclerotic papilloma (n=6), and micropa

146 03) revealed core biopsy diagnoses of benign papilloma (n=38), atypical papilloma (n=15), sclerotic p

147 (n=38), atypical papilloma (n=15), sclerotic papilloma (n=6), and micropapilloma (n=4) in 57 women (m

148 increase in number or growth rate of benign papillomas nor an increase in the rate of progression to

149 125 follow-up tissue specimens of laryngeal papillomas, obtained from 70 patients who had had recurr

150 Papillomas of K14.ATF2(f/f) mice exhibit reduced express

151 336 also induced near-complete regression of papillomas of TPA-treated Hras(G12V) knock-in mice.

152 ere not identified in exophytic or oncocytic papillomas or non-ISP-associated SNSCC, suggesting that

153 Novel papilloma outgrowths appeared expressing intense, basal

154 nt progression and the intense expression in papilloma outgrowths, identifies a novel, significant an

155 3 transgenic versus 2 +/- 1.5 nontransgenic papillomas per mouse), yet they were more differentiated

156 Moreover, in a papilloma-prone background, a reduced tumor burden was o

157 Here, we develop a papilloma pseudovirus-based oral immunotherapeutic appro

158 Papilloma recurrence is more common in children and adol

159 ERK and cyclin D1 were lowered in late-stage papillomas returning to elevated levels, alongside incre

160 nevi (SD, +/- 0.57) and 0.5 for conjunctival papilloma (SD, +/- 0.83).

161 ound that Kras(G12D) induced redundant skin, papillomas, shortened nails, and hair loss.

162 BPV-1-induced papillomas show characteristics of repressed NOTCH signa

163 -bromo-4-deoxyuridine labeling in Delta5PTEN papillomas showed that a second promotion mechanism cent

164 ection of normal skin, hyperplastic skin and papillomas showed that amplification occurred only at th

165 K14.ROCK(er)/HK1.ras(1205) cohorts exhibited papillomas similar to HK1.ras(1205) controls; however, K

166 owed that amplification occurred only at the papilloma stage.

167 lacking epidermal Mek1 protein develop fewer papillomas than both wild-type and Mek2-null mice follow

168 ethylbenz(a)anthracene (DMBA) developed more papillomas than like-treated nontransgenic mice, whereas

169 was much less susceptible to virion-induced papillomas than the muzzle or tail.

170 evealed that FGF22 null mice developed fewer papillomas than wild type controls, suggesting a potenti

171 Prkar1a(+/-) mice also developed more papillomas than wild-type animals.

172 hibited by TPA-induced K14.cre/PTEN(flx/flx) papillomas that also lacked endogenous c-ras(Ha) activat

173 13-acetate, which typically generates benign papillomas that occasionally progress to squamous cell c

174 TPA, 58% of K5-PKCalpha mice developed skin papillomas that progressed to carcinoma, whereas wild-ty

175 illomas ( approximately 20%); (ii) transient papillomas that spontaneously regress, typically within

176 The few papillomas that were developed displayed high levels of

177 2 matched those of corresponding intraductal papillomas that were involved by or were separate from t

178 In benign F1 papillomas, this imbalance is reversed, possibly by sele

179 Thus, the progression of GOF p53 papillomas to carcinoma was marked by the acquisition of

180 unctions as a suppressor of progression from papillomas to invasive squamous carcinomas.

181 ssion after papilloma development caused the papillomas to regress with an associated increase in apo

182 d reduced the malignant conversion of benign papillomas to SCCs.

183 beta1 transgene stimulated the conversion of papillomas to SCCs.

184 growth and prohibits progression from benign papillomas to SCCs.

185 Endo/Ectocervical Disease II (FUTURE II) and PApilloma TRIal against Cancer In young Adults (PATRICIA

186 o/Ectocervical Disease (FUTURE I/II) and the Papilloma Trial Against Cancer in Young Adults (PATRICIA

187 post hoc analysis of the phase III PATRICIA (PApilloma TRIal against Cancer In young Adults) trial (N

188 ysis after 4 years of follow-up in PATRICIA (PApilloma TRIal against Cancer In young Adults).

189 8 antibody levels at enrollment in PATRICIA (Papilloma Trial Against Cancer in Young Adults; NCT00122

190 8 benign papillomas, 10 (67%) of 15 atypical papillomas, two (50%) of four micropapillomas, and one (

191 se analysis of independent TIL isolates from papillomas versus carcinomas exposed a clear association

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 99% of cervical cancers are caused by human papilloma virus (HPV), measurement of HPV (HPV test) was

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

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

213 -3a differentially regulates different human papilloma virus (HPV)-16 variants that are associated wi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

234 Human papilloma virus has shown differential levels of prevale

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

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

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

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

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

240 s typically associated with anogenital human papilloma virus infection.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 e to elimination of foreskin harboring human papilloma virus.

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

274 es are available against rotavirus and human papilloma virus.

275 tegies against oncogenesis mediated by human papilloma virus.

276 reasing percentage are associated with human papilloma virus.

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

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

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

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

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

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

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

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

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

286 the most effective, as it reduced cumulative papilloma volumes by 96.9% overall, relative to those of

287 E2, E6, or E7 protein significantly reduced papilloma volumes relative to those of the controls.

288 Cumulative papilloma volumes were computed for analysis of the data

289 up (micropapillomas and sclerotic and benign papillomas) was compared with high-risk atypical papillo

290 )/HK1.ras(1205) histotypes comprised a mixed papilloma/well-differentiated squamous cell carcinoma (w

291 oma, 7 epidermoid dysplasias, and 4 squamous papillomas were evaluated with microscopy and biomarkers

292 e transplanted dogs that developed cutaneous papillomas were maintained for >3 1/2 years post-BMT for

293 SKH1 mice with persistent papillomas were treated by using a candidate preventive/

294 tages of GOF p53 tumor progression (that is, papillomas), whereas it is implicated at a later stage i

295 tradecanoylphorbol-13-acetate (TPA)-promoted papillomas, whereas HK1.ras/K14.cre/PTEN(flx/flx) cohort

296 in mice induced an even greater incidence of papillomas, which either harbored Hras(G12V) amplificati

297 ma in 14, intraductal papillomatosis in two, papilloma with adjacent foci of atypical ductal hyperpla

298 lele dramatically reduced the number of skin papillomas with Hras mutations, consistent with Hras as

299 port the case of a patient with chronic oral papillomas with resolution after quadrivalent HPV vaccin

300 tetradecanoylphorbol-13-acetate-induced skin papillomas, with increased latency and greatly reduced i