ライフサイエンスコーパス: papilloma

1 It may resemble conjunctival squamous papilloma.

2 with a lesion that resembled a conjunctival papilloma.

3 o the development of chemically induced skin papillomas.

4 of the tumor suppressor PTEN causes squamous papillomas.

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

6 compared with high indices in dysplasias and papillomas.

7 tinocytes, which are precursor cells to skin papillomas.

8 promoter in normal-appearing skin and benign papillomas.

9 er promotes the malignant conversion of skin papillomas.

10 ha mutations were detected in carcinomas and papillomas.

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

12 se conditions, CD34KO mice failed to develop papillomas.

13 pontaneous skin tumors, mainly squamous cell papillomas.

14 bserved in carcinomas compared with those in papillomas.

15 ally induced mouse cSCCs, compared to benign papillomas.

16 th calreticulin can rapidly clear persistent papillomas.

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

18 neoplasia (classic) and seven arising within papillomas.

19 ly half of the mice also developed cutaneous papillomas.

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

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

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

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

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

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

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

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

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

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

30 its expression was maintained in transgenic papillomas and cancer.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 Examination of human papillomas and squamous cell carcinomas (SCCs) revealed

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 Papillomas bearing the mutation showed increased Erk act

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

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

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

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

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

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

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

74 milarly suppress tumor formation by adjacent papilloma cells.

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

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

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

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

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

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

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

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

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

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

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

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

87 competes with apoptosis during initiation of papilloma development.

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

89 The papillomas displayed a normal cytokeratin pattern but ex

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

91 treated animals and included hyperkeratoses, papillomas, dysplasias, and cancers.

92 14-CreER(tam)/LSL-K-ras(G12D) mice developed papillomas exclusively in the oral mucosa within 1 month

93 uPAR genetic deficiency decreased papilloma formation and accelerated keratinocyte differe

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

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

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

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

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

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

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

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

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

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

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

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

106 re partially resistant to chemically induced papilloma formation.

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

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

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

110 tiation and promotion are required steps for papilloma formation.

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

112 expression increases the number of epidermal papillomas formed after carcinogen treatment.

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

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

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

116 (T), hyperplastic epidermis and/or squamous papilloma (Hyp/Pap), poorly-differentiated (PDSCC), or w

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

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

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

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

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

122 sease that presents with recurrent growth of papillomas in the upper airway.

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

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

125 Papillomas included lesions with benign and dysplastic p

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

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

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

129 12V) allele copy number was increased in all papillomas induced by TPA.

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

131 Conjunctival papilloma is a benign epithelial tumor occurring in both

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

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

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

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

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

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

138 125 follow-up tissue specimens of laryngeal papillomas, obtained from 70 patients who had had recurr

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

140 336 also induced near-complete regression of papillomas of TPA-treated Hras(G12V) knock-in mice.

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

142 Novel papilloma outgrowths appeared expressing intense, basal

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

144 3 transgenic versus 2 +/- 1.5 nontransgenic papillomas per mouse), yet they were more differentiated

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

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

147 Papilloma recurrence is more common in children and adol

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

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

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

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

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

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

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

155 owed that amplification occurred only at the papilloma stage.

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

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

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

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

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

161 13-acetate, which typically generates benign papillomas that occasionally progress to squamous cell c

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

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

164 The few papillomas that were developed displayed high levels of

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

166 rotocol potentiated the conversion of benign papillomas to carcinomas by elevating p38MAPK and MAPK/E

167 thereby preventing the progression of benign papillomas to carcinomas.

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

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

170 growth and prohibits progression from benign papillomas to SCCs.

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

172 beta1 transgene stimulated the conversion of papillomas to SCCs.

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

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

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

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

177 8 antibody levels at enrollment in PATRICIA (Papilloma Trial Against Cancer in Young Adults; NCT00122

178 tric sensors used for the detection of human papilloma, vaccinia, dengue, Ebola, influenza A, human i

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

180 ere collected from women with healthy, human papilloma virus (HPV) +/- cervical intraepithelial neopl

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

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

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

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

185 High-risk subtypes of the human papilloma virus (HPV) are the cause of the disease in mo

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

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

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

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

190 er the past decades owing to increased human papilloma virus (HPV) exposure.

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

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

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

194 noma (HNSCC) associated with high-risk human papilloma virus (HPV) infection is a growing clinical pr

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

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

197 In cervical cancer cells, human papilloma virus (HPV) protein E7 binds to Rb, releasing

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

199 the aerodigestive tract caused by the Human Papilloma Virus (HPV) that manifests as profoundly alter

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

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

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

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

204 99% of cervical cancers are caused by human papilloma virus (HPV), measurement of HPV (HPV test) was

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

206 -3a differentially regulates different human papilloma virus (HPV)-16 variants that are associated wi

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

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

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

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

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

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

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

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

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

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

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

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

219 rus (EBV), hepatitis B virus (HBV) and human papilloma virus (HPV; for example, HPV16 or HPV18).

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

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

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

223 milies and as SPCs are associated with human papilloma virus and smoking related cancers.

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

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

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

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

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

229 Human papilloma virus has shown differential levels of prevale

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

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

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

233 cess bodyweight (three provinces), and human papilloma virus infection (one province).

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

235 s typically associated with anogenital human papilloma virus infection.

236 types suggest that life style related human papilloma virus infections contributed to the observed f

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

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

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

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

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

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

243 A PCR screening detected human papilloma virus type 45 DNA (high-risk subtype), and foc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 ts tumour growth in the B16F10-OVA and human papilloma virus-E6/E7 tumour models in mice.

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

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

262 n ligase E6AP (UBE3A) is implicated in human papilloma virus-induced cervical tumorigenesis and sever

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

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

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

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

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

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

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

270 e to elimination of foreskin harboring human papilloma virus.

271 es are available against rotavirus and human papilloma virus.

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

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

274 tegies against oncogenesis mediated by human papilloma virus.

275 reasing percentage are associated with human papilloma virus.

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

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

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

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

280 tion of PPIs that discriminate between human papilloma viruses (HPVs) with high and low oncogenic pot

281 be infected by more than 200 types of human papilloma viruses (HPVs), and persistent HPV infections

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

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

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

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

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

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

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

289 Cumulative papilloma volumes were computed for analysis of the data

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

291 Rhinosporidiosis and papilloma were the predominant diagnostic hypotheses (28

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

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