ライフサイエンスコーパス: SCC

1 SCC connectivity was investigated with closely connected

2 SCC lesions have higher levels of the H3K27 methyltransf

3 SCC-25 cells, a human squamous cell carcinoma cell line,

4 SCCs can also originate from simple or pseudo-stratified

5 SCCs frequently resist chemotherapy through still unknow

6 cancer genome atlas (TCGA) and a panel of 24 SCC cell lines to classify three disease segments within

7 pCR was achieved in 30 patients (22%); 37% SCC and 17% adenocarcinoma.

8 After vaccination, he developed 4.44 SCCs and 0 BCCs per year, a 62.5% reduction in SCCs and

9 a population-based case-control study of 487 SCC cases and 462 age- and gender-matched controls.

10 After vaccination, she developed 1.84 SCCs and 0 BCCs per year, a 66.5% reduction in SCCs and

11 CSC regulatory mechanisms change in advanced SCC, correlating with aggressive tumor growth and enhanc

12 arly SCC CSC, were downregulated in advanced SCC.

13 w that their frequency increases in advanced SCCs.

14 occurrence, and risk factors for aggressive SCC after retransplantation.

15 ransplant SCC have a high risk of aggressive SCC.

16 Twenty aggressive SCC developed over the study period.

17 iomarker-directed trials for FGFR1-amplified SCC require assessment of FGFR1 protein expression and u

18 l therapeutic strategies for FGFR1-amplified SCC with low FGFR1 protein expression.

19 Anal SCC tumor specimens derived from the AIDS and Cancer Spe

20 ns of PD-1/PD-L1 checkpoint blockade in anal SCC, irrespective of patient HIV status.

21 IC infiltration or PD-L1 expression in anal SCC.

22 n levels was observed in HIV-associated anal SCCs (fold change, 12.69; P < .001).

23 tumor immune microenvironment (TME) in anal SCCs from HIV-positive and HIV-negative patients.

24 s demonstrate an immune-reactive TME in anal SCCs from HIV-positive patients and support clinical inv

25 ubsets, and gene expression profiles in anal SCCs from HIV-positive vs HIV-negative patients.

26 between KIR and HLA modify risks of BCC and SCC and that KIR encoded by the B genes provides selecti

27 h RTDs on sun-exposed body sites for BCC and SCC are in keeping with sun exposure as the primary etio

28 Former smokers had similar risks for BCC and SCC as never smokers.

29 that the anatomical distribution of BCC and SCC differ, few have compared them directly in well-defi

30 mpare the anatomical distribution of BCC and SCC in a population-based sample in Queensland, Australi

31 mpare the anatomical distribution of BCC and SCC in a population-based sample in Queensland, Australi

32 about the anatomical distribution of BCC and SCC may provide insight into their diagnoses and causes.

33 greatest differences in RTDs between BCC and SCC were on the hand (BCC:SCC ratio, 1:14) and the back

34 CD4 count, VL, and subsequent NMSC (BCC and SCC).

35 stage, or patients' survival time in EAC and SCC.

36 decreased significantly in hyperplastic and SCC lesions.

37 rized by increased metastatic potential, and SCC progression is associated with an expansion of CSC.

38 ark, is also prevalent in human lung SCC and SCC regions within ADSCC tumours.

39 ported at baseline; newly diagnosed BCCs and SCCs were ascertained through data linkage and verified

40 ric energy densities of LIBs with SCC anode (SCC-LIBs) and the potential improvement over graphite-LI

41 us squamous cell carcinoma (SCC), anogenital SCC, inability to extract cSCC data from other malignanc

42 (HR, 0.98; 95% CI, 0.87-1.12), including any SCC.

43 SCT recipients had an increased risk of BCC, SCC, and MM, with respective HRs of 3.1 (95% CI, 1.9-5.2

44 CT recipients have an increased risk of BCC, SCC, and MM.

45 tio, 1:14) and the back and/or buttocks (BCC:SCC ratio, 8:1).

46 Ds between BCC and SCC were on the hand (BCC:SCC ratio, 1:14) and the back and/or buttocks (BCC:SCC r

47 ifferences in glycolytic rate and VB between SCC and AC are relevant for research in targeting agents

48 tations in esophageal squamous cell cancers (SCCs).

49 The social cost of carbon (SCC) is a central concept for understanding and implemen

50 used to calculate the social cost of carbon (SCC) is either undocumented, difficult to trace, or base

51 ded melanoma (12%), squamous cell carcinoma (SCC) (9%), lymphoma (7%), and others.

52 istory of cutaneous squamous cell carcinoma (SCC) after a first kidney transplantation who received a

53 otes nonmelanocytic squamous cell carcinoma (SCC) after kidney transplantation.

54 including cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), in part as a result

55 pregulation in skin squamous cell carcinoma (SCC) and demonstrate that TCF7L1 overexpression increase

56 t can progress into squamous cell carcinoma (SCC) and invasive SCC if left untreated.

57 ncrease the risk of squamous cell carcinoma (SCC) and other skin cancers in organ transplant recipien

58 ransplant cutaneous squamous cell carcinoma (SCC) are few and appear contradictory.

59 their functions in squamous cell carcinoma (SCC) are unclear.

60 the first time that squamous cell carcinoma (SCC) EVs were enriched with the C-terminal fragment of d

61 carcinoma (BCC) and squamous cell carcinoma (SCC) from healthy tissue.

62 the development of squamous cell carcinoma (SCC) in lung transplant recipients, by attempting to acc

63 carcinoma (BCC) and squamous cell carcinoma (SCC) in Mohs micrographic surgery fresh-tissue specimens

64 carcinoma (BCC) or squamous cell carcinoma (SCC) in QSkin, a prospective study of skin cancer (N = 4

65 st the formation of squamous cell carcinoma (SCC) in several models.

66 Anal squamous cell carcinoma (SCC) is associated with both human papillomavirus and HI

67 l response; one had squamous cell carcinoma (SCC) of the anus and one had SCC of the head and neck.

68 Patients with squamous cell carcinoma (SCC) of the cervix or vulva have limited therapeutic opt

69 tration and risk of squamous cell carcinoma (SCC) of the skin in a U.S. population.

70 rate were higher in squamous cell carcinoma (SCC) than in adenocarcinoma (AC), whereas VB was lower (

71 urine model of skin squamous cell carcinoma (SCC) that nuclear FAK regulates Runx1-dependent transcri

72 carcinomas (ADC) to squamous cell carcinoma (SCC) through deletion of Lkb1 (Stk11) in autochthonous a

73 d incidence rate of squamous cell carcinoma (SCC) was highest among black persons, while adenocarcino

74 ll metaplasia (CM), squamous cell carcinoma (SCC), and squamous epithelium (SE) cases.

75 auses oropharyngeal squamous cell carcinoma (SCC), and the prevalence of oropharyngeal SCC is higher

76 a were noncutaneous squamous cell carcinoma (SCC), anogenital SCC, inability to extract cSCC data fro

77 carcinoma (BCC) and squamous cell carcinoma (SCC), are the most common cancers among fair-skinned pop

78 carcinoma (BCC) and squamous cell carcinoma (SCC), are the most common cancers among fair-skinned pop

79 n cancer, including squamous cell carcinoma (SCC), melanoma (MM), and Merkel cell carcinoma (MCC) in

80 Lung squamous cell carcinoma (SCC), strongly associated with smoking, is treated prima

81 ymphocytes (TIL) in squamous cell carcinoma (SCC), using a systems biologic approach to integrate pub

82 tumor types such as squamous cell carcinoma (SCC).

83 carcinoma (BCC) and squamous cell carcinoma (SCC).

84 tally induced mouse squamous cell carcinoma (SCC).

85 ocarcinoma (AC) and squamous cell carcinoma (SCC).

86 er types, including squamous cell carcinoma (SCC).

87 pouch model of oral squamous cell carcinoma (SCC).

88 AD) but not in lung squamous cell carcinoma (SCC).

89 ially excised skin squamous cell carcinomas (SCC) is characterized by increased metastatic potential,

90 mewhat stronger in squamous cell carcinomas (SCC, OR = 4.90) than in urothelial carcinomas (UC, OR =

91 Cs), consisting of squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs), are the most com

92 Squamous cell carcinomas (SCCs) are heterogeneous tumors sustained by tumor-propag

93 rus (HPV)-positive squamous cell carcinomas (SCCs) arise.

94 Squamous cell carcinomas (SCCs) derived from interfollicular epidermis (IFE) are g

95 umor suppressor in squamous cell carcinomas (SCCs).

96 found in 10-20% of squamous cell carcinomas (SCCs).

97 dermatofibromas, 2 squamous cell carcinomas [SCCs]) was selected and shown to attendees of a dermosco

98 llomavirus (HPV)-associated uterine cervical SCC, the third-leading cause of death by cancer in women

99 ded (FFPE) biopsy specimens from 48 cervical SCCs and 23 vulvar SCCs.

100 amples of FFPE tissue from cases of cervical SCCs (n = 48) and vulvar SCCs (n = 23) were retrieved fr

101 responses were significantly lower in KT-CNI-SCC than KT-mTORi-SCC and NoKT-SCC and predicted SCC rel

102 Moreover, 25 KT-CNI-SCC were switched to mTOR-i and evaluated after 12 month

103 transplant patients with SCC on CNI (KT-CNI-SCC) or mTOR-i (KT-mTORi-SCC), 25 nontransplants develop

104 he stratum adjusted correlation coefficient (SCC), for quantifying the similarity between Hi-C intera

105 embly supramolecular coordination complexes (SCCs) bearing triazine and porphyrin faces with promisin

106 of Si composition in a Si-carbon composite (SCC) based anode to maximize the volumetric energy densi

107 , on the risk of developing biopsy-confirmed SCC.

108 conditions, the subgenual cingulate cortex (SCC) exhibited increased functional connectivity with th

109 ng a bilateral subcallosal cingulate cortex (SCC) seed was applied to 122 patients from the Predictio

110 Mammary quarter milk somatic cell count (SCC) and N-acetyl-beta-d-gluconaminidase (NAGase) activi

111 ral cracks including stress corrosion crack (SCC) and rolling contact fatigue (RCF).

112 ur findings characterize ZNF750 as a crucial SCC-specific suppressor and uncover its novel anticancer

113 Cutaneous SCC occurrence (n = 6,169) was associated with 1.44-fold

114 Cutaneous SCC occurrence after transplantation could serve as a ma

115 Cutaneous SCC was also associated with increased risk of human pap

116 ive HNSCC (13 of 30 tumors [43%]), cutaneous SCC (11 of 21 tumors [52%]), basal cell carcinoma (3 of

117 th an increased risk of aggressive cutaneous SCC after retransplantation.

118 t was the occurrence of aggressive cutaneous SCC after the second transplantation.

119 and suggest a shared etiology for cutaneous SCC and other SCC in the setting of immunosuppression.

120 were particularly elevated for non-cutaneous SCC, including those of the oral cavity/pharynx (HR, 5.6

121 ngs highlight the possibility that cutaneous SCC development, and perhaps BCC development, may be dri

122 st that transplant recipients with cutaneous SCC, but not BCC, have an increased risk of developing o

123 xtract cSCC data from other malignancy data, SCC in situ, Marjolin ulcer, and genetic disorders predi

124 AR2 is highly overexpressed in p53-deficient SCC cell lines compared with normal primary keratinocyte

125 , while hair follicle (HF) stem cell-derived SCCs frequently exhibit EMT, efficiently form secondary

126 7hi participants were more likely to develop SCC during follow-up (hazard ratio, 2.9; 95% confidence

127 ansplantation, 17 (33.3%) patients developed SCC in dialysis and 39 (73.6%) after the second transpla

128 (KT-mTORi-SCC), 25 nontransplants developing SCC (NoKT-SCC) and 6 healthy controls.

129 sample of 863 patients with newly diagnosed SCC of the oral cavity, oropharynx, larynx, or nasophary

130 s standard in social cost of carbon dioxide (SCC) models, and of average utilitarianism (AU), which i

131 r similarities to multiple carcinogen-driven SCCs from diverse sites, suggesting that cuSCC may serve

132 significantly more highly-expressed in EAC, SCC and glandular lesions than in SE and more in EAC tha

133 Catenin and EGFR signaling, induced in early SCC CSC, were downregulated in advanced SCC.

134 tify renal transplant recipients at elevated SCC risk.

135 c disparities in the incidence of esophageal SCC over time in the United States, while disparities in

136 nd predicts for poor prognosis of esophageal SCC, shedding light upon the tumor promoting oncogenic a

137 or proliferation in vitro and in established SCC tumors in vivo.

138 h Dsg2/green fluorescence protein-expressing SCC cells, green fluorescence protein signal was detecte

139 The first SCC developed in 47 patients with a functional graft and

140 r posttransplant skin cancer overall and for SCC, MM, and MCC were calculated per 100000 person-years

141 tandardized incidence ratios (SIRs) and, for SCC, multivariable Poisson regression analysis of SIR ra

142 ty of a prospective connectomic approach for SCC DBS surgery, this pilot study used the four-bundle t

143 adults (55-69 years) were 2-fold higher for SCC on the scalp (0.38 [95% CI, 0.00-0.81] vs 1.07 [95%

144 implications include targeted monitoring for SCC among HIV-infected individuals, particularly those w

145 Odds ratios (OR) for SCC associated with the frequency of rice consumption we

146 lub cells are the likely cells-of-origin for SCC transitioned tumours.

147 ticipants were followed up prospectively for SCC development.

148 Specific subtype rates for SCC, MM, and MCC were 812, 75, and 2 per 100000 person-y

149 the 1983-1987 period, the unadjusted SIR for SCC was 102.7 (95%, 85.8-122.1), declining to 21.6 (95%

150 aft organ, and sex, a decline in the SIR for SCC was found, with SIR peaking in patients who underwen

151 CI, 95%-100%) (P = .15) after training; for SCC, they were 73% (95% CI, 65%-81%) and 89% (95% CI, 72

152 Furthermore, SCC EVs activated Erk1/2 and Akt signaling and enhanced

153 sents a connectomic approach to guide future SCC DBS studies.

154 he strongest immunologic predictor of future SCC and correlated with increasing CD8(+) T cell differe

155 cell carcinoma (SCC) of the anus and one had SCC of the head and neck.

156 (range, 1.2 to 6.7 months), six of whom had SCC.

157 deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor

158 several distinct CSC populations coexist in SCC and that tumor initiation and metastatic potential o

159 is review compares the properties of CSCs in SCC with normal stem cells in the skin, summarizes curre

160 ich was due mainly to reduced disparities in SCC.

161 identify p53-independent CCAR2 functions in SCC and to examine its role in tumorigenesis.

162 lated with poor prognosis in LUAD but not in SCC.

163 umor promoting oncogenic aspect of Notch1 in SCC.

164 and VB were less heterogeneous in AC than in SCC (Friedman analysis of variance).

165 factor receptor (FGFR) inhibitor therapy in SCC, which contrasts to the relatively high rates of res

166 However, the precise role of ZNF750 in SCC cell biology remains unclear.

167 5, acts as an epithelial stem cell marker in SCCs in vivo.

168 Cs and 0 BCCs per year, a 66.5% reduction in SCCs and a 100% reduction in BCCs.

169 Cs and 0 BCCs per year, a 62.5% reduction in SCCs and a 100% reduction in BCCs.

170 ne dysfunction might contribute to increased SCC risk.

171 o squamous cell carcinoma (SCC) and invasive SCC if left untreated.

172 95% CI, 1.51-18.80; P = .01), and laryngeal SCCs (OR, 2.71; 95% CI, 1.00-7.43; P = .05), whereas gam

173 -30.75; P = .01, respectively) and laryngeal SCCs (OR, 7.49; 95% CI, 1.10-51.04; P = .04 and OR, 5.31

174 ity (OR, 4.5; 95% CI, 0.6-34.7) or laryngeal SCCs (OR, 0.11; 95% CI, 0.01-834.80).

175 In later SCCs, 4HT cessation became irrelevant as endogenous ROCK

176 GLI1 mRNA was highly expressed in human lung SCC and portended a poor prognosis.

177 K27me3 mark, is also prevalent in human lung SCC and SCC regions within ADSCC tumours.

178 Inhibition of GLI1 in human lung SCC cell lines suppressed tumor cell clonogenicity and p

179 nists did not affect GLI1 expression in lung SCC cells.

180 , our work identifies three subtypes of lung SCC that differ in drug sensitivity and shows a novel me

181 ion factor GLI1 as a critical driver of lung SCC.

182 tumor-specific T cell responses against main SCC-derived antigens using the IFN-gamma enzyme-linked i

183 No association between RS-PCR types and milk SCC was found; however, NAGase activity was significantl

184 [40.2%]) and the trunk (1305 [33.9%]); most SCCs were on the head and/or neck (435 [33.4%]) and uppe

185 signaling changes observed in advanced mouse SCC.

186 this YAP1 phosphorylation in human and mouse SCC tumors with low/negative expression of alphaE-cateni

187 g FOXP3 + Treg cells were higher in KT-mTORi-SCC (P < 0.05).

188 nificantly lower in KT-CNI-SCC than KT-mTORi-SCC and NoKT-SCC and predicted SCC relapses (area under

189 erved, reaching similar levels than KT-mTORi-SCC and NoKT-SCC patients.

190 SCC on CNI (KT-CNI-SCC) or mTOR-i (KT-mTORi-SCC), 25 nontransplants developing SCC (NoKT-SCC) and 6

191 an effective, accessible model for multiple SCC types and that common treatment and prevention strat

192 was highly up-regulated in the head and neck SCCs, and EVs isolated from sera of patients with SCC we

193 sment model (IAM) in order to estimate a new SCC.

194 s were are at higher risk for subsequent new SCC but not BCC, with a dose-response relationship betwe

195 Patient 1 had a mean of 12 new SCCs and 2.25 new BCCs per year before vaccination.

196 Patient 2 had a mean of 5.5 new SCCs and 0.92 new BCCs per year before vaccination.

197 The numbers of new SCCs and BCCs after the first dose of the quadrivalent H

198 wer in KT-CNI-SCC than KT-mTORi-SCC and NoKT-SCC and predicted SCC relapses (area under the curve = 0

199 ng similar levels than KT-mTORi-SCC and NoKT-SCC patients.

200 SCC), 25 nontransplants developing SCC (NoKT-SCC) and 6 healthy controls.

201 nd tumor-specific T cell responses than NoKT-SCC, and intratumoral and circulating FOXP3 + Treg cells

202 ue set of biomarkers for risk assessments of SCC and UC.

203 volumetric and gravimetric energy density of SCC-LIBs with constrained volume is predicted to be less

204 e more likely to make a correct diagnosis of SCC and hemangioma in color (P < .001 for both compariso

205 Furthermore, in vivo growth of SCC harboring amplifications of the PI3K gene PIK3CA was

206 that is inactivated in the vast majority of SCC tumors, leaving the role of CCAR2 in p53-null tumors

207 is sufficient to attenuate the migration of SCC cells, leading to decreased wound closure.

208 o promote carcinogenesis in murine models of SCC.

209 plex between FAK and Runx1 in the nucleus of SCC cells and showed that FAK interacted with a number o

210 sumption may be related to the occurrence of SCC in the United States, especially among those with re

211 a 1.5-fold (95% CI: 1.1, 2.0) higher odds of SCC compared with those who reported no rice consumption

212 thioprine risk estimates and the outcomes of SCC, BCC and KC.

213 iquely inhibited the malignant phenotypes of SCC cells both in vitro and in vivo.

214 ion, and previous disease were predictive of SCC development during follow-up.

215 he CD57hi phenotype is a strong predictor of SCC development and recurrence in this cohort of long-te

216 The rate of SCC decreased over time in all racial/ethnic groups, and

217 cause of detection bias) but higher rates of SCC.

218 ations of chromosomes 12, 13, 17 and risk of SCC (OR = 7.06, 6.91 and 6.23, respectively).

219 The risk of SCC after organ transplantation has declined significant

220 stable transplant recipients at high risk of SCC and analyzed phenotypically by flow cytometry.

221 Still, the risk of SCC in organ transplant recipients remains much higher t

222 ent NMSC overall and a 222% increase risk of SCC in particular, suggesting that subsequent SCC risk i

223 ate showed a significantly increased risk of SCC in relation to azathioprine exposure (1.56, 95% conf

224 nazole was associated with increased risk of SCC of the skin in lung transplant recipients.

225 refully weighed versus the potential risk of SCC.

226 = 0.4-0.9) but significantly higher risks of SCC (hazard ratio = 2.3; 95% confidence interval = 1.5-3

227 shed risk estimates to evaluate the risks of SCC, basal cell carcinoma (BCC), keratinocyte cancers (K

228 er, Notch1 is activated in a small subset of SCC cells at the invasive tumor front and predicts for p

229 the challenges for CSC-targeted treatment of SCC.

230 charge recombination due to the addition of SCCs.

231 eterminants implicated in the development of SCCs by recent large-scale genomic, genetic, and epigene

232 A reduction of SCCs and BCCs was observed in 2 patients after administr

233 sily examined, in the majority of cases oral SCC is diagnosed in its late stages.

234 The low detection rate of early oral SCC is a considerable clinical issue.

235 ormed as part of the routine work-up in oral SCC.

236 man papilloma virus-associated oropharyngeal SCC, we hypothesized that adding cetuximab to CRT would

237 with positive association for oropharyngeal SCC (OR, 22.4; 95% CI, 1.8-276.7), but not for oral cavi

238 a (SCC), and the prevalence of oropharyngeal SCC is higher among men than women in the United States.

239 tion precedes the incidence of oropharyngeal SCC.

240 ences in risk for HPV-positive oropharyngeal SCC.

241 shared etiology for cutaneous SCC and other SCC in the setting of immunosuppression.

242 , have an increased risk of developing other SCC.

243 ds for the risk of skin cancer, particularly SCC, after organ transplantation.

244 320 patients were screened, and 85 patients (SCC n = 29, AC n = 56) were included in the study.

245 Decreased (less positive) SCC connectivity with the right parahippocampal gyrus an

246 Occurrence of first posttransplant SCC, melanoma, or Kaposi sarcoma of the skin.

247 splantation with a history of posttransplant SCC have a high risk of aggressive SCC.

248 than KT-mTORi-SCC and NoKT-SCC and predicted SCC relapses (area under the curve = 0.837; P < 0.05).

249 pathological characteristics of the previous SCC and discussed on an individual patient basis.

250 Subsequent new primary SCCs had a strong association with lower CD4 and higher

251 ymal transition (EMT) are coupled to promote SCC tumor initiation in concert with transforming growth

252 taining cell cycle progression and promoting SCC tumorigenesis.

253 For the central case, the real SCC grows at 3% per year over the period to 2050.

254 ut recover after mTOR-i conversion, reducing SCC relapses.

255 protein 3 (IGFBP3), and that this regulates SCC cell-cycle progression and tumor growth in vivo Furt

256 and reliable evaluation of reproducibility, SCC can also be used to quantify differences between Hi-

257 ded clear margins, residual BCC, or residual SCC.

258 improve treatment of chemotherapy-resistant SCCs.

259 raepithelial neoplasia (CIN) vs SCC revealed SCC with greater diffuse involvement (1% vs 8%, P < .000

260 Finally, high-grade and recurrent human skin SCC recapitulated the signaling changes observed in adva

261 or growth in a xenograft model of human skin SCC.

262 n the chemically induced mouse model of skin SCC.

263 the peritumoral stroma of HPV8-positive skin SCC.

264 ave not been previously associated with skin SCC CSC, were upregulated in late CSC and promoted tumor

265 For some SCCs, particularly those in immunocompromised patients,

266 could only be observed at the cancer stage (SCC), where HPV oncoproteins are highly expressed, suppo

267 ubcallosal cingulate deep brain stimulation (SCC DBS) for depression demonstrated the common impact o

268 Previously identified measures to stratify SCC risk have limited use, however.

269 CC in particular, suggesting that subsequent SCC risk is associated with immune dysfunction.

270 Using the summed SCC functional connectivity scores for these three regio

271 The evidence indicates that SCCs from various body sites, while clinically treated a

272 These findings indicate a key role for the SCC, a region previously implicated in altruistic decisi

273 The difference in the SCC between the two population scenarios under TU is com

274 pressive Complex 2 (PRC2) subunit EED in the SCC lesions.

275 pulation scenario entails an increase in the SCC of 85% under TU vs. 5% under AU.

276 both approaches, as population increases the SCC increases, but optimal peak temperature decreases.

277 The porosity of the SCC anode is adjusted to accommodate the volume expansio

278 The study estimates that the SCC is $31 per ton of CO2 in 2010 US$ for the current pe

279 vity of the following three regions with the SCC was differentially associated with outcomes of remis

280 ineurin inhibitors (CNI) could contribute to SCC development, whereas conversion to mammalian target

281 germline knockout of Lgr6 are predisposed to SCC development, through a mechanism that includes compe

282 ivities/p-Mypt1 inactivation, progression to SCC required loss of compensatory p21 expression.

283 net costs of $8.5 ton(-1), leading the total SCC to more than double.

284 and neck squamous cell carcinoma (HNSCC) UM-SCC-1 cells both in in vitro three-dimensional culture a

285 f miR-375 expression on protein levels in UM-SCC-1 cells.

286 G2-M cell-cycle arrest and cell death in UM-SCC-46 cells.

287 o invasion assays with an OSCC cell line (UM-SCC-1).

288 sion in vitro and pulmonary metastases of UM-SCC-1 cells in vivo.

289 junctival intraepithelial neoplasia (CIN) vs SCC revealed SCC with greater diffuse involvement (1% vs

290 pecimens from 48 cervical SCCs and 23 vulvar SCCs.

291 m cases of cervical SCCs (n = 48) and vulvar SCCs (n = 23) were retrieved from the archives of Brigha

292 xpression in a subset of cervical and vulvar SCCs and identifies a class of patients that are rationa

293 ce interval 1.07-11.06) were associated with SCC compared with those unexposed after controlling for

294 ble volumetric energy densities of LIBs with SCC anode (SCC-LIBs) and the potential improvement over

295 alysis in 59 kidney transplant patients with SCC on CNI (KT-CNI-SCC) or mTOR-i (KT-mTORi-SCC), 25 non

296 and EVs isolated from sera of patients with SCC were enriched in Dsg2 C-terminal fragment and epider

297 vel CSC-targeted therapies for patients with SCC with poor prognoses.

298 in dose-expansion cohorts for patients with SCC.

299 es to classify three disease segments within SCC.

300 ish quiescent from proliferative TPCs within SCCs.