ライフサイエンスコーパス: SCC

1 SCC arises due to ultraviolet light exposure and is asso

2 SCC cells were transplanted into immune-compromised or i

3 SCC incidence was unrelated to treatment with vitamin D

4 SCC PRS at P-value threshold 1 x 10(-5) was the most sig

5 SCC received mitomycin in case of tumoral resection marg

6 SCCs are generally synthesized in solution, with isolate

7 ix international cohorts and totaling 19,149 SCC cases and 680,049 controls.

8 including 404 melanomas, 1367 BCCs, and 232 SCCs.

9 In Experiment 3, SCC analysis was conducted on images it was not trained

10 e expression of the UV-biomarker genes in 31 SCC and normal skin (NS) pairs and 10 AK/NS pairs was qu

11 ch surgery rates were similar between the 39 SCC and 15 miSCC.

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

13 and later were diagnosed with CIS (n = 59), SCC (n = 32), or remained healthy (n = 3).

14 Additionally, SCC utilized a new approach to count overlapping cells w

15 and promotes distant metastasis in advanced SCCs.

16 Here, we show that CSCs of mouse advanced SCCs (L-CSCs) express CXCR4 and CXCR7, both receptors of

17 n and metastasis in human and mouse advanced SCCs, and suggest that CXCR4 and/or PDGFR inhibitors cou

18 ated, along CXCR4 in tumor cells of advanced SCCs.

19 ransplant SCC have a high risk of aggressive SCC.

20 Twenty aggressive SCC developed over the study period.

21 The second control contained an SCC(M1) insertion.

22 cooperates with SOX2 and TRP63 to sustain an SCC-specific transcriptional feed-forward circuit that m

23 Anal SCC incidence in SOTR was elevated vs the general popula

24 ial and consistent evidence of elevated anal SCC incidence in SOTR.

25 d meta-analyses evaluating incidence of anal SCC (standardized incidence ratio [SIR] vs general popul

26 (HR: 0.60, 95% CI: 0.56-0.63, P < 0.001) and SCC (HR: 0.58, 95% CI: 0.53-0.63, P < 0.001).

27 with high PD-L1 expression (TPS >= 50%) and SCC, the Expert Panel recommends single-agent pembrolizu

28 letion of eIF4E in human SCC cells (A431 and SCC-13) reduced eIF4G and proteins that regulate the cel

29 r tools to classify and risk stratify AK and SCC lesions, which will complement histopathologic diagn

30 While genetic drivers of BCC and SCC development have been extensively characterized, BSC

31 Principal component analysis of BCC and SCC driver genes further demonstrate the genetic similar

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

33 Using these GWAS, BCC and SCC PRS were calculated for each sample across three Eur

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

35 self-renewal, aberrant differentiation, and SCC growth in mice and humans, providing clues for devel

36 decreased significantly in hyperplastic and SCC lesions.

37 t 2, performance analytics of OCFU, IMJM and SCC were compared.

38 ompared to those detected via OCFU, IMJM and SCC.

39 as not associated with risks of melanoma and SCC, vitamin D intake was associated with slightly incre

40 as performed in 93.3% and 20.5% of miSCC and SCC, respectively (P < .001).

41 y was performed in 0% and 92.0% of miSCC and SCC, respectively (P < .001).

42 s 14.8%, including 20% and 12% for miSCC and SCC, respectively (P = .079).

43 Gill pore papillae were absent and SCCs were sparse during the larval stage and in newly tr

44 ere differentially expressed between AKs and SCCs, while 10 genes were uniquely expressed in the more

45 ween benign and transformation-prone AKs and SCCs.

46 ations and potential regulators for BCCs and SCCs that likely impact the divergent oncogenic pathways

47 enewing and differentiating into supra-basal SCC cells, which lack proliferative potential.

48 the Pt(II)-based building block in Pt-based SCCs.

49 RID1A mutations occur after PTCH1 but before SCC driver mutations, indicating that ARID1A mutations m

50 ence of the synergetic hybridization between SCCs and MOFs.

51 lae during the parasitic juvenile stage, but SCCs were abundant on prominent papillae in migrating an

52 (CIS) and invasive squamous cervical cancer (SCC).

53 n a cohort of 108 squamous cell lung cancer (SCC) patients.

54 s less than 5% to the social cost of carbon (SCC) under alternative discount rates and estimates of t

55 is overexpressed in squamous cell carcinoma (SCC) and associated with poor prognosis and survival.

56 osen from published squamous cell carcinoma (SCC) and basal cell carcinoma (BCC) nontransplant GWAS.

57 carcinoma (BCC) and squamous cell carcinoma (SCC) are both derived from epidermal keratinocytes but a

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

59 arcinoma (IEC), and Squamous Cell Carcinoma (SCC) are generally considered to be advancing stages of

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

61 Murine squamous cell carcinoma (SCC) can be initiated by hair follicle stem cells (HFSCs

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

63 ells (TPCs) control squamous cell carcinoma (SCC) growth by self-renewing and differentiating into su

64 Epidermal squamous cell carcinoma (SCC) is a common and highly invasive form of cancer.

65 Squamous cell carcinoma (SCC) is a global public health burden originating in epi

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

67 Cutaneous squamous cell carcinoma (SCC) is one of the most common cancers in the United Sta

68 splasia to invasive squamous cell carcinoma (SCC) of the conjunctiva.

69 AKs) and aggressive squamous cell carcinoma (SCC) subtypes.

70 in cancer model for squamous cell carcinoma (SCC) that can be effectively challenged by adoptive cyto

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

72 the burden of anal squamous cell carcinoma (SCC), and its surrogates, in SOTR.

73 lower proportion of squamous cell carcinoma (SCC), and more positive lymph nodes.

74 inoma (ADC) but not squamous cell carcinoma (SCC), even though the stroma is fibrotic in both histoty

75 cancers, including squamous cell carcinoma (SCC), involves surgical resection with negative cancer m

76 also occur in skin Squamous Cell Carcinoma (SCC)-associated CAFs, in which CSL is decreased.

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

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

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

80 invasive cutaneous squamous cell carcinoma (SCC).

81 ncogenic driver in squamous cell carcinomas (SCC).

82 Squamous cell carcinomas (SCCs) account for the majority of cancer mortalities.

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

84 Skin squamous cell carcinomas (SCCs) are a major cause of death in patients who have un

85 Squamous cell carcinomas (SCCs) arising from aerodigestive or anogenital epitheliu

86 hat CAFs from skin squamous cell carcinomas (SCCs) display chromosomal alterations, with heterogeneou

87 ifferentiated skin squamous cell carcinomas (SCCs) exhibit aggressive growth and enhanced metastasis

88 man papillomas and squamous cell carcinomas (SCCs) revealed that TC-PTP expression was significantly

89 ologic subtypes of squamous cell carcinomas (SCCs) were identified-SCCs with exophytic and invasive c

90 cancers, 113 were squamous cell carcinomas (SCCs), and 34 were adenocarcinoma/adenosquamous carcinom

91 cancers, primarily squamous cell carcinomas (SCCs), progress either slowly or aggressively.

92 cinomas (BCCs) and squamous cell carcinomas (SCCs), respectively.

93 inomas (BCCs), and squamous cell carcinomas (SCCs).

94 umor suppressor in squamous cell carcinomas (SCCs).

95 ntained empty SCCmec cassettes, 1.6% carried SCC(M1), <1% had spa deletions, and <1% contained SCCmec

96 matched larynx SCC compared with oral cavity SCC and oropharynx SCC.

97 , gustatory, and solitary chemosensory cell (SCC) systems detect chemical stimuli in vertebrates.

98 Solitary chemosensory cells (SCCs) and their innervating fibers are located in the re

99 Solitary chemosensory cells (SCCs) are epithelial sentinels that utilize bitter Tas2r

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

101 in stimulation of the subcallosal cingulate (SCC DBS) has been studied as a potential treatment for s

102 crete supramolecular coordination complexes (SCCs) has attracted considerable attention within the fi

103 Supramolecular coordination compounds (SCCs) represent the power of coordination chemistry meth

104 stologically concerning from less concerning SCCs (AUC 1, precision score 1, recall 0.714).

105 re uniquely expressed in the more concerning SCCs.

106 nd MIC on time to sputum culture conversion (SCC) and treatment outcome in patients with MDR-TB.

107 Spike count correlations (SCCs) are ubiquitous in sensory cortices, are characteri

108 mples were collected for somatic cell count (SCC) and colony forming units (CFU).

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

110 er hospitalization for a sickle cell crisis (SCC) is extremely high.

111 nd therapeutic target discovery in cutaneous SCC.

112 Here, we report the largest cutaneous SCC meta-analysis to date, representing six internationa

113 lymorphisms (SNPs) associated with cutaneous SCC.

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

115 iderably among tumors derived from different SCC lines.

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

117 t is still challenging to construct discrete SCCs with high fluorescence quantum yields and tunable f

118 to tune the emission wavelengths of discrete SCCs in the same solvent.

119 uning of the emission wavelength of discrete SCCs.

120 he present study, we show that ACTL6A drives SCC cell proliferation, spheroid formation, invasion and

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

122 Cytochrome P450 side-chain cleavage enzyme (SCC or CYP11A1) catalyzes cholesterol to pregnenolone co

123 chanism to maintain the aggressive epidermal SCC phenotype.

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

125 nconi anemia (FA) are a paradigm for extreme SCC susceptibility caused by germline loss-of-function m

126 Few SCCs were located on small nub-like papillae during the

127 male genital, 1.77 for cervical and 2.29 for SCC skin CISs.

128 ons with tumor cells but are dispensable for SCC metastasis.

129 teristics and time after hospitalization for SCC.

130 30-day readmission after hospitalization for SCC.

131 Among patients hospitalized for SCC, 30-day readmissions were frequent throughout the mo

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

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

134 We found SCC to be highly accurate and efficient in quantifying c

135 and other vertebrates and suggest that gill SCC function may be important during the feeding juvenil

136 ing molecules or genetic absence of gingival SCCs (gSCCs) increases the bacterial load, reduces bacte

137 Although several strains harboured SCC-borne fusidic acid resistance (fusC) (n = 181), eryt

138 and determines cell fate in mouse and human SCC.

139 directly regulates NRG1 expression in human SCC cell lines and that NRG1 is a critical component of

140 ing RNA-mediated depletion of eIF4E in human SCC cells (A431 and SCC-13) reduced eIF4G and proteins t

141 amous cell carcinomas (SCCs) were identified-SCCs with exophytic and invasive components associated w

142 Here, we present the self-assembly of Pd(II) SCCs within the confined space of a pre-formed MOF (SCCs

143 ch signaling is altered but not abolished in SCC cells.

144 sought to determine whether Ldh activity in SCC is critical for tumorigenesis or simply a marker of

145 ulation, and keratinocyte differentiation in SCC susceptibility.

146 AD and JDP2 in BCC pathogenesis and FOXP1 in SCC pathogenesis.

147 er in BCC, intragenic regulation of FOXP1 in SCC, and WNT5A promoter in both subtypes) and validated

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

149 Despite its importance in SCC, the upstream regulation of DeltaNp63alpha is poorly

150 32 inhibited the phosphorylation of c-Jun in SCC cell line in a dose-dependent manner.

151 inhibitor attenuated FLIP protein levels in SCC cells.

152 Here we assessed the role of macrophages in SCC behavior.

153 AFs in the clinical failure of nintedanib in SCC and supports that patients with ADC may benefit from

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

155 Postoperative proton therapy, performed in SCC only, was associated with a lower risk for relapse.

156 tify those that are commonly de-regulated in SCC representing candidates for prognosis and therapeuti

157 selective epigenetic repression of SMAD3 in SCC-TAFs in the clinical failure of nintedanib in SCC an

158 the contributions and limitations of TAMs in SCC progression.

159 n MAPK pathway and its downstream targets in SCC-R cells.

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

161 e identity of natural stimuli and changes in SCCs are independent of changes in response mean.

162 promoting immune environment was detected in SCCs and the perilesional skin of cancer-prone DLE patie

163 ntify a lineage-specific function of NRG1 in SCCs of diverse anatomic origin.

164 an established lineage-survival oncogene in SCCs, therapeutic strategies have not been developed to

165 une response and cell activation pathways in SCCs.

166 structured internal dynamics and patterns in SCCs.

167 s higher in moderate dysplasias and invasive SCCs than in hyperplasias and mild dysplasias, although

168 with papillary lesions (pSCCs) and invasive SCCs without exophytic histology (iSCCs).

169 7 proliferation index in size matched larynx SCC compared with oral cavity SCC and oropharynx SCC.

170 ge in HNSCC from non-smokers and that larynx SCC from non-smokers have a greater number of signature

171 se observations support a model where larynx SCC are characterized by slower growth and increased sus

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

173 r work provides a powerful resource for lung SCC biology and suggests therapeutic opportunities based

174 histology-proven invasive conjunctival miSCC/SCC treated between 2002 and 2017.

175 thin the confined space of a pre-formed MOF (SCCs@MOF) and its post-assembly metalation to give a Pd(

176 We used mouse SCC cells derived from tumors harboring a Kras(G12D) act

177 to detect and localize primary head and neck SCC on WSI with an AUC of 0.916 for patients in the SCC

178 ith poorer overall survival in head and neck SCC patients.

179 red with radiation therapy than HPV-negative SCCs.

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

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

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

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

184 >= 50%) and non-squamous cell carcinoma (non-SCC), the Expert Panel recommends single-agent pembroliz

185 For most patients with non-SCC and either negative (0%) or low positive (1% to 49%)

186 95% CI: 0.66, 0.90; Ptrend = 0.0006) but not SCC (HR: 1.08; 95% CI: 0.75, 1.55; Ptrend = 0.68), altho

187 n new avenues in both the synthesis of novel SCCs and their use in heterogeneous metal-based supramol

188 V1 activity cannot account for the observed SCC patterns and conclude that the stimulus dependence o

189 stently, forcing global DNA demethylation of SCC-TAFs with 5-AZA rescued TGFbeta1/SMAD3 activation, w

190 that smoking and/or the anatomic location of SCC in the proximal airways, which are more exposed to c

191 o promote carcinogenesis in murine models of SCC.

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

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

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

195 c insights on the selective poor response of SCC-TAFs to nintedanib.

196 reduced fibrosis and nintedanib response of SCC-TAFs was associated with increased promoter methylat

197 The risk of SCC after organ transplantation has declined significant

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

199 nation with vitamin D may reduce the risk of SCC, but not BCC.

200 refully weighed versus the potential risk of SCC.

201 = 0.4-0.9) but significantly higher risks of SCC (hazard ratio = 2.3; 95% confidence interval = 1.5-3

202 participants enrolled in a clinical trial of SCC DBS for treatment-resistant depression.

203 iffuse staining was seen in 95% (108/113) of SCCs, and 81% (29/34) of adenocarcinoma/adenosquamous ca

204 and conclude that the stimulus dependence of SCCs is a natural consequence of structured internal dyn

205 rsely correlated with the increased grade of SCCs.

206 we demonstrate that stimulus specificity of SCCs in V1 can be directly manipulated by altering the a

207 pecific modulations in the fine structure of SCCs as stimulus identity and, more importantly, stimulu

208 tic stimuli to measure the fine structure of SCCs in V1 of awake behaving macaques and assessed their

209 We show that the fine structure of SCCs is specific to the identity of natural stimuli and

210 nd clinically actionable molecular subset of SCCs that are uniquely amenable to HER2 blocking therapi

211 Reports of incident BCC or SCC were confirmed from pathology records.

212 r these tumors originally derive from BCC or SCC.

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

214 atin 15-positive stem cells and a human oral SCC cell line, FaDu, which has NRAS amplification and SM

215 We used a combination of an oropharyngeal SCC tissue microarray, HNSCC cell lines, and patient-der

216 compared with oral cavity SCC and oropharynx SCC.

217 the chorion (microinvasive; miSCC) or over (SCC).

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

219 Lampreys also possess SCCs that are particularly numerous on cutaneous papilla

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

221 osed to cigarette smoke particles, may prime SCC-TAFs to stronger SMAD3 epigenetic repression, becaus

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

223 ied as having bipolar II disorder) receiving SCC DBS for 4-8 years.

224 nd splenic macrophages, resulting in reduced SCC volumes.

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

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

227 erations associated with erlotinib resistant SCC-R cells.

228 utant MAP2K1 (p.K57E) in erlotinib resistant SCC-R cells.

229 improve treatment of chemotherapy-resistant SCCs.

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

231 ways blocks distant metastasis of human PD/S-SCCs.

232 Quarters of MSC group of cows had similar SCC log/mL in milk compared to infected quarters of ATB

233 Therefore, we created SimpylCellCounter (SCC), an automated method to quantify cells that express

234 In an orthotopic model of skin SCC, genetic or pharmacological inhibition of NOTCH1 act

235 herapeutic target for abrogating lethal skin SCCs in patients who have undergone or will undergo orga

236 , eIF4G, and eIF4A1 in human and murine skin SCCs.

237 of these findings in patient samples of skin SCCs shows a strong correlation between the expression o

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

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

240 fibrosis is actually higher in ADC-TAFs than SCC-TAFs in vitro and patient samples.

241 The current study demonstrates that SCC is a novel, automated tool to quantify cells in brai

242 We find that SCC is directly imported into the mitochondrial matrix,

243 gill pores, and on the dorsal fins and that SCCs are particularly numerous on these papillae.

244 Here we report that SCCs are present in mouse gingival junctional epithelium

245 lides with an AUC of 0.944 and 0.995 for the SCC and thyroid carcinoma testing groups, respectively.

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

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

248 WSI with an AUC of 0.916 for patients in the SCC testing group and 0.954 for patients in the thyroid

249 Following integration of the SCC C terminus into the TIM23 complex, amino acids 141 t

250 own cells is required for suppression of the SCC cell phenotype, suggesting that p21(Cip1) is a media

251 nsights on the function and evolution of the SCC system in vertebrates.

252 ignificant attention has been devoted to the SCC system.

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

254 The SCCs are microvillous cells that were first discovered o

255 The SCCs were distinguished from the surrounding epithelial

256 d into the gill pore papillae, as far as the SCCs and serotonergic fibers extended from the underlyin

257 These findings show similarities between the SCCs in lampreys and other vertebrates and suggest that

258 These SCCs@MOFs catalyze the coupling of boronic acids and/or

259 tudy revealed that macrophages contribute to SCC expansion through interactions with tumor cells but

260 rovide evidence that TIP60 may contribute to SCC progression by increasing DeltaNp63alpha protein lev

261 stand how genetic risk factors contribute to SCC, studies of ESPC biology are imperative.

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

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

264 tration density change during progression to SCC.

265 ological changes occur during progression to SCC.

266 periods readmitted with diagnoses related to SCC.

267 ust and sustained antidepressant response to SCC DBS.

268 was associated with a 29-day longer time to SCC (hazard ratio [HR] 0.57, 95% confidence interval [CI

269 istance was associated with a longer time to SCC.

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

271 tal-catalyzed reactions in which traditional SCCs tend to decompose, and retain their structural inte

272 in response to immune-activating treatments, SCC typically do not regress.

273 UM-SCC-11A and UM-SCC-12 both produce 17beta-estradiol, but

274 UM-SCC-11A and UM-SCC-12 both produce 17beta-estradiol, but only UM-SCC-12

275 duction by LSCC cell lines UM-SCC-11A and UM-SCC-12 was examined.

276 rcinoma (HNSCC) cell lines (UM-SCC-47 and UM-SCC-22B, respectively) to grow tumor xenografts in athym

277 HNSCC UM-SCC-1 and UM-SCC-47 cells were cultured in 2D monoculture and compare

278 Conversely, UM-SCC-47 exhibited a more constant drug response across cu

279 HNSCC UM-SCC-1 and UM-SCC-47 cells were cultured in 2D monocultur

280 uamous cell carcinoma (HNSCC) cell lines (UM-SCC-47 and UM-SCC-22B, respectively) to grow tumor xenog

281 a-estradiol production by LSCC cell lines UM-SCC-11A and UM-SCC-12 was examined.

282 17beta-estradiol, but only UM-SCC-12, not UM-SCC-11A, xenograft tumors grow larger in vivo in respons

283 2 both produce 17beta-estradiol, but only UM-SCC-12, not UM-SCC-11A, xenograft tumors grow larger in

284 The results showed UM-SCC-1 drug response significantly changed in the differe

285 A reductase-focused shRNA screen in UT-SCC-74B cells similarly identified mitochondrial respira

286 In UT-SCC-74B cells, evofosfamide oxidized cytochromes a, b, a

287 tochondrial DNA and biochemical assays in UT-SCC-74B cells.

288 The best model to classify AKs versus SCCs (area under curve (AUC) 0.814, precision score 0.83

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

290 skin and provide 3D epidermal models wherein SCC prevention can now be explored.

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

292 We discover eight novel loci associated with SCC, confirm all previously associated loci, and perform

293 sceptible strains showed no association with SCC in crude or adjusted analyses (HR 0.98, 95% CI 0.73-

294 d slightly worse relapse rates compared with SCC.

295 and 68 (3%) participants were diagnosed with SCC.

296 For most patients with SCC and either negative (0%) or low positive PD-L1 (TPS

297 In 2016, readmission among patients with SCC incurred an additional 95,445 hospitalization days r

298 from 11 patients (five with BCC and six with SCC) undergoing Mohs surgery.

299 tained SCCmec variants other than those with SCC(M1) These data suggest that genetic variations that

300 that suppress the association of Tim50 with SCC ablate metabolic activity.