ライフサイエンスコーパス: BCC

1 BCC is primarily driven by the Sonic Hedgehog (Hh) pathw

2 er vaccination, he developed 4.44 SCCs and 0 BCCs per year, a 62.5% reduction in SCCs and a 100% redu

3 r vaccination, she developed 1.84 SCCs and 0 BCCs per year, a 66.5% reduction in SCCs and a 100% redu

4 duals who received a diagnosis of at least 1 BCC in 2011 or 2012 revealed distinct geographic areas w

5 Among 138 BCCs from 62 patients (43 males and 19 females; mean [SD

6 2 years, participants reported a mean of 25 BCCs (median, 11; range, 0-250).

7 ifetime, participants reported a mean of 257 BCCs (median, 160; range, 0-2200).

8 Our genetic profiling of 293 BCCs found the highest mutation rate in cancer (65 mutat

9 g of 2,636 Icelanders and imputed into 4,572 BCC patients and 266,358 controls.

10 Of the 116, 88 had a BCC first, of whom 74% subsequently developed only BCCs,

11 Finally, in a BCC mouse model, keratinocyte-specific D3 depletion mark

12 articipants: This retrospective study used a BCC registry to determine rates of BCC by census block g

13 UVR does produce D3, UVR fails to accelerate BCC carcinogenesis, thus mirroring the plateauing in hum

14 adiation-treated Ptch1(+/-) mice accelerates BCC carcinogenesis in male mice, in which UVR does not p

15 ntegrated into existing therapy for advanced BCC as it becomes increasingly used.

16 f currently available therapies for advanced BCC warrants further prospective study.

17 ugs are approved for use in locally advanced BCC (laBCC), with vismodegib also approved for metastati

18 patients with recurrent or locally advanced BCC and that combined use of currently available therapi

19 Among the patients with locally advanced BCC, 5 had T3bN0M0 disease at presentation; 1 each had T

20 Ten patients had locally advanced BCC; 2 had basal cell nevus syndrome.

21 We report 2 cases of recurrent, advanced BCC treated from April 1, 2012, through October 31, 2014

22 odegib, are effective therapies for advanced BCCs.

23 Nutrient level affected BCC more in hypolimnia than in epilimnia, likely due to

24 PD-1 immunotherapy may have activity against BCCs, including in those that have been previously treat

25 t at tendril surfaces, but tendrils were all BCC tungsten metal.

26 49; 95% CI: 1.11, 11.0; P-trend = 0.01), and BCC (HR(T3vs.T1): 7.44; 95% CI: 1.57, 35.3; P-trend = 0.

27 85; 95% CI: 1.06, 3.23; P-trend = 0.03), and BCC (HR(T3vs.T1): 1.78; 0.98, 3.24; P-trend = 0.05).

28 nce of NMSC in the US population in 2012 and BCC and SCC in the 2012 Medicare fee-for-service populat

29 tifiable differences between the healthy and BCC skin samples.

30 ciation between 21 distinct genetic loci and BCC risk.

31 and 0.02 for overall skin cancer, NMSC, and BCC, respectively.

32 eased risk of overall skin cancer, NMSC, and BCC.

33 h risk of melanoma than with risk of SCC and BCC in men (multivariable-adjusted hazard ratios were 2.

34 with melanoma risk, but not risk of SCC and BCC, when compared with sunburns at other body sites (fa

35 tivariable model adjusting for age, sex, and BCC location, PD-L1 staining intensity in tumor cells in

36 ociations between azathioprine treatment and BCC (0.96, 95% CI 0.66-1.40) or KC (0.84, 95% CI 0.59-1.

37 uctive factors or exogenous estrogen use and BCC.

38 lex relationship between exposure to UVR and BCC incidence.

39 The numbers of new SCCs and BCCs after the first dose of the quadrivalent HPV vaccin

40 A reduction of SCCs and BCCs was observed in 2 patients after administration of

41 We estimated annual BCC incidence rates by age, sex, and race/ethnicity and

42 /MAPK activation emerged from the antecedent BCC tumors.

43 ounterintuitive conclusion that UVR has anti-BCC carcinogenic effects that can explain, at least in p

44 Their mean (SD) age at BCC diagnosis was 56 (16) years, and 68.9% (n = 124) wer

45 BCNS-BCCs appear to have reduced mutator phenotype compared w

46 However, compared with sporadic BCCs, BCNS-BCCs have a significantly lower mutational load, lower p

47 Interestingly, BCNS-BCCs are more responsive to SMO inhibitors than sporadic

48 O mutations at baseline, explaining why BCNS-BCCs lack intrinsic resistance to SMO inhibitors.

49 ted States are difficult to quantify because BCCs are not reportable tumors.

50 tallographically related to the parent beta (BCC) matrix.

51 The greatest differences in RTDs between BCC and SCC were on the hand (BCC:SCC ratio, 1:14) and t

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

53 Basal cell cancers (BCCs) are characterized by upregulation of Hedgehog path

54 samples diagnosed for basal cell carcinoma (BCC) and compared with healthy skin samples.

55 Patients with basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (SCC) (often

56 ciation with cutaneous basal-cell carcinoma (BCC) and linked to a germline SNP rs700635.

57 of local recurrence of basal cell carcinoma (BCC) and ocular complications following ESB to the lower

58 ogy on differentiating basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) from healthy tiss

59 ter training to detect basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) in Mohs micrograp

60 le people develop both basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) or one type exclu

61 ncers (KCs), including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), are the most com

62 ncers (KCs), including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), are the most com

63 cer (NMSC), defined as basal cell carcinoma (BCC) and squamous cell carcinoma (SCC).

64 ulation-based study of basal cell carcinoma (BCC) and squamous cell carcinomas (SCC).

65 Basal cell carcinoma (BCC) are common in this age group and treatment is often

66 inical significance in basal cell carcinoma (BCC) are unknown to date.

67 effect of UVR on human basal cell carcinoma (BCC) epidemiology is complex-the incidence rises until a

68 Basal cell carcinoma (BCC) incidence is increasing, particularly in young peop

69 Basal cell carcinoma (BCC) is characterized by frequent loss of PTCH1, leading

70 Basal cell carcinoma (BCC) is the most common cancer worldwide with an annual

71 Basal cell carcinoma (BCC) is the most common type of skin cancer and is usual

72 Basal cell carcinoma (BCC) of the skin is the most common malignant neoplasm i

73 oking and incidence of basal cell carcinoma (BCC) or squamous cell carcinoma (SCC) in QSkin, a prospe

74 microRNA-21 (miR21) in basal cell carcinoma (BCC) skin tumors.

75 l carcinoma (SCC), and basal cell carcinoma (BCC)) in prospective studies simultaneously, and little

76 approved for advanced basal cell carcinoma (BCC), and shows promise in clinical trials for SONIC HED

77 d therapy for advanced basal cell carcinoma (BCC), and their long-term effects, such as increased ris

78 nt or locally advanced basal cell carcinoma (BCC), and will inevitably be integrated into existing th

79 ntly elevated in human basal cell carcinoma (BCC), coinciding with increased primary cilia formation

80 ll carcinoma (SCC) and basal cell carcinoma (BCC), in part as a result of immunosuppressive medicatio

81 uate the risks of SCC, basal cell carcinoma (BCC), keratinocyte cancers (KCs) overall and other skin

82 to first appearance of basal cell carcinoma (BCC), squamous cell carcinoma (SCC), or malignant melano

83 skin cancer, including basal cell carcinoma (BCC), the most common cancer, have been increasing over

84 Basal cell carcinoma (BCC), the most common human cancer, results from aberran

85 rimary risk factor for basal cell carcinoma (BCC), the most common human malignancy.

86 nfer risk of cutaneous basal cell carcinoma (BCC), we conduct a genome-wide association study (GWAS)

87 in medulloblastoma and basal cell carcinoma (BCC), where inhibitors targeting the Shh pathway compone

88 tor-treated metastatic basal cell carcinoma (BCC).

89 with risk of cutaneous basal cell carcinoma (BCC).

90 a superficial type of basal cell carcinoma (BCC).

91 ated in a majority of basal cell carcinomas (BCC).

92 Basal cell carcinomas (BCCs) are diagnosed by clinical evaluation, which can in

93 Advanced basal cell carcinomas (BCCs) frequently acquire resistance to Smoothened (SMO)

94 The incidence of basal cell carcinomas (BCCs) is increasing globally, but incidence rates in the

95 Human basal cell carcinomas (BCCs) very frequently carry p53 mutations, and p53 loss

96 carcinomas (SCCs) and basal cell carcinomas (BCCs), are the most common human malignant neoplasms.

97 f developing numerous basal cell carcinomas (BCCs).

98 f developing numerous basal cell carcinomas (BCCs).

99 ed the impact of MSCs on breast cancer cell (BCC) dormancy.

100 ction of substance P in breast cancer cells (BCCs) is caused by the enhancement of tachykinin (TAC)1

101 f-renewal properties of breast cancer cells (BCCs).

102 therapy response, we sought to characterize BCCs in the setting of BCNS.

103 ce-weighted bacterial community composition (BCC) differed and that inter-lake BCC varied more for PA

104 icated that bacterial community composition (BCC) varied between reservoir and catchment, within catc

105 In contrast, BCC (n = 3,669) was not associated with overall risk of

106 entropically stabilized body-centered cubic (BCC) crystals due to the thermal excitations of the crys

107 the previously reported body-centered cubic (BCC) or face-centered-cubic (FCC) types, the major struc

108 eres self-organize in a body-centered cubic (BCC) periodic array, rarely encountered for self-assembl

109 tly reported disordered body-centered cubic (BCC) phase.

110 grees C, an equilibrium body-centered cubic (BCC) structure forms, whereas below TOOT the Frank-Kaspe

111 The recently discovered body-centered cubic (BCC) Ta-Nb-Hf-Zr-Ti high-entropy alloy superconductor ap

112 rial simple cubic (SC), body centered cubic (BCC), and face centered cubic (FCC) crystal structures a

113 it remains unexplored in body-centred cubic (BCC) nanoscale crystals.

114 llicle stem cell populations readily develop BCC-like tumors.

115 ple keratinocyte cancers: 65 (56%) developed BCC exclusively (range 2-8 per person); 18 (16%) develop

116 ,000 were calculated for those who developed BCC exclusively, SCC exclusively, or BCC and SCC.

117 s self-reported at baseline; newly diagnosed BCCs and SCCs were ascertained through data linkage and

118 It is worthy to note that the disordered BCC phase at 27.8 GPa is not observed here.

119 tu in an oncogenic mutant Smo (SmoM2)-driven BCC mouse model prevented the formation of BCC through s

120 supporting a role of UV exposure in driving BCC development in BCNS individuals.

121 dy suggest that INTU is indispensable during BCC tumorigenesis and that its aberrant upregulation is

122 that Intu performs a permissive role during BCC formation.

123 aled distinct geographic areas with elevated BCC rates.

124 munohistochemical staining on formalin-fixed BCCs from a dermatology clinic were examined in masked f

125 ) for SCC, and 1.18 (95% CI: 1.06, 1.32) for BCC) but not in women.

126 Measures of diagnostic accuracy for BCC were estimated.

127 pattern of RTDs did not differ with age for BCC.

128 for melanomas from 5 days to 2 days, and for BCC from 2 days to 1 day.

129 body irradiation was a major determinant for BCC.

130 However, for BCC, the low RTD on the hand and high RTDs on less sun-e

131 en HLA-C and the activating gene KIR2DS3 for BCC (Pinteraction = 0.005).

132 ulation, the age-adjusted procedure rate for BCC and SCC were 3280 and 3278 per 100,000 beneficiaries

133 also demonstrates equal incidence rates for BCC and SCC in the Medicare population.

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

135 The high RTDs on sun-exposed body sites for BCC and SCC are in keeping with sun exposure as the prim

136 The high RTDs on sun-exposed body sites for BCC and SCC are in keeping with sun exposure as the prim

137 % CI, 90%-96%) (P = .18) after training; for BCC, they were 83% (95% CI, 59%-100%) and 92% (95% CI, 8

138 lifetime (disease burden), risk factors for BCCs.

139 lifetime (disease burden), risk factors for BCCs.

140 ates and identify potential risk factors for BCCs.

141 ates and identify potential risk factors for BCCs.

142 n RTDs between BCC and SCC were on the hand (BCC:SCC ratio, 1:14) and the back and/or buttocks (BCC:S

143 en the KIR B haplotype and p53 alteration in BCC tumors, with a higher likelihood that KIR B carriers

144 Although the requirement for Hedgehog in BCC is well established, the identity of disease-initiat

145 our study identifies a disease mechanism in BCC involving mutations in regulatory noncoding elements

146 w insights into the deformation mechanism in BCC nanostructures.

147 dence of the involvement of TH metabolism in BCC tumorigenesis.

148 ovides selective pressure for altered p53 in BCC tumors.

149 structures (SWSs) are frequently present in BCC.

150 LATS1 suggested their potential relevance in BCC tumorigenesis.

151 Strikingly, in BCC patients treated with Smo inhibitor, squamous cell c

152 5% reduction in SCCs and a 100% reduction in BCCs.

153 5% reduction in SCCs and a 100% reduction in BCCs.

154 A total of 28,951 incident BCC cases were documented over 3.74 million person-years

155 Novel findings of increased BCC risk associated with MHT in women experiencing natur

156 alcohol intake was associated with increased BCC risk in both women and men (both P-trend < 0.0001).

157 n UVR accelerates ionizing radiation-induced BCC carcinogenesis.

158 on of D3 inhibits ionizing radiation-induced BCC tumorigenesis.

159 ALB/c mice were injected with Msi1-knockdown BCCs.

160 mposition (BCC) differed and that inter-lake BCC varied more for PA than for FL fractions.

161 In low-nutrient lakes, BCC differences between PA and FL fractions were larger

162 .046) as potential risk factors for lifetime BCC severity.

163 tly associated with the severity of lifetime BCC.

164 of beta-carotene but longer treatments made BCC prooxidant, showing that samples that underwent dras

165 with vismodegib also approved for metastatic BCC (mBCC).

166 tment is a feasible treatment for metastatic BCC.

167 Five men with metastatic BCC who experienced relapse after SMO inhibitor treatmen

168 ted expression of GALNT14 in lung-metastatic BCCs.

169 t aberrant hedgehog signaling in microscopic BCCs activates p53 in part via Arf (that is, the oncogen

170 In our adjusted models, BCC burden increased by 4% per year of age and by 6% per

171 Most BCC patients experience significant clinical benefit on

172 Most BCCs were on the head and/or neck (1547 [40.2%]) and the

173 Although most BCCs are sporadic, rare individuals with basal cell nevu

174 associated with significant risk of multiple BCC tumors (OR, 2.39; 95% confidence interval, 1.10-5.21

175 At 100 muM, BCC lost its antioxidant properties and became pro-oxida

176 ns, and p53 loss markedly accelerates murine BCC carcinogenesis.

177 keratinocytes significantly restrains murine BCC tumorigenesis and demonstrate the counterintuitive c

178 reated BCCs compared with 60 treatment-naive BCCs was significantly different in tumor cells (32% vs

179 or topical chemotherapy) vs treatment-naive BCCs.

180 nucleation mechanism of defects in nanoscale BCC crystals.

181 Here we show the discovery of four new BCC susceptibility loci: 2p24 MYCN (rs57244888[C], OR=0.

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

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

184 adults aged 25-75 years by recording all new BCCs and SCCs for 16 years in people with no previous ke

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

186 ndicating increased risk of developing a non-BCC malignancy.

187 Hazard ratio for non-BCC malignancies after vismodegib exposure, adjusting fo

188 Most non-BCC malignancies were cutaneous squamous cell carcinomas

189 high diagnostic specificity for nonpigmented BCC.

190 plant recipients with cutaneous SCC, but not BCC, have an increased risk of developing other SCC.

191 t higher risk for subsequent new SCC but not BCC, with a dose-response relationship between risk and

192 Although most cases of BCC are sporadic, some forms are inherited, such as Baze

193 methodology to identify spatial clusters of BCC and identify such clusters in a northern California

194 istically significant geographic clusters of BCC as determined by spatial scan statistics.

195 formation mechanism in nanoscale crystals of BCC tungsten.

196 f any SWS was associated with a diagnosis of BCC (2.3 [1.5-3.6]; P < .001).

197 come; the secondary outcome was diagnosis of BCC compared with amelanotic melanoma.

198 Diagnosis of BCC with dermoscopy compared with all other diagnoses co

199 blotches and/or strands for the diagnosis of BCC.

200 ndicated that the anatomical distribution of BCC and SCC differ, few have compared them directly in w

201 e and compare the anatomical distribution of BCC and SCC in a population-based sample in Queensland,

202 e and compare the anatomical distribution of BCC and SCC in a population-based sample in Queensland,

203 owledge about the anatomical distribution of BCC and SCC may provide insight into their diagnoses and

204 vasively the main histopathologic feature of BCC lesions: nests of basaloid cells showing palisading

205 emiology and clinicopathological features of BCC in the very elderly to guide clinicians and policy m

206 t reveals several characteristic features of BCC lesions.

207 n BCC mouse model prevented the formation of BCC through suppressing primary cilia formation and Hh s

208 on, current smokers had a lower incidence of BCC (possibly because of detection bias) but higher rate

209 The incidence of BCC among the very elderly is high and increasing.

210 clusters with modestly elevated incidence of BCC.

211 ation between sun exposure and occurrence of BCC.

212 ding deeper insight into the pathogenesis of BCC.

213 be caused by long-chain-oxidized-products of BCC.

214 dy used a BCC registry to determine rates of BCC by census block group, and used spatial scan statist

215 High and increasing incidence rates of BCC in the very elderly were found ranging from 13 to 12

216 hat included age-specific incidence rates of BCC in the very elderly.

217 The ratio of BCC to SCC treated in Medicare beneficiaries was 1.0.

218 The risk of BCC after allogeneic HSCT was seen only in patients cond

219 , which is associated with increased risk of BCC and breast cancer, is protective against prostate ca

220 firm a previous finding of increased risk of BCC associated with MHT.

221 Elevated risk of BCC was associated with late age at natural menopause (h

222 Risk of BCC was not associated with age at menarche, parity, age

223 The risk of BCC was similar for allogeneic HSCT recipients and RTRs,

224 eic HSCT recipients had an increased risk of BCC, SCC, and MM, with respective HRs of 3.1 (95% CI, 1.

225 ic HSCT recipients have an increased risk of BCC, SCC, and MM.

226 To identify young individuals at risk of BCC, we assessed existing melanoma or overall skin cance

227 ent smokers had significantly lower risks of BCC (hazard ratio = 0.6; 95% confidence interval = 0.4-0

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

229 a two-stage genome-wide association study of BCC, totalling 17,187 cases and 287,054 controls.

230 es themselves, contributes to suppression of BCC carcinogenesis.

231 Objective: To describe the burden of BCCs in patients with BCNS in the United States and iden

232 To describe the burden of BCCs in patients with BCNS in the United States and iden

233 ce: Patients with BCNS have a high burden of BCCs.

234 Patients with BCNS have a high burden of BCCs.

235 er understanding of geographic clustering of BCCs can help target screening and prevention efforts.

236 istically significant geographic clusters of BCCs, adjusting for age, sex, and socioeconomic status.

237 ition, GALNT14 supports continuous growth of BCCs in the lung by not only inducing macrophage infiltr

238 f noninvasive, label-free in vivo imaging of BCCs that could reduce the time from consultation to tre

239 vide an updated estimate of the incidence of BCCs, highlight the changing epidemiologic findings, and

240 Number of BCCs in the past 2 years and over lifetime (disease burd

241 Main Outcomes and Measures: Number of BCCs in the past 2 years and over lifetime (disease burd

242 ly, cannibalism of MSCs enhanced survival of BCCs deprived of nutrients but suppressed their tumorige

243 hypothesize that UVR has opposing effects on BCC carcinogenesis-stimulatory via mutagenesis and inhib

244 e research should focus more specifically on BCC in the very elderly, together with prognostication a

245 and 2 previous large prospective studies on BCC are in line with these results, epidemiologic litera

246 rst, of whom 74% subsequently developed only BCCs, and 28 had SCC first, of whom 64% subsequently dev

247 Our early-onset BCC risk prediction model incorporating MC1R and indoor

248 veloped BCC exclusively, SCC exclusively, or BCC and SCC.

249 gene) in biopsy specimens of normal skin or BCC before and after treatment.

250 that cutaneous SCC development, and perhaps BCC development, may be driven in part by HPV in immunoc

251 advanced or metastatic orbital or periocular BCC or basal cell nevus syndrome and can obviate orbital

252 advanced or metastatic orbital or periocular BCC or basal cell nevus syndrome treated with the Hedgeh

253 s, exogenous estrogen use, and first primary BCC while accounting for sun exposure, personal sun sens

254 the risks for a subsequent BCC after a prior BCC diagnosis and of a subsequent SCC after a prior SCC

255 the risk for a subsequent BCC after a prior BCC diagnosis and the risk for a subsequent SCC after a

256 ths after undergoing ESB for a biopsy-proven BCC.

257 A man in his 60s presented with a recurrent BCC within the radiation field 10 months after undergoin

258 ions, which included clear margins, residual BCC, or residual SCC.

259 riptome profiles revealed that the resulting BCCs acquired a unique molecular signature enriched in p

260 rine risk estimates and the outcomes of SCC, BCC and KC.

261 nally extracted from another natural source (BCC), and a synthetic one (BCS), was assessed during an

262 thologically indistinguishable from sporadic BCCs.

263 e responsive to SMO inhibitors than sporadic BCCs, with minimal development of resistance.

264 However, compared with sporadic BCCs, BCNS-BCCs have a significantly lower mutational lo

265 ced mutator phenotype compared with sporadic BCCs, which may contribute to their relatively more indo

266 Among the 14 counties studied, BCC incidence ranged from 661 to 1598 per 100000 person-

267 ndary analyses of the risks for a subsequent BCC after a prior BCC diagnosis and of a subsequent SCC

268 ondary analyses of the risk for a subsequent BCC after a prior BCC diagnosis and the risk for a subse

269 hanism by which p53 is activated to suppress BCC carcinogenesis.

270 Ten BCC lesions were imaged in vivo in 9 patients prior to b

271 We estimate that BCCs occur in approximately 2 million Americans annually

272 nd mRNA stabilization analyses indicate that BCCs contain the factor needed to increase TAC1 translat

273 The BCC incidence rates were standardized to the age, sex, a

274 titutes a conclusive route for detecting the BCC condition on a cellular level compared to the health

275 S phase is created by oxygen-ordering in the BCC Fe matrix.

276 Incidence rates did not differ by sex in the BCC-only, SCC-only, or mixed groups, but they increased

277 tates effectively double the strength of the BCC matrix above that provided by grain size reduction a

278 Compared to the healthy skin samples, the BCC samples' profiles exhibit significantly diminished l

279 reas the sigma phase grows directly when the BCC phase is cooled below TOOT and vice versa upon heati

280 s exhibit regular cellular pattern while the BCC skin samples indicate lack of regular cell pattern.

281 The main MPM feature associated with the BCC lesions involved nests of basaloid cells present in

282 e alloys, which maintains coherency with the BCC matrix up to at least 913 degrees C.

283 However, 85% of the BCCs also harbored additional driver mutations in other

284 Eighty-five percent of the BCCs harbored mutations in Hh pathway genes (PTCH1, 73%

285 served that MSCs sequentially surrounded the BCCs, promoted formation of cancer spheroids, and then w

286 to be targeted as a therapeutic approach to BCC.

287 Further interventions to prevent and treat BCCs in patients with BCNS are needed.

288 Treated BCCs (including those recurrent after surgery, radiother

289 stochemical staining intensity of 78 treated BCCs compared with 60 treatment-naive BCCs was significa

290 L1 expression in treatment-naive and treated BCCs.

291 tem, identified using a previously validated BCC registry.

292 Of these, 3846 KCs (74.7%) were BCCs.

293 mented neoplasms evaluated, 287 (62.8%) were BCCs, 106 (23.2%) were squamous cell carcinoma, 39 (8.5%

294 e and liquor were positively associated with BCC risk.

295 ]; P < .001) were positively associated with BCC.

296 ly spherical nanoparticles crystallized with BCC symmetry experimentally yield single crystals with w

297 Clinical experience with BCC patients shows that continuous exposure to vismodegi

298 Participants were higher-risk patients with BCC diagnosed from January 1, 1998, to December 31, 2014

299 r 31, 2012), we studied 147093 patients with BCC from Kaiser Permanente Northern California, a large,

300 Imaging in patients with BCC was performed at the University of California-Irvine