ライフサイエンスコーパス: BCC

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

10 at is, (011)(BCC) || ( 1 1 1)(FCC) and [100](BCC) || [ 11 0](FCC) .

11 67,332 women, including 404 melanomas, 1367 BCCs, and 232 SCCs.

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

13 ears with periocular (n=6) or orbital (n=15) BCC.

14 novel eutectoid nano-lamellar (FCC + L1(2))/(BCC + B2) microstructure that has been discovered in a r

15 2 years, participants reported a mean of 25 BCCs (median, 11; range, 0-250).

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

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

18 Simulation results indicate that Cr, as a BCC stabilizing element, exhibits a tendency to segregat

19 ual inverse phase transition sequence from a BCC phase to a sigma phase was observed by increasing an

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

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

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

23 so led to the precipitation of an additional BCC phase Cr(67)Fe(13)Mn(18.5)Ni(1.5), which was confirm

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

25 odegib, are effective therapies for advanced BCCs.

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

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

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

29 0.72; 95% CI: 0.54, 0.96; Ptrend = 0.02) and BCC (HR: 0.77; 95% CI: 0.66, 0.90; Ptrend = 0.0006) but

30 rameters, desired thicknesses of the FCC and BCC phases in the laminates can be achieved.

31 tifiable differences between the healthy and BCC skin samples.

32 ciation between 21 distinct genetic loci and BCC risk.

33 cer risk in women, particularly melanoma and BCC.

34 between a Pro-vegetarian dietary pattern and BCC.

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

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

37 to monthly community-level AM screenings and BCC sessions was highly effective at improving screening

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

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

40 lex relationship between exposure to UVR and BCC incidence.

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

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

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 tallographically related to the parent beta (BCC) matrix.

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

51 r demonstrate the genetic similarity between BCC and BSC.

52 We find that the interface is rough in both BCC and FCC cases.

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

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

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

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

57 Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are both derived

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

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

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

63 h the features of both 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 ttern with the risk of basal cell carcinoma (BCC) is little understood and has scarcely been investig

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

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

71 ll carcinoma (SCC) and basal cell carcinoma (BCC) nontransplant GWAS.

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

73 ion alters the risk of basal cell carcinoma (BCC) or invasive cutaneous squamous cell carcinoma (SCC)

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

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

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

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

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

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

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

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

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

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

86 1.57 (0.64-3.86), for basal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs), respectively.

87 Basal cell carcinomas (BCCs) depend on Hedgehog (Hh)/Gli signaling, but can dev

88 uals develop multiple basal cell carcinomas (BCCs) of the skin.

89 Basal cell carcinomas (BCCs) rely on Hedgehog (HH) pathway growth signal amplif

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

91 including melanomas, basal cell carcinomas (BCCs), and squamous cell carcinomas (SCCs).

92 hog pathway output in basal cell carcinomas (BCCs), and we have previously shown that resistant BCCs

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

94 rlin syndrome-related basal cell carcinomas (BCCs), with loss of function of Ptc1 being the most comm

95 f developing numerous basal cell carcinomas (BCCs).

96 f developing numerous basal cell carcinomas (BCCs).

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

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

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

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

101 ions included behavior change communication (BCC) on nutrition, health, and hygiene practices (both s

102 e-appropriate behavior change communication (BCC) on nutrition, health, and hygiene practices and a m

103 es (including behavior change communication [BCC] sessions, home visits, and integrated community cas

104 The Burkholderia cepacia complex (BCC) can cause severe lung infections in patients with c

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

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

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

108 of colloidal crystals: body-centered cubic (BCC) crystals and face-centered cubic (FCC) crystals.

109 ere established between body-centered cubic (BCC) crystals and their liquid using charged colloidal p

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

111 entered cubic (FCC) and body-centered cubic (BCC) metals.

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

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

114 alline (DQC) phase, and body-centered cubic (BCC) phase, is reported.

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

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

117 final SL structure from body-centered cubic (BCC) to face-centered cubic (FCC) through a series of bo

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

119 A single-phase body-centered-cubic (BCC) refractory HEA, NbTaTiVZr, using thermodynamic mode

120 ed lattice in the Fe(0) body-centered-cubic (BCC) structure and lower electron-transfer resistance, p

121 g nanometer layers of a body-centered-cubic (BCC) structure.

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

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

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

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

126 that Intu performs a permissive role during BCC formation.

127 aled distinct geographic areas with elevated BCC rates.

128 e the effects of the type and spacing of FCC/BCC interfaces on the deformation and spall behavior.

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

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

131 Measures of diagnostic accuracy for BCC were estimated.

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

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

134 body irradiation was a major determinant for BCC.

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

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

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

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

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

140 % CI, 90%-96%) (P = .18) after training; for BCC, they were 83% (95% CI, 59%-100%) and 92% (95% CI, 8

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

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

143 ates and identify potential risk factors for BCCs.

144 ates and identify potential risk factors for BCCs.

145 e modifications and potential regulators for BCCs and SCCs that likely impact the divergent oncogenic

146 whether these tumors originally derive from BCC or SCC.

147 support the genetic derivation of BSCs from BCCs and highlight potential factors involved in modulat

148 Using these GWAS, BCC and SCC PRS were calculated for each sample across t

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

150 ely target LYPD3+/TACSTD2+/LY6D+ nMRTF human BCCs ex vivo, opening an avenue for improving combinator

151 A panel of sporadic human BCCs showed increased staining of both Dsg2 and phosphor

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

153 utative regulation events (FGFR2 enhancer in BCC, intragenic regulation of FOXP1 in SCC, and WNT5A pr

154 ion factors that implicated SMAD and JDP2 in BCC pathogenesis and FOXP1 in SCC pathogenesis.

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

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

157 ovides selective pressure for altered p53 in BCC tumors.

158 structures (SWSs) are frequently present in BCC.

159 LATS1 suggested their potential relevance in BCC tumorigenesis.

160 ms represents a powerful signal amplifier in BCCs with implications for zinc finger-based signal tran

161 pment and Wnt signaling pathways enriched in BCCs and enriched immune response and cell activation pa

162 5% reduction in SCCs and a 100% reduction in BCCs.

163 5% reduction in SCCs and a 100% reduction in BCCs.

164 APK activation, and primary cilia removal in BCCs potentiated Ras/MAPK pathway activation.

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

166 ntake was associated with slightly increased BCC risk, albeit with no heterogeneity across skin cance

167 n UVR accelerates ionizing radiation-induced BCC carcinogenesis.

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

169 Our results provide insights into BCC treatment and identify the primary cilium as an impo

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

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

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

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

174 tly associated with the severity of lifetime BCC.

175 Ptrend = 0.014) were associated with a lower BCC risk.

176 line but who later reported a physician-made BCC diagnosis during the follow-up period.

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

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

179 tment is a feasible treatment for metastatic BCC.

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

181 ted expression of GALNT14 in lung-metastatic BCCs.

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

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

184 group also received age-appropriate monthly BCC and SQ-LNS for children >6 months of age.

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

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

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

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

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

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

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

192 or topical chemotherapy) vs treatment-naive BCCs.

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

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

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

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

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

198 Most non-BCC malignancies were cutaneous squamous cell carcinomas

199 high diagnostic specificity for nonpigmented BCC.

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

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

202 itamin D may reduce the risk of SCC, but not BCC.

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

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

205 e cohort we identified 101 incident cases of BCC.

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

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

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

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

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

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

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

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

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

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

216 While genetic drivers of BCC and SCC development have been extensively characteri

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

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

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

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

221 clusters with modestly elevated incidence of BCC.

222 s offered for the preferential nucleation of BCC over FCC in metallic alloys.

223 ation between sun exposure and occurrence of BCC.

224 with a 72% relative reduction in the odds of BCC (OR: 0.28; 95% CI: 0.10, 0.77; Ptrend = 0.014); the

225 ding deeper insight into the pathogenesis of BCC.

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

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

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

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

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

231 terns may be associated with a lower risk of BCC, but confirmatory studies are required.

232 vegetarian dietary pattern] with the risk of BCC, conducting a nested case-control study (4 controls

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

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

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

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

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

238 es themselves, contributes to suppression of BCC carcinogenesis.

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

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

241 Patients with BCNS have a high burden of BCCs.

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

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

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

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

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

247 insights about the cancer prone phenotype of BCCs in GS patients, including biomarkers/targets for ea

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

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

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

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

252 mpared with naive or Gorlin syndrome patient BCCs.

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

254 egib therapy for locally advanced periocular BCC.

255 dvanced and metastatic orbital or periocular BCC treated with vismodegib in 2012-2017 at 2 tertiary m

256 ehog signaling downstream of Ptc1 to promote BCC development through the activation of phosphorylated

257 in children 6-23 months of age and provided BCC to caregivers.

258 ression of Dsg2 in ASZ001 cells, a Ptc1(-/-) BCC cell line, induced Stat3 phosphorylation and further

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

260 Strikingly, Smoothened inhibitor-resistant BCCs have an increased mutational load in ciliome genes,

261 Gene set enrichment analysis of resistant BCCs with a low HH pathway signature showed increased Ra

262 and we have previously shown that resistant BCCs increase GLI1 deacetylation through atypical protei

263 Although the resistant BCCs usually maintain HH pathway activation, squamous ce

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

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

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

267 acZ) mice) resulted in increased spontaneous BCC formation at 3 and 6 months, respectively.

268 Sporadic BCCs also overexpress Dsg2, a desmosomal cadherin normal

269 thologically indistinguishable from sporadic BCCs.

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

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

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

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

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

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

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

277 ed to play a role in virulence in either the BCC or B. pseudomallei Since many of these TCS are invol

278 Separate from the BCC is Burkholderia pseudomallei, which is the causative

279 The mobility of the BCC interface is greater than that of the FCC interface.

280 accelerate the nucleation and growth of the BCC phase during irradiation.

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

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

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

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

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

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

287 to be targeted as a therapeutic approach to BCC.

288 -)/ODC(t)/C57BL/6) that is more sensitive to BCCs growth as compared with Ptch1(+/+)/ODC(t)/C57BL/6 l

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

290 Treated BCCs (including those recurrent after surgery, radiother

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

292 L1 expression in treatment-naive and treated BCCs.

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

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

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

296 n cancers, except positive associations with BCC risk.

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

298 y, 200 (9%) participants were diagnosed with BCC and 68 (3%) participants were diagnosed with SCC.

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

300 mor-normal pairs from 11 patients (five with BCC and six with SCC) undergoing Mohs surgery.