1 terized by high incidence and early onset of
non-melanoma and melanoma skin cancers.
2 We examined
non-melanoma cancer cell lines containing oncogenic Ras
3 in cells (keratinocytes and fibroblasts) and
non-melanoma cancer cells.
4 al evidence of MITF(E318K)'s contribution to
non-melanoma cancer risk among individuals with low inhe
5 s is not yet established, nor is the risk of
non-melanoma cancer to gene carriers.
6 o predict for long-term survivorship in most
non-melanoma cancers.
7 ase reporter gene expression in melanoma and
non-melanoma cell lines.
8 melanoma cells, the presence of interfering
non-melanoma cells, were tested and optimized over diffe
9 patients underwent ECT for the treatment of
non-melanoma head and neck cancers.
10 monitis (P = 0.028), an effect replicated in
non-melanoma ICB recipients (n = 58, P = 0.044).
11 ability to distinguish between melanoma and
non-melanoma images, achieving F-measures of 92.769%, 93
12 was no difference in (18)F-FDG uptake in the
non-melanoma-
involved spleen.
13 tions in p53 were detected in 11/23 (48%) of
non melanoma skin cancers in renal allograft recipients
14 was for prostate cancer (77.0% in April) and
non-melanoma skin cancer (72.4% in April).
15 's lymphoma (SIR=28.56, 95% CI, 7.68-73.11),
non-melanoma skin cancer (estimated SIR> or =3.16) and f
16 nsplant recipients have an increased risk of
non-melanoma skin cancer (NMSC) compared to in the gener
17 This approach is limited because
non-melanoma skin cancer (NMSC) is predominantly formed
18 Non-melanoma skin cancer (NMSC) is the most common cance
19 Non-melanoma skin cancer (NMSC) is the most common malig
20 Non-melanoma skin cancer (NMSC) represents a significant
21 sue injury, represents a clinical marker for
non-melanoma skin cancer (NMSC) risk.
22 genes was related to EMAST in a series of 61
non-melanoma skin cancer (NMSC) tumors.
23 Given the high incidence of
non-melanoma skin cancer (NMSC), a preventative interven
24 sociation between UVB and the development of
non-melanoma skin cancer (NMSC), controlling for known c
25 type are risk factors for the development of
non-melanoma skin cancer (NMSC), including basal cell ca
26 buting factor in ultraviolet B (UVB)-induced
non-melanoma skin cancer (NMSC), which consists primaril
27 neous beta-HPV infection and a high risk for
non-melanoma skin cancer (NMSC).
28 genes are associated with susceptibility to
non-melanoma skin cancer (NMSC).
29 iseases is associated with decreased risk of
non-melanoma skin cancer (NMSC).
30 oming available, especially for treatment of
non-melanoma skin cancer and Barrett's oesophagus, and i
31 cell carcinoma (SCC) is the most aggressive
non-melanoma skin cancer and is dramatically increased i
32 is associated with solid cancers, including
non-melanoma skin cancer and lung cancer, and that CHIP
33 dent cancer cases were documented (excluding
non-melanoma skin cancer and non-aggressive prostate can
34 r transmission from donors with a history of
non-melanoma skin cancer and selected cancers of the CNS
35 ln399gln) is associated with a lower risk of
non-melanoma skin cancer and suggest that the etiology o
36 for the majority of the approximately 10,000
non-melanoma skin cancer deaths in the United States ann
37 s, leading to more than one million cases of
non-melanoma skin cancer diagnosed annually in the Unite
38 en shown to contribute to the development of
non-melanoma skin cancer in humans.
39 om an incident survey of all newly diagnosed
non-melanoma skin cancer in New Hampshire, and controls
40 een implicated in the increased incidence of
non-melanoma skin cancer in transplant recipients, most
41 Non-melanoma skin cancer is a disease primarily afflicti
42 The development of extensive and severe
non-melanoma skin cancer is an extremely common complica
43 Diagnosis of
non-melanoma skin cancer is made clinically and confirme
44 mulation of genetic change and behaviour for
non-melanoma skin cancer is not straightforward.
45 This approach is limited because
non-melanoma skin cancer is predominantly formed on body
46 Non-melanoma skin cancer is the most common cancer world
47 Currently, the only effective treatment for
non-melanoma skin cancer is the removal of the tumors af
48 73 malignancies other than
non-melanoma skin cancer occurred (SIR 0.9 [95% CI 0.7-1
49 =50% size of alar subunit) after excision of
non-melanoma skin cancer on the alar lobule.
50 Non-melanoma skin cancer represents the most common canc
51 mouse model of UVB-induced inflammation and
non-melanoma skin cancer to further define sex discrepan
52 have a prevalent cancer at baseline (except
non-melanoma skin cancer) and had provided data on oral
53 43; and with skin cancer (Bowen's disease or
non-melanoma skin cancer), 378.
54 al thrombosis, thrombophilia, cancer (except
non-melanoma skin cancer), liver disease, chronic kidney
55 antified for all cancers combined, excluding
non-melanoma skin cancer, and 33 specific cancer types.
56 TP53 is an accepted UVR target in human
non-melanoma skin cancer, but is not thought to have a m
57 an early warning sign of progression toward
non-melanoma skin cancer, if ignored.
58 6 women were diagnosed with cancer excluding
non-melanoma skin cancer, in Denmark.
59 iagnosed with cancer before 1986 (other than
non-melanoma skin cancer, n=2076) and those with missing
60 serious infections, herpes zoster infection,
non-melanoma skin cancer, other malignancies, major card
61 HPV DNA was detected in 15 of 20 (75%)
non-melanoma skin cancer, seven of 17 (41.2%) dysplastic
62 Non-melanoma skin cancer, the most common neoplasia afte
63 rincipal aetiological factor associated with
non-melanoma skin cancer, the most prevalent group of ma
64 suggested an association between eczema and
non-melanoma skin cancer, while the remaining study fail
65 CI 0.57-0.91, p=0.0042), owing primarily to
non-melanoma skin cancer.
66 A confers an increased risk for melanoma and
non-melanoma skin cancer.
67 HPV8 and 77) are suspected to be involved in
non-melanoma skin cancer.
68 ll-recognized etiologic factor for cutaneous
non-melanoma skin cancer.
69 ynamic therapy (PDT) is widely used to treat
non-melanoma skin cancer.
70 tis, viral warts, molluscum contagiosum, and
non-melanoma skin cancer.
71 asal alar lobule after two-layer excision of
non-melanoma skin cancer.
72 story of photosensitizing medication use and
non-melanoma skin cancer.
73 as for the identification of target cells in
non-melanoma skin cancer.
74 facing to reduce or prevent aging-associated
non-melanoma skin cancer.
75 are novel loci conferring susceptibility to
non-melanoma skin cancer.
76 ated by UV irradiation, the primary cause of
non-melanoma skin cancer.
77 omponent in the development of aging-related
non-melanoma skin cancer.
78 e development and progression of UVB-induced
non-melanoma skin cancer.
79 tologists treat actinic keratoses to prevent
non-melanoma skin cancer.
80 s a significant factor in the development of
non-melanoma skin cancer.
81 dministration of ARD on at least one type of
non-melanoma skin cancer.
82 arge, population-based case-control study of
non-melanoma skin cancer.
83 disorders (18.2%), prostate cancers (18.2%),
non-melanoma skin cancers (18.2%), and breast cancers (1
84 r of sunburns, tanning ability and number of
non-melanoma skin cancers (NMSCs) among 10 183 European
85 Non-melanoma skin cancers (NMSCs) are among the most com
86 Non-melanoma skin cancers (NMSCs) are the most common ma
87 e of overall de novo malignancies (excluding
non-melanoma skin cancers [NMSCs]), post-transplantation
88 nts as evidenced by the fact that 80% of all
non-melanoma skin cancers are diagnosed in patients over
89 treatment of pre-cancerous skin lesions and
non-melanoma skin cancers are not completely effective.
90 issue and ease of observation, acceptance of
non-melanoma skin cancers as model carcinomas has been h
91 We have demonstrated that
non-melanoma skin cancers express functional purinergic
92 Photodynamic therapy (PDT) to manage
non-melanoma skin cancers has garnered great attention o
93 The rising incidence and morbidity of
non-melanoma skin cancers has generated great interest i
94 Another group of HPVs causes
non-melanoma skin cancers in genetically predisposed or
95 trum of HPV types are also commonly found in
non-melanoma skin cancers in immunocompromised individua
96 ity for all incident cancer cases, excluding
non-melanoma skin cancers, diagnosed between 2002 and 20
97 For example, unlike
non-melanoma skin cancers, melanoma is not restricted to
98 In 2023, excluding
non-melanoma skin cancers, there were 18.5 million (95%
99 st examples of video-mosaics of melanoma and
non-melanoma skin cancers, to demonstrate potential clin
100 tive and site-specific approach for managing
non-melanoma skin cancers.
101 mental factors contribute to pathogenesis of
non-melanoma skin cancers.
102 The incidence of keratinocyte-derived (
non-melanoma)
skin cancers is increasing rapidly.
103 In 28 patients with BRAF-mutant
non-melanoma solid tumours, apparent antitumour activity
104 elanoma with untreated brain metastases, and
non-melanoma solid tumours.
105 culating levels of FGF2 were associated with
non-melanoma tumor formation in vivo.
106 Of 60
non-melanoma tumors, none displayed nuclear Mitf stainin
107 lanoma and permit its broader application to
non-melanoma tumors.
108 lung, ovary, pancreas, kidney, and malignant
non-melanoma)
using cis protein Mendelian randomisation