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 s is not yet established, nor is the risk of
non-melanoma cancer to gene carriers.
5 ase reporter gene expression in melanoma and
non-melanoma cell lines.
6 melanoma cells, the presence of interfering
non-melanoma cells, were tested and optimized over diffe
7 patients underwent ECT for the treatment of
non-melanoma head and neck cancers.
8 was no difference in (18)F-FDG uptake in the
non-melanoma-
involved spleen.
9 tions in p53 were detected in 11/23 (48%) of
non melanoma skin cancers in renal allograft recipients
10 's lymphoma (SIR=28.56, 95% CI, 7.68-73.11),
non-melanoma skin cancer (estimated SIR> or =3.16) and f
11 This approach is limited because
non-melanoma skin cancer (NMSC) is predominantly formed
12 Non-melanoma skin cancer (NMSC) is the most common malig
13 Non-melanoma skin cancer (NMSC) represents a significant
14 sue injury, represents a clinical marker for
non-melanoma skin cancer (NMSC) risk.
15 genes was related to EMAST in a series of 61
non-melanoma skin cancer (NMSC) tumors.
16 Given the high incidence of
non-melanoma skin cancer (NMSC), a preventative interven
17 sociation between UVB and the development of
non-melanoma skin cancer (NMSC), controlling for known c
18 type are risk factors for the development of
non-melanoma skin cancer (NMSC), including basal cell ca
19 buting factor in ultraviolet B (UVB)-induced
non-melanoma skin cancer (NMSC), which consists primaril
20 genes are associated with susceptibility to
non-melanoma skin cancer (NMSC).
21 iseases is associated with decreased risk of
non-melanoma skin cancer (NMSC).
22 oming available, especially for treatment of
non-melanoma skin cancer and Barrett's oesophagus, and i
23 cell carcinoma (SCC) is the most aggressive
non-melanoma skin cancer and is dramatically increased i
24 dent cancer cases were documented (excluding
non-melanoma skin cancer and non-aggressive prostate can
25 r transmission from donors with a history of
non-melanoma skin cancer and selected cancers of the CNS
26 ln399gln) is associated with a lower risk of
non-melanoma skin cancer and suggest that the etiology o
27 for the majority of the approximately 10,000
non-melanoma skin cancer deaths in the United States ann
28 s, leading to more than one million cases of
non-melanoma skin cancer diagnosed annually in the Unite
29 en shown to contribute to the development of
non-melanoma skin cancer in humans.
30 om an incident survey of all newly diagnosed
non-melanoma skin cancer in New Hampshire, and controls
31 een implicated in the increased incidence of
non-melanoma skin cancer in transplant recipients, most
32 Non-melanoma skin cancer is a disease primarily afflicti
33 The development of extensive and severe
non-melanoma skin cancer is an extremely common complica
34 Diagnosis of
non-melanoma skin cancer is made clinically and confirme
35 mulation of genetic change and behaviour for
non-melanoma skin cancer is not straightforward.
36 This approach is limited because
non-melanoma skin cancer is predominantly formed on body
37 Non-melanoma skin cancer is the most common cancer world
38 Currently, the only effective treatment for
non-melanoma skin cancer is the removal of the tumors af
39 73 malignancies other than
non-melanoma skin cancer occurred (SIR 0.9 [95% CI 0.7-1
40 =50% size of alar subunit) after excision of
non-melanoma skin cancer on the alar lobule.
41 Non-melanoma skin cancer represents the most common canc
42 mouse model of UVB-induced inflammation and
non-melanoma skin cancer to further define sex discrepan
43 43; and with skin cancer (Bowen's disease or
non-melanoma skin cancer), 378.
44 TP53 is an accepted UVR target in human
non-melanoma skin cancer, but is not thought to have a m
45 an early warning sign of progression toward
non-melanoma skin cancer, if ignored.
46 iagnosed with cancer before 1986 (other than
non-melanoma skin cancer, n=2076) and those with missing
47 HPV DNA was detected in 15 of 20 (75%)
non-melanoma skin cancer, seven of 17 (41.2%) dysplastic
48 Non-melanoma skin cancer, the most common neoplasia afte
49 rincipal aetiological factor associated with
non-melanoma skin cancer, the most prevalent group of ma
50 ll-recognized etiologic factor for cutaneous
non-melanoma skin cancer.
51 ynamic therapy (PDT) is widely used to treat
non-melanoma skin cancer.
52 tis, viral warts, molluscum contagiosum, and
non-melanoma skin cancer.
53 asal alar lobule after two-layer excision of
non-melanoma skin cancer.
54 story of photosensitizing medication use and
non-melanoma skin cancer.
55 as for the identification of target cells in
non-melanoma skin cancer.
56 facing to reduce or prevent aging-associated
non-melanoma skin cancer.
57 are novel loci conferring susceptibility to
non-melanoma skin cancer.
58 A confers an increased risk for melanoma and
non-melanoma skin cancer.
59 ated by UV irradiation, the primary cause of
non-melanoma skin cancer.
60 omponent in the development of aging-related
non-melanoma skin cancer.
61 e development and progression of UVB-induced
non-melanoma skin cancer.
62 tologists treat actinic keratoses to prevent
non-melanoma skin cancer.
63 s a significant factor in the development of
non-melanoma skin cancer.
64 dministration of ARD on at least one type of
non-melanoma skin cancer.
65 arge, population-based case-control study of
non-melanoma skin cancer.
66 HPV8 and 77) are suspected to be involved in
non-melanoma skin cancer.
67 r of sunburns, tanning ability and number of
non-melanoma skin cancers (NMSCs) among 10 183 European
68 Non-melanoma skin cancers (NMSCs) are among the most com
69 Non-melanoma skin cancers (NMSCs) are the most common ma
70 nts as evidenced by the fact that 80% of all
non-melanoma skin cancers are diagnosed in patients over
71 treatment of pre-cancerous skin lesions and
non-melanoma skin cancers are not completely effective.
72 issue and ease of observation, acceptance of
non-melanoma skin cancers as model carcinomas has been h
73 We have demonstrated that
non-melanoma skin cancers express functional purinergic
74 The rising incidence and morbidity of
non-melanoma skin cancers has generated great interest i
75 Another group of HPVs causes
non-melanoma skin cancers in genetically predisposed or
76 trum of HPV types are also commonly found in
non-melanoma skin cancers in immunocompromised individua
77 ity for all incident cancer cases, excluding
non-melanoma skin cancers, diagnosed between 2002 and 20
78 For example, unlike
non-melanoma skin cancers, melanoma is not restricted to
79 st examples of video-mosaics of melanoma and
non-melanoma skin cancers, to demonstrate potential clin
80 mental factors contribute to pathogenesis of
non-melanoma skin cancers.
81 The incidence of keratinocyte-derived (
non-melanoma)
skin cancers is increasing rapidly.
82 In 28 patients with BRAF-mutant
non-melanoma solid tumours, apparent antitumour activity
83 elanoma with untreated brain metastases, and
non-melanoma solid tumours.
84 culating levels of FGF2 were associated with
non-melanoma tumor formation in vivo.
85 Of 60
non-melanoma tumors, none displayed nuclear Mitf stainin
86 lanoma and permit its broader application to
non-melanoma tumors.