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1 ed with RT (xerostomia, mucositis, and local skin toxicity).
2 hough it is efficacious, erlotinib can cause skin toxicity.
3 ulation in the skin and heart and eliminated skin toxicity.
4 th the observed moist desquamation radiation skin toxicity.
5 mpletion of chemoradiation or on recovery of skin toxicity.
6 mcitabine, including two instances of severe skin toxicity.
7 creening and showed potential for predicting skin toxicity.
9 atin cohort (panitumumab v control) included skin toxicity (36% v 1%), diarrhea (24% v 13%), infectio
10 f 219 patients vs 39 [18%] of 218 patients), skin toxicity (41 [19%] vs none), lethargy (45 [21]% vs
11 gefitinib vs six [3%] of 225 on placebo) and skin toxicity (46 [21%] vs two [1%]), both mostly grade
13 s584547 were found to be novel risk loci for skin toxicity and dysphagia in NPC patients receiving ra
14 ivery vectors and diagnostic agents, but the skin toxicity and irritation potential of QDs are unknow
17 29 reported grade 2 toxicities, with grade 2 skin toxicities being the most frequent (16 of 67; 24%).
18 only shows reasonable accuracy in predicting skin toxicity but also enables cross-study comparison an
20 e potential of Raman spectroscopy to predict skin toxicity due to tyrosine kinase inhibitors treatmen
22 incidence of protocol-specified >or= grade 2 skin toxicities during the 6-week skin treatment period
23 incidence of protocol-specified >or= grade 2 skin toxicities during the 6-week skin treatment period.
24 inhibitors, which are known to induce severe skin toxicity; for this pilot study, three patients were
25 had interruption of oncologic therapy due to skin toxicity; four of six (67%) were successfully recha
28 dverse events of immediate radiotherapy were skin toxicity (grade 1 in 50 [54%] and grade 2 in four [
29 delay surgery but induced unexpected severe skin toxicity, hampering domatinostat dose escalation.
30 4 +/- 5 ug mL(-1) revealed no acute in vitro skin toxicity (IC(50): 95 ug mL(-1)) and skin sensitizat
31 verse events in the treatment group included skin toxicity, impaired activity, damage to surrounding
32 ive and reactive skin treatment for specific skin toxicities in patients with mCRC for any EGFR inhib
36 97, rs4848598, and rs2091255 correlated with skin toxicity in patients of EBV positive, late stage (I
38 f Raman spectroscopy to detect apparition of skin toxicity in patients treated with tyrosine kinase i
40 Thus, a comprehensive understanding of the skin toxicity mechanisms involving the AhR, as well as t
43 s one [<1%] in the erlotinib group), whereas skin toxicity (one [<1%] vs 22 [16%]) was the most frequ
49 d according to the National Cancer Institute skin toxicity scale, offering a basis for describing cut
50 ionated radiotherapy group had grade 3 acute skin toxicity than in the conventional fractionated radi
52 ructed tissues were exposed to drugs causing skin toxicity, the thickness evaluation of epidermal lay
56 In contrast to other reports, development of skin toxicity was a statistically significant predictor
63 atoh et al. define a mechanism for acneiform skin toxicity wherein EGFR/MEK inhibitors cooperate with
64 synthesis by the spheroids and evaluation of skin toxicity with chemical agents showed a correlation
65 lains the basis underlying sorafenib-induced skin toxicity, with important implications for the thera