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1 hance arsenic efflux but may also impact the carcinogenic process.
2 stric epithelial cells may contribute to the carcinogenic process.
3 ctor receptor (EGFR), a critical gene in the carcinogenic process.
4 state of chromosomal instability during the carcinogenic process.
5 he accumulation of mutations and enhance the carcinogenic process.
6 standing of racial disparities in cancer and carcinogenic process.
7 s, an effect that could directly inhibit the carcinogenic process.
8 and c-fos, and may thereby contribute to the carcinogenic process.
9 ing in a mutation that may contribute to the carcinogenic process.
10 l may be important during the nickel-induced carcinogenic process.
11 survive to cause mutations that initiate the carcinogenic process.
12 ammalian cells and putative initiator of the carcinogenic process.
13 an potentially serve as a biomarker for this carcinogenic process.
14 ells in dysplastic foci and thus promote the carcinogenic process.
15 onal novel DNA repair genes important to the carcinogenic process.
16 ming proteins, which might contribute to the carcinogenic process.
17 ncoproteins is believed to contribute to the carcinogenic process.
18 t a possible role for its involvement in the carcinogenic process.
19 s are thought to play essential roles in the carcinogenic process.
20 igenicity have implicated this enzyme in the carcinogenic process.
21 rations occur from the very beginning of the carcinogenic process.
22 consequent mutations initiate the multistep carcinogenic process.
23 tation landscape of melanoma reveals diverse carcinogenic processes across its subtypes, some unrelat
24 malfunction arises as an early event in this carcinogenic process and has been demonstrated in patien
25 dge results in a better understanding of the carcinogenic process and improved predictive power, with
27 er, whether AKR1C isoforms contribute to the carcinogenic process and oxidize potent PAH trans-dihydr
28 human cancers suggests a common role in the carcinogenic process and possible application as a tumor
29 ery might be involved in naturally occurring carcinogenic processes and/or other numerous biological
30 Although pertinent roles of AEG-1 in the carcinogenic process are established, its potential func
32 by arresting, slowing down, or reversing the carcinogenic process before invasion into surrounding ti
33 of TGF-beta responsiveness might promote the carcinogenic process, both through direct effects on cel
34 ve normal cells and becomes defective during carcinogenic processes, e.g., by an inactivation of the
35 ples were analyzed representing the stepwise carcinogenic process from preneoplastic lesions (cirrhos
36 C have comparable suppressive effects on the carcinogenic process in a variety of in vivo and in vitr
40 the involvement of CLIP2 in the fundamental carcinogenic processes including apoptosis, mitogen-acti
43 ition of the role of small oval cells in the carcinogenic process led to a new hypothesis that HCC ar
44 d, in the last decade, as key players in the carcinogenic process, with many candidates identified as
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