219) Tumor formation is inhibited in nude mouse |
220) 1-deficient NPC cell lines could suppress tumor formation and angiogenesis in vitro |
221) tive function of SAA1.5 in suppression of tumor formation and angiogenesis. |
222) Notch1 deficiency led to a reduced early tumor formation and lower activity of MAPK |
223) ced, whereas knockdown suppressed, HT1080 tumor formation in nude mice. |
224) licate in the NHP brain and did not cause tumor formation. |
225) -/-) ) mice were highly resistant to skin tumor promotion by CHRY. |
226) ne a novel mechanism associated with skin tumor promotion by the anthrone class of t |
227) With a tumor promotion model, the JB6 Cl41.5a cel |
228) lycoprotein, is a rate-limiting factor in tumor promotion of skin carcinogenesis. |
229) a]PDE regulates signaling pathways during tumor promotion remains unclear. |
230) tivator of transcription 1 (Stat1) during tumor promotion using the mouse skin multi |
231) -related genes (Prkg1, Gnao1 and Rgs9) in tumor samples and an enrichment of Apobec1 |
232) d human fibroblasts from normal ovary and tumor samples and epithelial ovarian cance |
233) alysis was performed using primary breast tumor samples from 50 postmenopausal women |
234) oordinate expression of S100A4 and SAA in tumor samples from colorectal carcinoma pa |
235) Solid tumor samples typically contain multiple d |
236) hybrid mice revealed features specific to tumor samples. |
237) nt differences in cancer cell morphology, tumor size (P = 0.742), Ki-67 labeling ind |
238) < 0.05) and was highly related to tumor size and TNM stage (P < 0.05) |
239) eatment and repair procedures, as well as tumor size and location. |
240) not impact in the latency of diagnosis or tumor size but the recognition of signific |
241) servations over the course of 1 year, the tumor size increased. |
242) nography on B scan showed a growth of the tumor size. |
243) tical downstream target of MEN1-dependent tumor suppression and is required for tumo |
244) concentration, the DA group showed a 95% tumor suppression rate without any recurre |
245) After 12 d of treatment, the tumor suppression rates of 75% and 84% wer |
246) t or senescence, to exert its function in tumor suppression. |
247) r, studies have also reported its role in tumor suppression. |
248) , which contributes to the role of p53 in tumor suppression. |
249) ession is significantly down-regulated in tumor tissue and CRC cell lines compared w |
250) on, short half-life, low concentration in tumor tissue and systemic toxicity. |
251) , 62 pairs of samples from patients whose tumor tissue showed hypermethylation of AN |
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