266) l the potential mechanism of lidamycin on tumor initiating cells and the benefit for |
267) Recently, tumor initiating cells are considered as t |
268) evaluate the effect of lidamycin on Huh7 tumor initiating cells in vitro. |
269) , we evaluated the effect of lidamycin on tumor initiating cells of hepatocellular c |
270) ts suggest that lidamycin suppressed Huh7 tumor initiating cells via GSK3β/β-caten |
271) In addition to loss of tumor suppressive function, tumor-associat |
272) that induction of apoptosis is a key p53 tumor suppressive function. |
273) owever, indicate that other undefined p53 tumor suppressive functions are operative |
274) retinoblastoma (Rb) and p53 have critical tumor suppressive functions in retinoblast |
275) enesis, and identify essential Rb and p53 tumor suppressive functions in vivo. |
276) In addition, lidamycin restrained tumor volume and incidence in vivo. |
277) the semiquantitative evaluation of total tumor volume in the node when a whole node |
278) The results showed the tumor volume of GLUT-1-siRNA-MG63 cells xe |
279) ring rats indicated significantly reduced tumor volume with cisplatin-loaded targete |
280) line that encompassed at least 90% of the tumor volume. |
281) f the zebrafish Danio rerio as an in vivo tumor model for studying non-targeted effe |
282) Subcutaneous tumor model in nude mice was used to obser |
283) rvical lymph node metastasis in an animal tumor model. |
284) arison to a comparable Myc-driven mammary tumor model. |
285) properties, drug delivery applications to tumor sites and future perspectives. |
286) be used for targeting anticancer drugs to tumor sites as they behave similar to long |
287) d that the residence time of AR-DTX-PM at tumor sites was longer than its commercial |
288) accumulation of therapeutic drugs at the tumor sites. |
289) In addition, these tumor suppressors have important roles in |
290) RING-finger E3s serve as oncoproteins or tumor suppressors in HCC under specific co |
291) a signaling network involving established tumor suppressors including LKB1, TSC2 and |
292) nscripts, can lead to loss-of-function in tumor suppressors or activation of oncogen |
293) miR-106b induced by TGF-β determines the tumor-promoting effects of TGF-β in breas |
294) er cells acquire the ability to evade the tumor-suppressing effects of TGF-β, yet s |
295) This can explain why SAA1.5 has no tumor-suppressive effects. |
296) ents, of whom a majority had laparoscopic tumor excision and partial myocutaneous gl |
297) cases were successfully treated regarding tumor excision by practicing right hemicol |
298) gnosis of an ectopic lymph node or benign tumor, excision via the oral cavity was pe |
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