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We surmise that the application of high-content, high-throughput technologies to heterotypic experimental settings that involve not only malignant cells but also various other components of the tumor microenvironment (including endothelial, mesenchymal and immune cells) is the key for the development of efficient strategies to restore the sensitivity of multiple human neoplasms to CDDP.
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One recent detailed study of the multiple clinical specimen of human neoplasms reported that proliferation rate of endothelial cells within the vasculature of normal human organs has been reported to be <0.01%, whereas 2%to9%9% of endothelial cells in tumor-associated vessels divide daily [ 46].
The oncosuppressor TP53, which is mutated or inactivated in more than 50% of all human neoplasms, is widely known for its ability to orchestrate a transcriptional stress response that can have multiple outcomes including senescence and cell death [ 1].
Numerical chromosomal instability is a ubiquitous feature of human neoplasms.
There is growing biomedical interest in survivin as a diagnostic and prognostic factor in human neoplasms.
Yonezawa, S., Goto, M., Yamada, N., Higashi, M. & Nomoto, M. Expression profiles of MUC1, MUC2, and MUC4 mucins in human neoplasms and their relationship with biological behavior.
Oncocytic tumors are a peculiar subset of human neoplasms in which mitochondria have been proven to have a prominent role.
Kras mutations are among the most common genetic abnormalities in human neoplasms, including cholangiocarcinomas, pancreatic cancer and colon cancer.
It is maintained that there are six identifiable biological capacities that are acquired during the development of human neoplasms [130].
Investigators also found multiple human bones.
More generally, breaks of chromosomal band 19q13 have been reported in a variety of human neoplasms.
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