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Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Eun-Kyung Lim, Taekhoon Kim, Soonmyung Paik, Seungjoo Haam, Yong-Min Huh, Kwangyeol Lee
As described earlier, cancer cells undergo a series of changes via mutation and eventually acquire a number of abilities, dubbed as hallmarks for cancer [29, 30], such as self-sufficiency in growth signals, insensitivity to antigrowth signals, evasion of apoptosis, limitless replication, sustained angiogenesis, tissue invasion and metastasis, deregulation of cellular energetics, and escape from immune destruction, which distinguishes cancer cells from normal cells. The detailed discussion of these hallmarks does not need to be repeated here, but it should be stressed that a thorough understanding of cancer metabolism is imperative for successful design of nanomaterial-based theranostic agents.
The Role of Nanotechnology in the Treatment of Drug Resistance Cancer
Published in Bhaskar Mazumder, Subhabrata Ray, Paulami Pal, Yashwant Pathak, Nanotechnology, 2019
Sandipan Dasgupta, Anup Kumar Das, Paulami Pal, Subhabrata Ray, Bhaskar Mazumder
After a sufficient amount of anticancer drug has entered, accumulated, and inhibited its cellular targets, the outcome is dependent on how the cancer cell reacts. Ideally, anticancer drug-induced damage results in cancer cell death. However, several intrinsic adaptive responses are triggered that promote cancer cell survival. Additionally, the pathways that regulate cell death through apoptosis frequently become dysfunctional, which has become one of the hallmarks of cancer (Hanahan and Weinberg, 2000).
Hazard Characterization and Dose–Response Assessment
Published in Ted W. Simon, Environmental Risk Assessment, 2019
Cancer is still viewed in a monolithic way—as a single disease; thinking of cancer as a group of diseases with multiple interacting causal factors is more accurate. The hallmarks of cancer were identified in the early 21st century, and include sustaining a blood supply, cells acquiring a limitless ability to replicate, insensitivity to controls on growth, the ability to escape programmed cell death, and other features. These acquired hallmarks provide malignant cells with a Darwinian selective advantage over normal cells: in short, cancer cells can scavenge resources, are essentially immortal, and in a very real sense, parasitize the host. The six original hallmarks of cancer are: self-sufficiency in growth signals;evasion of apoptosis;insenstivity to anti-growth signals;sustained angiogenesis;tissue invasion and metastasis;limitless replicative potential.4 The four next-generation hallmarks added in 2011 are: dysregulation of cellular energetics;avoidance of immune destruction;genomic instability and mutation;tumor-promoting inflammation.5 These hallmarks are acquired capabilities of cells that are necessary for tumor growth and progression. The hallmarks are intended to serve as a general set of clinical targets for development of new drugs and treatment protocols. The authors also mention epigenetic changes, but in 2010 did not have sufficient information on the relationship of epigenetics and cancer to add another hallmark.
MicroRNA-122 overexpression promotes apoptosis and tumor suppressor gene expression induced by microcystin-leucine arginine in mouse liver
Published in International Journal of Environmental Health Research, 2022
Rui Wang, Haohao Liu, Xingde Du, Ya Ma, Zhihui Tian, Shiyu Zhang, Linjia Shi, Hongxiang Guo, Huizhen Zhang
The induction of apoptosis caused by DNA damage in precancerous lesions can remove potentially harmful cells, thereby blocking tumor growth. Deregulation of this death process is associated with unchecked cell proliferation, development and progression of cancer and cancer resistance to drug therapies Fulda (2009). For these reasons, deregulation of apoptosis is considered one of the hallmarks of cancer. It had been reported that miR-122 could serve as a pro-apoptotic factor in suppressing hepatocellular carcinoma cell migration and invasion Wang et al. (2018). Studies have shown that miR-122 can participate in apoptosis of liver cancer cells by regulating many pathways such as the programmed cell death 4 (PDCD4) signaling pathway Wang et al. (2018).