Fundamentals of Cancer Detection, Treatment, and Prevention. Surya K. DeЧитать онлайн книгу.
option compared to surgery, radiation, and chemotherapy. Over the past few decades, scientists have discovered new ways to boost the human body's immune response to cancer. Currently, immunotherapy consists of either stimulating the immune system to more effectively overcome cancer or supplementing the immune system with special synthetic proteins or other tools that work against cancer cells [47,52,53,62,63]. An example of immunotherapy is the development of the HPV vaccine, which is now recommended by the US Centers for Disease Control and Prevention (CDC).
1.11.6 Hormone Therapy
It is a consideration for some cancers, such as breast or prostate cancer, that are sensitive to hormones. Drugs are available, which block the body's normal signals to produce certain hormones, preventing hormone‐dependent cancers from continued growth. Although this sounds simple, any drugs that change the natural processes of the body include risk of side effects. Hormone therapy is frequently used with other treatments, and specialists work with each patient to determine when and how to administer it, the amount and duration of doses, and to gauge individual responses to treatment [65,66].
1.11.7 Stem Cell Transplant
It is a method used to restore the body's ability to produce new blood cells after a patient has undergone other forms of aggressive cancer treatment [5]. For certain types of cancer, very high doses of chemotherapy or radiation are required to destroy the cancer cells, but cells that produce blood are also destroyed in the process. In this case, stem cells are administered along with a blood transfusion. Stem cells are collected either from the patient before cancer treatment or from a donor. After stem cell treatment, it takes two to four weeks for an individual's body to recover and begin producing blood cells again. As with other treatments, there are risks involved, including the possibility that the stem cells will not settle in the bone marrow and begin producing blood cells as intended. When that occurs, it is deemed a failed treatment, and the process may be repeated.
1.11.8 Precision Medicine
It differs from other forms of cancer treatment in that it is focused on genetic changes particular to each individual's cancer to determine the most effective treatment options for countering it. Although precision medicine may involve various forms of traditional cancer treatment, it considers the genetic particularities of each individual's cancer to offer a more specialized treatment plan [68–74].
References
1 1 Nandini, D.B. (2017). Cancer cell nucleus: an insight. J. Mol. Biomark. Diagn. S2: 026.
2 2 Papetti, M. and Herman, I. (2002). Mechanisms of normal and tumor‐derived angiogenesis. Am. J. Physiol. Cell Physiol. 282 (5): C947–C970.
3 3 Eales, K., Hollinshead, K., and Tennant, D. (2016). Hypoxia and metabolic adaptation of cancer cells. Oncogenesis 5 (1): e190.
4 4 Song, Q., Merajver, S.D., and Li, J.Z. (2015). Cancer classification in the genomic era: five contemporary problems. Hum. Genomics 9: 27.
5 5 Yadav, U.P., Singh, T., Kumar, P. et al. (2020). Metabolic adaptations in cancer stem cells. Front. Oncol. 10: 1010. Published 25 June 2020. https://doi.org/10.3389/fonc.2020.01010.
6 6 Baylin, S.B. and Ohm, J.E. (2006). Epigenetic gene silencing in cancer – a mechanism for early oncogenic pathway addiction? Nat. Rev. Cancer 6 (2): 107–116. https://doi.org/10.1038/nrc1799. PMID: 16491070.
7 7 Merlo, L.M., Pepper, J.W., Reid, B.J., and Maley, C.C. (2006). Cancer as an evolutionary and ecological process. Nat. Rev. Cancer 6 (12): 924–935. https://doi.org/10.1038/nrc2013. Epub 2006 Nov 16. PMID: 17109012.
8 8 Croce, C.M. (2008). Oncogenes and cancer. N. Engl. J. Med. 358 (5): 502–511. https://doi.org/10.1056/NEJMra072367. PMID: 18234754.
9 9 Lahtz, C. and Pfeifer, G.P. (2011). Epigenetic changes of DNA repair genes in cancer. J. Mol. Cell Biol. 3 (1): 51–58. https://doi.org/10.1093/jmcb/mjq053. PMID: 21278452; PMCID: PMC3030973.
10 10 Han, Y., Chen, W., Li, P., and Ye, J. (2015). Association between coeliac disease and risk of any malignancy and gastrointestinal malignancy: a meta‐analysis. Medicine 94 (38): e1612. https://doi.org/10.1097/MD.0000000000001612. PMID: 26402826; PMCID: PMC4635766.
11 11 Cuozzo, C., Porcellini, A., Angrisano, T. et al. (2007). DNA damage, homology‐directed repair, and DNA methylation. PLoS Genet. 3 (7): e110. https://doi.org/10.1371/journal.pgen.0030110. Erratum in: PLoS Genet. 2017 Feb 10;13(2):e1006605. PMID: 17616978; PMCID: PMC1913100.
12 12 Vogelstein, B., Papadopoulos, N., Velculescu, V.E. et al. (2013). Cancer genome landscapes. Science 339 (6127): 1546–1558. https://doi.org/10.1126/science.1235122. PMID: 23539594; PMCID: PMC3749880.
13 13 Fearon, E.R. (1997). Human cancer syndromes: clues to the origin and nature of cancer. Science 278 (5340): 1043–1050. https://doi.org/10.1126/science.278.5340.1043. PMID: 9353177.
14 14 Hisada, M., Garber, J.E., Fung, C.Y. et al. (1998). Multiple primary cancers in families with Li‐Fraumeni syndrome. J. Natl. Cancer Inst. 90: 606–611.
15 15 Kushi, L.H., Doyle, C., McCullough, M. et al. (2012). American Cancer Society guidelines on nutrition and physical activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA Cancer J. Clin. 62 (1): 30–67. https://doi.org/10.3322/caac.20140. PMID: 22237782.
16 16 Kim, S.H., Shin, D.W., Kim, S.Y. et al. (2016). Terminal versus advanced cancer: do the general population and health care professional share a common language? Cancer Res. Treat. 48 (2): 759–767.
17 17 Danaei, G., Vander Hoorn, S., Lopez, A.D. et al. (2005). Causes of cancer in the world: comparative risk assessment of nine behavioural and environmental risk factors. Lancet 366 (9499): 1784–1793. https://doi.org/10.1016/S0140-6736(05)67725-2. PMID: 16298215.
18 18 Cappellani, A., Di Vita, M., Zanghi, A. et al. (2012). Diet, obesity and breast cancer: an update. Front. Biosci. (Schol. Ed.) 4: 90–108. https://doi.org/10.2741/253. PMID: 22202045.
19 19 Quinn, B.A., Wang, S., Barile, E. et al. (2016). Therapy of pancreatic cancer via an EphA2 receptor‐targeted delivery of gemcitabine. Oncotarget 7 (13): 17103–17110. https://doi.org/10.18632/oncotarget.7931. PMID: 26959746; PMCID: PMC4941374.
20 20 Scortegagna, M., Lau, E., Zhang, T. et al. (2015). PDK1 and SGK3 contribute to the growth of BRAF‐mutant melanomas and are potential therapeutic targets. Cancer Res. 75 (7): 1399–1412. https://doi.org/10.1158/0008-5472.CAN-14-2785. Epub 2015 Feb 24. PMID: 25712345; PMCID: PMC4383687.
21 21 Wu, B., Wang, S., De, S.K. et al. (2015). Design and characterization of novel EphA2 agonists for targeted delivery of chemotherapy to cancer cells. Chem. Biol. 22 (7): 876–887. https://doi.org/10.1016/j.chembiol.2015.06.011. Epub 2015 Jul 9. PMID: 26165155; PMCID: PMC4515144.
22 22 Lind, M.J. (2008). Principles of cytotoxic chemotherapy. Medicine 36 (1): 19–23.
23 23 Nastoupil, L.J., Rose, A.C., and Flowers,