Mutation Mechanisms of Breast Cancer among the Female Population in China

Author(s): Asmaa Amer, Ahmed Nagah, Tianhai Tian*, Xinan Zhang*

Journal Name: Current Bioinformatics

Volume 15 , Issue 3 , 2020


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Abstract:

Background: Cancer is a genetic disease caused by the accumulation of gene mutations. It is important to derive the number of driver mutations that are needed for the development of human breast cancer, which may provide insights into the tumor diagnosis and therapy.

Objective: This work is designed to investigate whether there is any difference for the mutation mechanism of breast cancer between the patients in the USA and those in China. We study the mechanisms of breast cancer development in China, and then compare these mechanisms with those in the USA.

Methods: This work designed a multistage model including both gene mutation and clonal expansion of intermediate cells to fit the dataset of breast cancer in China from 2004 to 2009.

Results: Our simulation results show that the maximum number of driver mutations for breast epithelium stem cells of females in China is 13 which is less than the 14 driver mutations of females in the USA. In addition, the two-hit model is the optimal one for the tumorigenesis of females in China, which is also different from the three-hit model that was predicted as the optimal model for the tumorigenesis of females in the USA.

Conclusion: The differences of the mutation mechanisms between China and the USA reflect a variety of lifestyle, genetic influences, environmental exposure, and the availability of mammography screening.

Keywords: Breast cancer, multistage model, age-specific incidence rate, Chi square test, mutation, tumorigenesis.

[1]
Michor F, Iwasa Y, Nowak MA. Dynamics of cancer progression. Nat Rev Cancer 2004; 4(3): 197-205.
[http://dx.doi.org/10.1038/nrc1295] [PMID: 14993901]
[2]
Vogelstein B, Kinzler KW. The Genetic Basis of Human Cancer. 2nd ed. McGraw-Hill 2002.
[3]
Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell 2011; 144(5): 646-74.
[http://dx.doi.org/10.1016/j.cell.2011.02.013] [PMID: 21376230]
[4]
Loeb LA, Loeb KR, Anderson JP. Multiple mutations and cancer. Proc Natl Acad Sci USA 2003; 100(3): 776-81.
[http://dx.doi.org/10.1073/pnas.0334858100] [PMID: 12552134]
[5]
Loeb LA. Mutator phenotype may be required for multistage carcinogenesis. Cancer Res 1991; 51(12): 3075-9.
[PMID: 2039987]
[6]
Tomlinson I, Bodmer W. Selection, the mutation rate and cancer: ensuring that the tail does not wag the dog. Nat Med 1999; 5(1): 11-2.
[http://dx.doi.org/10.1038/4687] [PMID: 9883827]
[7]
Wood LD, Parsons DW, Jones S, et al. The genomic landscapes of human breast and colorectal cancers. Science 2007; 318(5853): 1108-13.
[http://dx.doi.org/10.1126/science.1145720] [PMID: 17932254]
[8]
Armitage P, Doll R. The age distribution of cancer and a multi-stage theory of carcinogenesis. Br J Cancer 1954; 8(1): 1-12.
[http://dx.doi.org/10.1038/bjc.1954.1] [PMID: 13172380]
[9]
Knudson AG Jr. Mutation and cancer: statistical study of retinoblastoma. Proc Natl Acad Sci USA 1971; 68(4): 820-3.
[http://dx.doi.org/10.1073/pnas.68.4.820] [PMID: 5279523]
[10]
Moolgavkar SH, Knudson AG Jr. Mutation and cancer: a model for human carcinogenesis. J Natl Cancer Inst 1981; 66(6): 1037-52.
[http://dx.doi.org/10.1093/jnci/66.6.1037] [PMID: 6941039]
[11]
Moolgavkar SH, Dewanji A, Venzon DJ. A stochastic two-stage model for cancer risk assessment. I. The hazard function and the probability of tumor. Risk Anal 1988; 8(3): 383-92.
[http://dx.doi.org/10.1111/j.1539-6924.1988.tb00502.x] [PMID: 3201016]
[12]
Luebeck EG, Moolgavkar SH. Multistage carcinogenesis and the incidence of colorectal cancer. Proc Natl Acad Sci USA 2002; 99(23): 15095-100.
[http://dx.doi.org/10.1073/pnas.222118199] [PMID: 12415112]
[13]
Zhang X, Simon R. Estimating the number of rate limiting genomic changes for human breast cancer. Breast Cancer Res Treat 2005; 91(2): 121-4.
[http://dx.doi.org/10.1007/s10549-004-5782-y] [PMID: 15868439]
[14]
Zhang X, Fang Y, Zhao Y, Zheng W. Mathematical modeling the pathway of human breast cancer. Math Biosci 2014; 253: 25-9.
[http://dx.doi.org/10.1016/j.mbs.2014.03.011] [PMID: 24680645]
[15]
Li L, Tian T, Zhang X. Mutation mechanisms of human breast cancer. J Comput Biol 2018; 25(4): 396-404.
[http://dx.doi.org/10.1089/cmb.2017.0111] [PMID: 29265879]
[16]
Simon R, Zhang X. On the dynamics of breast tumor development in women carrying germline BRCA1 and BRCA2 mutations. Int J Cancer 2008; 122(8): 1916-7.
[http://dx.doi.org/10.1002/ijc.23323] [PMID: 18098285]
[17]
Li T, Mello-Thoms C, Brennan PC. Descriptive epidemiology of breast cancer in China: incidence, mortality, survival and prevalence. Breast Cancer Res Treat 2016; 159(3): 395-406.
[http://dx.doi.org/10.1007/s10549-016-3947-0] [PMID: 27562585]
[18]
Li J, Zhang BN, Fan JH, et al. A nation-wide multicenter 10-year (1999-2008) retrospective clinical epidemiological study of female breast cancer in China. BMC Cancer 2011; 11: 364.
[http://dx.doi.org/10.1186/1471-2407-11-364] [PMID: 21859480]
[19]
Leong SP, Shen ZZ, Liu TJ, et al. Is breast cancer the same disease in Asian and Western countries? World J Surg 2010; 34(10): 2308-24.
[http://dx.doi.org/10.1007/s00268-010-0683-1] [PMID: 20607258]
[20]
Lee H, Li JY, Fan JH, et al. Risk factors for breast cancer among Chinese women: a 10-year nationwide multicenter cross-sectional study. J Epidemiol 2014; 24(1): 67-76.
[http://dx.doi.org/10.2188/jea.JE20120217] [PMID: 24270059]
[21]
Wang Q, Li J, Zheng S, et al. Breast cancer stage at diagnosis and area-based socioeconomic status: a multicenter 10-year retrospective clinical epidemiological study in China. BMC Cancer 2012; 12: 122.
[http://dx.doi.org/10.1186/1471-2407-12-122] [PMID: 22455370]
[22]
Lu WL, Li HX, Qian BY, et al. The clinical characteristics and prognosis of Chinese early stage breast cancer patients: a retrospective study. Breast J 2010; 16(3): 331-3.
[http://dx.doi.org/10.1111/j.1524-4741.2010.00903.x] [PMID: 20210801]
[23]
Wang J, Wu Q, Hu XT, Tian T. An integrated platform for reverse engineering protein-gene interaction network. Methods 2016; 110: 3-13.
[http://dx.doi.org/10.1016/j.ymeth.2016.08.001] [PMID: 27514497]
[24]
Bar-Joseph Z, Gerber G, Simon I, Gifford DK, Jaakkola TS. Comparing the continuous representation of time-series expression profiles to identify differentially expressed genes. Proc Natl Acad Sci USA 2003; 100(18): 10146-51.
[http://dx.doi.org/10.1073/pnas.1732547100] [PMID: 12934016]
[25]
Vogelstein B, Kinzler KW. Cancer genes and the pathways they control. Nat Med 2004; 10(8): 789-99.
[http://dx.doi.org/10.1038/nm1087] [PMID: 15286780]
[26]
Negrini S, Gorgoulis VG, Halazonetis TD. Genomic instability--an evolving hallmark of cancer. Nat Rev Mol Cell Biol 2010; 11(3): 220-8.
[http://dx.doi.org/10.1038/nrm2858] [PMID: 20177397]
[27]
Tubbs A, Nussenzweig A. Endogenous DNA damage as a source of genomic instability in cancer. Cell 2017; 168(4): 644-56.
[http://dx.doi.org/10.1016/j.cell.2017.01.002] [PMID: 28187286]
[28]
Lengauer C, Kinzler KW, Vogelstein B. Genetic instability in colorectal cancers. Nature 1997; 386(6625): 623-7.
[http://dx.doi.org/10.1038/386623a0] [PMID: 9121588]


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VOLUME: 15
ISSUE: 3
Year: 2020
Page: [253 - 259]
Pages: 7
DOI: 10.2174/1574893615666191220141548
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