I recommend you read more on the multi-hit theory of carcinogesis to better understand the these observed dynamics

Thank you@ Yeboah Kwaku Opoku but does the multi hit theory apply to all the types of cancers and does it really explain the differences in the rates at which cells form cancer on exposure to a carcinogen.

I think the multi hit theory explains the continuous accumulation of mutations or stressors which causes some cells to develop cancers over time. But what i am trying to understand is that, for epithelium cells that have been introduced to the same amount of carcinogen for a certain duration and intensity. Why do some of the cells become cancer faster. What accounts for the differences in the susceptibility of the cells to cancer?

I will be very glad to understand this.

Amended on 11 January 2019

I would like to express my opinion.

Cancer (hepatocellular carcinoma/HCC) is due to co-integration of +ssRNA vira HIV-1 and Flavivirus (HCV, Hog cholera virus/Classical swine fever virusor/CSFV and/or GB virus C/GBV-HGV/GBV-C) (please see file; HepG2 Fucoidan). Flavivirus seems to be integrated by the help of reverse transcriptase (RT) and integrase (IN) of the HIV-1. Pacreatic cancer seems to be due to co-infection of HIV-1 and human coronavirus/HCoV (our unpublished result). It is important that these cancer inducing virus is only co-infected to the cancer tissue.

Genome polyprotein (Hog cholera virus/Classical swine fever virus/CSFV) is present only HCC tissue of named No.6 (Japanese, male; who has happily survived) at a low concentration of 0.74 μg/mg of tissue protein. LC (liver cirrhosis) tissue of No.6 has no CSFV. This patient (with HCV) has survived due not to be infected by HIV-1, but infected by SIV. Effect of SIV on inate immune system seems to be weaker than HIV-1.

It is noteworthy that cancer marker-proteins are not present in Humans; i.e., Immuno therapy to human cancer can not be possible. However, it is also noteworthy that disappearance of Apo B-100 is a marker of true liver cancer to leading patients to death (HepG2, and HCC tissue with PBC). This disappearance of Apo B-100 in HCC tissues seems to be occurred via the gene repression by Pegivirus of GB virusC/GBV-C in the case of HepG2 and Pestivirus of Hog cholera virus/Classical swine fever virus/CSFV in the case of HCC tissue with PBC.

Hepatoma HepG2 (cultured without fucoidan; American Caucasoid, male, who has sadly deceased) has 1st Envelope glycoprotein gp160 (HIV-1) at 15.8, 2nd Genome polyprotein (GB virus C/GBV-HGV/GBV-C) at 15.4, 3rd Spike glycoprotein (Human coronavirus/HCoV） at 10.0, and 4th Genome polyprotein (HCV) at 7.8 μg/mg of cell protein, respectively. Interestingly, healed hepatocyte HepG2 (cultured with fucoidan for 3 days) has no GB virus C/GBV-C (please see file; HepG2 fucoidan).

HCC tissue with PBC (Japanese, female; who has sadly deceased) has 1st Genome polyprotein (Hog cholera virus/Classical swine fever virus/CSFV) at 43.6, 2nd Genome polyprotein (HCV) at 35.4, 3rd Envelopment polyprotein/M polyprotein (Hantaanvirus/HTNV/Prospect hill virus/PHV) at 34.7, and 4th Genome polyprotein (HAV) at 24.0 μg/mg of tissue protein, respectively.

It is also noteworthy that HepG2 unexpectedly has no HBV at all (please see again file; HepG2 fucoidan). HBV is present in a normal liver (pseudo-liver cancer) (my unpublished observation). Therefore, dsDNA virus such as HBV, Human papillomavirus/HPV, and SV-40 is not linked to the human cancer at all.

Stresses such as X-ray, radio wave, sulphite, mental stress, sleeplessness, and chemical carcinogen induce the activation or release of previously integrated viral genes of +ssRNA virus from the host human DNA of the cancer tissue (please see file; The Fascio effect).

Cancer is not caused by mutation, change of gene, or changes in gene expression at all (please see file; Feed by Measure).

Because

Somatic mutation theory is not correct theory for carcinogenesis

Thank you very much for your input @Mesut Tez and @Kou Hayakawa. Excuse me if i might have used mutation in my question wrongly. What i meant was, some cells form cancers more often than others. So aside the fact that different parts of the body are exposed to different concentrations of various carcinogens and also tissues having different proliferative potential, what factors again is responsible for the differences in the rate at which cells form cancers. I will be glad to understand this. Thank you very much.

because:

"Requisite driver mutations (...) are dependent upon the specific gene expression profile associated with cancer cell type (...)"

page 164 in:

https://www.researchgate.net/publication/326302952_Bioenergetics_of_life_disease_and_death_phenomena/stats

and also:

Kauffman S (1969a) Homeostasis and differentiation in random genetic control networks. Nature 224:177–178

Kauffman SA (1993) The origins of order. Oxford University Press, New York

Huang S, Ernberg I, Kauffman S (2009) Cancer attractors: a systems view of tumors from a gene network dynamics and developmental perspective. Semin Cell Dev Biol 20(7):869–876

Thank you so much @Rohan Chaubal and @Andrzej Kasperski your input has been very helpful.