I came across the two articles below in the literature recently, hope this helps.

A review article:

Stephanie A. Hills, John F.X. Diffley

DNA Replication and Oncogene-Induced Replicative Stress

Current Biology, Volume 24, Issue 13, 7 July 2014, Page 1563

A research article:

Bartkova et al.

Replication stress and oxidative damage contribute to aberrant constitutive activation of DNA damage signalling in human gliomas

Oncogene (2010) 29, 5095–5102; doi:10.1038/onc.2010.249

Thanks Fadi.These were very useful. 

Here is another study which I found meanwhile, with some clean concrete evidence :-

Cancer Biol Ther. 2010 Feb;9(3):246-52. Epub 2010 Feb 25.

DNA damage signaling is activated during cancer progression in human colorectal carcinoma.

Oka K1, Tanaka T, Enoki T, Yoshimura K, Ohshima M, Kubo M, Murakami T, Gondou T, Minami Y, Takemoto Y, Harada E, Tsushimi T, Li TS, Traganos F, Darzynkiewicz Z, Hamano K.

Good question - I shall be interested to hear of papers with quantitative information on endogenous DNA damage as cells move through the carcinogenic process. AS I suspect you know, genomic instability is considered a cancer hallmark of cancer and predictor of poor prognosis for some cancers. A key point is that DNA damage is constantly occurring in cells but mutagenesis is low due to DNA repair. So certain DNA lesions may have large biological effects if they are not efficiently and accurately removed by DNA repair, which can be defective in cancers, as best known for those with genetic DNA repair defects. Thus, therapeutic strategies can directly or indirectly target DNA damage or DNA damage responses that are reduced in many cancers. In cases of inherited DNA repair defects, such as those that cause Xeroderma pigmentosum, the increase in DNA damage is large and obvious during carcinogens. Similarly, endogenous damage has been measured to increase in peripheral blood lymphocytes of endometrial cancer patients with a family history of cancer - BMC Cancer 2014, 14:765 doi:10.1186/1471-2407-14-765: http://www.biomedcentral.com/1471-2407/14/765 . But following dame during cancer progression in mice for example would be interesting. 

Thanks John for your informative response and an interesting reference. I agree with you that genomic instability is one of the key carcinogenic event , maybe even a pre-dominant one.  I also agree that following real time dynamics of DNA-damage in the process of  carcinogenesis  would be indeed very vital for our understanding of its role in the process. But I think the field could move much faster with identification  of markers in addition to gH2AX. Interestingly, an extra allele of CHK1has been shown to promote transformation in mice PMID: 22370720.

An in-depth reading of the current article could may be of help.

Best regards

Robert