I have heard that there is a relation between cancers and bad luck, not heredity or lifestyle. Is there any published work on this point?
Cancer risk: bad behaviour, bad luck or bad journalism?
http://www.theguardian.com/science/grrlscientist/2015/jan/02/bad-luck-bad-journalism-and-cancer-rates
Many thanks Dr. Jasmin S. Nurkovic!
Yes Priyanka Srivastava, we're very serious. May be this hypothesis right. If thought in the problems which arisen due to depression with many proofs, may you think again in this hypothesis.
Mathematical mistakes makes results of Christian Tomasetti and Bert Vogelstein mean nothing.
"Choosing the distribution parameters so that the cumulative distribution function fits the incidence curve they get that only 13.5% of population is susceptible to colon and 22%-to prostate carcinomas. Unfortunately they use wrong formulas for Weibull distribution as well as for statistical criteria[5]and thus this conclusion is unfounded too. Nevertheless the main problem of this research is not the incorrect equalities but the hidden assumptions which, as it usually happens, are neither discussed nor even mentioned. "
……………
Medics usually tell us "Don’t treat yourself" and they are right as they have much more knowledge about diseases than we do. Maybe we may give them a similar advice: "Don’t do maths yourself", since we know it better?
https://www.researchgate.net/publication/310326046_Weibull_Distribution_Theory_of_Cancer_Age-Specific_Incidence_from_the_Mathematician%27s_Point_of_View
Article Weibull Distribution Theory of Cancer Age-Specific Incidence...
The following paper was brough up by Ijaz at the web Group of the Theodor-Billroth-Academy (TBA) at LinkedIn and it might be of importance for critical thinking:
Chronic inflammation initiates pancreatic carcinogenesis
- without K-ras mutations and
- in p53 absence
Oncogene 2017:
Abstract
Chronic inflammation (CI) is a risk factor for pancreatic cancer (PC) including the most common type, ductal adenocarcinoma (PDAC), but its role and the mechanisms involved are unclear. To investigate the role of CI in PC, we generated genetic mouse models with pancreatic specific CI in the presence or absence of TP53. Mice were engineered to express either cyclooxygenase-2 (COX-2) or IκB kinase-2 (IKK2), and TP53+/+ or TP53f/f specifically in adult pancreatic acinar cells by using a full-length pancreatic elastase promoter-driven Cre. Animals were followed for >80 weeks and pancreatic lesions were evaluated histologically and immunohistochemically. The presence of K-ras mutations was assessed by direct sequencing, locked nuclei acid (LNA)-based PCR, and immunohistochemistry. We observed that sustained COX-2/IKK2 expression caused histological abnormalities of pancreas, including increased immune cell infiltration, proliferation rate and DNA damage. A minority of animals with CI developed pre-neoplastic lesions, but cancer was not observed in any TP53+/+ animals within 84 weeks. In contrast, all animals with CI-lacking TP53 developed various subtypes of PC, including acinar cell carcinoma, ductal adenocarcinoma, sarcomatoid carcinoma and neuroendocrine tumors, and all died within 65 weeks. No evidence of K-ras mutations was observed. Variations in the activity of the Hippo, pERK and c-Myc pathways were found in the diverse cancer subtypes. In summary, chronic inflammation is extremely inefficient at inducing PC in the presence of TP53. However, in the absence of TP53, CI leads to the development of several rare K-ras-independent forms of PC, with infrequent PDAC. This may help explain the rarity of PDAC in persons with chronic inflammatory conditions.
http://www.nature.com/onc/journal/v36/n22/full/onc2016461a.html
http://www.nature.com/onc/journal/v36/n22/full/onc2016461a.html
Someone may be interested reading carefully the commentary written commentary by Dr. Stuart G. Baker, National Cancer Institute, Bethesda, MD, USA, which was brought up by Ijaz:
“The questionable premises underlying the search for cancer driver mutations and cancer susceptibility genes.”
Dr. Stuart G. Baker, National Cancer Institute, Bethesda, MD, USA
http://www.cognitivephilology.uniroma1.it/index.php/Organisms/article/view/13873/13628
http://www.cognitivephilology.uniroma1.it/index.php/Organisms/article/view/13873/13628
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