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		Biological bad luck blamed in two-thirds 
		of cancer cases 
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		[January 02, 2015] 
		By Will Dunham 
		WASHINGTON (Reuters) - Plain old bad luck 
		plays a major role in determining who gets cancer and who does not, 
		according to researchers who found that two-thirds of cancer incidence 
		of various types can be blamed on random mutations and not heredity or 
		risky habits like smoking. | 
        
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			 The researchers said on Thursday random DNA mutations accumulating 
			in various parts of the body during ordinary cell division are the 
			prime culprits behind many cancer types. 
 They looked at 31 cancer types and found that 22 of them, including 
			leukemia and pancreatic, bone, testicular, ovarian and brain cancer, 
			could be explained largely by these random mutations - essentially 
			biological bad luck.
 
 The other nine types, including colorectal cancer, skin cancer known 
			as basal cell carcinoma and smoking-related lung cancer, were more 
			heavily influenced by heredity and environmental factors like risky 
			behavior or exposure to carcinogens.
 
 Overall, they attributed 65 percent of cancer incidence to random 
			mutations in genes that can drive cancer growth.
 
			
			 
			"When someone gets cancer, immediately people want to know why," 
			said oncologist Dr. Bert Vogelstein of the Johns Hopkins University 
			School of Medicine in Baltimore, who conducted the study published 
			in the journal Science with Johns Hopkins biomathematician Cristian 
			Tomasetti.
 "They like to believe there's a reason. And the real reason in many 
			cases is not because you didn't behave well or were exposed to some 
			bad environmental influence, it's just because that person was 
			unlucky. It's losing the lottery."
 
 Tomasetti said harmful mutations occur for "no particular reason 
			other than randomness" as the body's master cells, called stem 
			cells, divide in various tissues.
 
 Tomasetti said the study indicates that changing one's lifestyle and 
			habits like smoking to avoid cancer risks may help prevent certain 
			cancers, but may not be as effective for others.
 
			
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			"Thus, we should focus more research and resources on finding ways 
			to detect such cancers at early, curable stages," Tomasetti added.
 The researchers charted the cumulative number of lifetime divisions 
			in the stem cells of a given tissue - for example, lungs or colon - 
			and compared that to the lifetime cancer risk in that tissue.
 
 Generally speaking, tissues that undergo more divisions - thus 
			increasing the probability of random mutations - were more prone to 
			tumors.
 
 The study did not cover all cancer types. Breast and prostate cancer 
			were excluded because the researchers were unable to ascertain 
			reliable stem cell division rates.
 
 (Reporting by Will Dunham; Editing by Mohammad Zargham)
 
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