Reduced Kidney Function Linked With Higher Risk Of Kidney And Urothelial Cancers.


Individuals with poor kidney function may require more intensive screening for these cancer types

Reduced kidney function may increase the risk of developing kidney and urothelial cancers, according to a study appearing in an upcoming issue of the Journal of the American Society of Nephrology (JASN). The findings suggest that patients with kidney disease may benefit from more intensive screenings for these types of cancer.

Chronic kidney disease and cancer are both major and growing public health problems. “While multiple studies have observed higher risks of cancer in persons with end-stage renal disease, the association of less severe kidney disease with cancer remains poorly understood,” said Alan Go, MD (Kaiser Permanente Northern California).

To investigate, Dr. Go and his colleagues analyzed information from nearly 1.2 million adult members of Kaiser Permanente in Northern California who were at least 40 years of age and who had no history of cancer, dialysis, or kidney transplantation. Kidney function was measured by estimated glomerular filtration rate (eGFR), with normal kidney function being over 60 ml/min/1.73m2 and kidney failure being below 15 ml/min/1.73m2.

During more than 6 million person-years of follow-up, 72,875 individuals developed cancer. (A person-year is the number of years of follow-up multiplied by the number of people in the study.) Among the major findings during follow-up:

Individuals with an eGFR of 45 to 59 had a 39% increased risk of kidney cancer (or renal cell carcinoma).
Individuals with an eGFR of 30 to 44 had an 81% increased risk of kidney cancer.
Individuals with an eGFR below 30 had a 100% (or a 2-fold) increased risk of kidney cancer.
Individuals with an eGFR below 30 had a 48% increased risk of urothelial cancer, which includes tumors in the bladder and ureters.
There were no significant links between eGFR and other cancer types such as prostate, breast, lung, and colorectal cancers.

The researchers noted that various biologic mechanisms may help to explain the links observed in this study. For example, kidney dysfunction causes a state of chronic inflammation and oxidative stress. “These and other mechanisms deserve further study in order to better define the link between kidney function and site-specific cancer risk,” said lead author Will Lowrance, MD, MPH (University of Utah).

In an accompanying editorial, Jonathan Hofmann, PhD and Mark Purdue, PhD (National Cancer Institute) noted that the study is “an important step forward in characterizing the relationship between chronic kidney disease and risk of renal cell carcinoma and other malignancies. Studies such as this further support an etiologic role of impaired renal function in the development of renal cell carcinoma.”

 

Source: American Society of Nephrology

 

Hebrew University Researchers Demonstrate Why DNA Breaks Down In Cancer Cells .


black-dna-dna-double-helix-dna-helicase-abstractdna-replication-model-145x88Damage to normal DNA is a hallmark of cancer cells. Although it had previously been known that damage to normal cells is caused by stress to their DNA replication when cancerous cells invade, the molecular basis for this remained unclear.

Now, for the first time, researchers at the Hebrew University of Jerusalem have shown that in early cancer development, cells suffer from insufficient building blocks to support normal DNA replication. It is possible to halt this by externally supplying the “building blocks,” resulting in reduced DNA damage and significant lower potential of the cells to develop cancerous features. Thus, hopefully, this could one day provide protection against cancer development.

In laboratory work carried out at the Hebrew University, Prof. Batsheva Kerem of the Alexander Silberman Institute of Life Sciences and her Ph.D. student Assaf C. Bester demonstrated that abnormal activation of cellular proliferation driving many different cancer types leads to insufficient levels of the DNA building blocks (nucleotides) required to support normal DNA replication.

Then, using laboratory cultures in which cancerous cells were introduced, the researchers were able to show that through external supply of those DNA building blocks it is possible to reactivate normal DNA synthesis, thus negating the damage caused by the cancerous cells and the cancerous potential. This is the first time that this has been demonstrated anywhere.

This work, documented in a new article in the journal Cell, raises the possibility, say the Hebrew University researchers, for developing new approaches for protection against precancerous development, even possibly creating a kind of treatment to decrease DNA breakage.

 

 

argin�C tm�>� �:� ne-height:11.25pt;background: white;vertical-align:baseline’>Furthermore, unlike meats, caffeinated beverages, and alcohol, fruits and vegetables do not improve the taste of cigarettes.

 

“Foods like fruit and vegetables may actually worsen the taste of cigarettes,” remarked Haibach in the statement.

The research team states that more research needs to be done to see if the results can be replicated. If the findings are replicated, the investigators will work to determine the mechanisms in fruit and vegetables that help smokers quit the habit. They also want to look into research based on other dietary factors and smoking cessation.

“It’s possible that an improved diet could be an important item to add to the list of measures to
help smokers quit. We certainly need to continue efforts to encourage people to quit and help them succeed, including proven approaches like quitlines, policies such as tobacco tax increases and smoke-free laws, and effective media campaigns,” concluded researchers in the statement.

 

Source:  redOrbit.com