Cancer Research

Can cancer biopsies spread more cancer? Some patients, and a few doctors think so. 

Fine needle aspiration is a minimally invasive technique that uses a thin and hollow needle to extract a few cells from a tumor mass. Some contend that a biopsy can cause some cancer cells to spread and it has become a strongly-held belief, but is it true?

It came about because some people who got biopsies did have cancer spread but it was so rare that answers were difficult to find. A recent study of more than 2,000 patients by researchers at Mayo Clinics concludes it is a myth and that patients who received a biopsy had a better outcome and longer survival than patients who did not have a biopsy.

Researchers have identified mutations which occur at four specific sites in what is known as the "hTERT promoter" in more than 75 percent of glioblastomas and melanomas.  

Telomerase is an enzyme largely responsible for the promotion of cell division. Within DNA, telomerase activation is a critical step for human carcinogenesis through the maintenance of telomeres. However, the activation mechanism during carcinogenesis - why cancer gets turned "on" - is not yet wholly understood. What is known is that transcriptional regulation of the human telomerase reverse transcriptase (hTERT) gene is the major mechanism for cancer-specific activation of telomerase.

Older men with locally advanced prostate cancer benefit by adding radiation treatment to hormone therapy versus hormone therapy alone, according to a new study which found that hormone therapy plus radiation reduced cancer deaths by nearly 50 percent in men aged 76 to 85 compared to men who only received hormone therapy.

Past studies have shown that 40 percent of men with aggressive prostate cancers are treated with hormone therapy alone, exposing a large gap in curative cancer care among "Baby Boomers" as they approach their their 70s. 

The gene TRK was shown to cause a small percentage of colon cancers in 1982 and then in 2013 and 2014, sequencing of tumor samples found fusions of the TRK family of genes in at least 11 tumor types, including lung, breast and melanoma . 

The TRK family of genes, including NTRK1, NTRK2 and NTRK3 are important in the developing nervous system. In the womb, these genes and the proteins they encode are essential for the growth and survival of new neurons. After birth, these genes are unneeded in many tissues and so are programmed to go dormant.

Some cancers wake them up - when improperly fused with other nearby genes, genes in the TRK family can restart their ability to signal cells to grow and become immortal, which in adult tissues can cause cancer.

There is no question there are genetic and environmental components to cancer but a statistical model that measures the proportion of cancer incidence across many tissue types finds that cancer is caused mainly by random mutations that occur when stem cells divide.

According to scientists from the Johns Hopkins Kimmel Cancer Center, two-thirds of adult cancer incidence across tissues can be explained primarily by "bad luck," when these random mutations occur in genes that can drive cancer growth, while the remaining third are due to environmental factors and inherited genes.

The implications of their model range from altering public perception about cancer risk factors to the funding of cancer research, they say.

New prostate screening guidelines recommend that the prostate-specific antigen (PSA) test not be used to screen for prostate cancer based on evidence that shows uncertain benefits and   an increased risk of harm. 

Prostate cancer is the most commonly diagnosed non-skin cancer in men and the third most common cause of death from cancer in men in Canada and elsewhere. In modern times, the prognosis for most prostate cancers is good with a 10-year survival rate of 95%. Prostate cancer is generally slow to progress and today is usually not life-threatening. 

The researchers at the Cancer Research UK Manchester Institute discovered that the ties which lash cells together - controlled by a protein called TIAM1 - are chopped up when cell maintenance work goes wrong.

Diagnostic screening systems for breast cancer like X-ray computed tomography (CT) and mammography are effective at detecting early signs of tumors but they subject patients to ionizing radiation and sometimes inflicting discomfort on women who are undergoing screening, because of the compression of the breast that is required to produce diagnostically useful images. 

Effective treatments for lung cancer has been challenging because so many genetic mutations play a role in the disease. Mutations, by their very definition, are difficult to predict, they occur due to random cosmic rays over time and in other natural ways, and can be aggravated by some aspects of the environment.

But by analyzing the DNA and RNA of lung cancers, researchers at the University of Michigan Comprehensive Cancer Center found that patients whose tumors contained a large number of gene fusions had worse outcomes than patients with fewer gene fusions. Gene fusions are a type of genetic anomaly found in cancers that occurs when genes get rearranged and fuse together. 

Although prostate cancer will affect over 23,000 U.S. men next year, the individual genes that initiate prostate cancer formation are poorly understood, but finding an enzyme that regulates this process could provide excellent new prevention approaches for the malignancy.

Sirtuin enzymes have been implicated in neurodegeneration, obesity, heart disease, and cancer and a new paper in The American Journal of Pathology finds that the loss of SIRT1 drives the formation of early prostate cancer (prostatic intraepithelial neoplasia) in mouse models of the disease.