New research may one one day help in the diagnosis and prognosis of the nation's number four cancer killer of men and number five cancer killer of women. The killer: pancreatic cancer.

Findings from an Ohio State University study show pancreatic cancer cells may leave signs in gene-related molecules called microRNAs.

Published in The Journal of the American Medical Association, this study examined pancreatic tissue from 65 people with the disease and 42 people with chronic inflammation of the pancreas, called chronic pancreatitis.

Canadian researchers have made an unexpected discovery in a molecule that appears to drastically boost the ability of standard drugs to kill breast cancer cells. Currently, the discovery has been confined to the lab -- but researchers hope the power of this molecule, the ANK peptide, can one day be used to counter drug resistance for many women with breast cancer.

Scientists from Queen's University say the ANK peptide, not a drug by itself, gives drugs like taxol and nocodazole more than triple the ability to kill breast cancer cells. One scientist says the process of enhancing drug effectiveness is much like adding flavor to coffee to make it taste better.

This is exciting news, but the results -- published Monday in the journal Cancer Research -- only apply to lab experiments at this point. Researchers must now proceed with testing the peptide-drug combination in lab mice. If successful, they will move on to human testing. The whole process could take years. But early results are so promising that application for a U.S. patent on the peptide has already been made.

According the medical experts, breast cancer patients can become resistant to some drugs depending on duration of treatment, dose of medication, and genetic makeup.

"This peptide would be able to give them another chance," said a researcher from this study. "For those who respond reasonably well, they will do even better; for those who don't respond to this drug treatment ... we greatly hope this will make the current drug more useful by extending its impact to a wider range of people, particularly those with a resistance problem."

Tamoxifen has been used successfully for over 20 years. The researchers know that over time Tamoxifen can lose its effectiveness. Many women diagnosed with Stage IV breast cancer that have tumors that are estrogen-receptor positive can be put on Tamoxifen to control the disease. After some time the patient becomes resistant to Tamoxifen and has to be switched to another drug.

A molecule, called disulfide benzamide or DIBA, could provide a way to overcome that resistance and restore the effectiveness of Tamoxifen. Findings are published in the December issue of Cancer Cell that show how mice engineered to develop Tamoxifen resistant tumors and human breast cancer cells in the lab were given the molecule. In both cases the tumor growth slowed.

William Farrar, head of the Cancer Stem Cell Section of the National Cancer Institute's Center for Cancer Research and the studies lead author, says "DIBA is what is known as a lead compound, which means it merely opens the door to suitable drugs." He also says that "DIBA itself is probably not appropriate for humans, because of solubility problems". The team plans to try and develop another compound fashioned after the properties of DIBA and hopeful have this be able to be administered orally.

One important aspect of the research was that it focused only on an acquired resistance to Tamoxifen over time. It did not study why some estrogen positive tumors initially are resistant to the drug.

An anti-viral molecule, TBK-1, that the body uses to fight viruses, seems to be vital to the survival of cancer cells. Blocking one enzyme, aldose reductase, was found to stop colon cancer cells in cell culture laboratory tests and in mice implanted with human colon cancer cells, according to University of Texas Southwestern Medical Center researchers.

"We got the surprise that this mechanism is involved in cancer cell survival, even though it's normally involved in immune response," stated Dr. Michael White, associate professor of cell biology at the University of Texas Southwestern Medical Center.

"We found something a little bit different -- an Achilles heel of cancer cells that's apparently broadly conserved among many types of solid tumors. This is making us think that there are many other surprises awaiting discovery regarding biological systems that are inappropriately subverted during development of cancer."

The discovery is called dramatic and could lead to new treatments for colon cancer. If blocking a single anti-viral molecule does shut down the biochemical signals that promote inflammation and colon cancer cell growth, as the researchers are reporting from the results of this study, it will be a dramatic discovery.