Biomedical researcher Trevor Marshall is currently at the “Understanding Aging” conference in UCLA where, in his talk, he will bring up an increasingly plausible possibility – namely that our stem cells can become infected with bacteria that contribute to the aging process. Serendipitously, a study released this week by a group of researchers at Ohio State University College of Medicine in Columbus provides evidence that Marshall may be on the right track. At a June 2nd meeting of the American Society of Clinical Oncology the team, under the direction of Sanford Barsky PhD, reported that data obtained from a study on organ transplant donors/recipients supports the hypothesis that many, if not all cancers, are caused when stem cells somehow go bad.

Stem cells allow our organs renew themselves over the course of time. As described by a recent article in the Economist, every organ and tissue in the body has its own collection of stem cells. When these cells divide, they produce two very different daughter cells. One resembles the parent stem cell and thus allows the process of regeneration in the same organ to continue. The progeny of the other differentiate into mature cells within the skin, kidney, lung or what have you. In a healthy organ, the stem cells divide only when needed—usually in response to injury or when other cells have died.

Because dividing cells have been associated with tumors, so have stem cells. The association is commonly explained by the hypothesis that under certain conditions, stem cells somehow lose control and begin to divide endlessly, causing a tumor to form. Based on this hypothesis, Barsky set out to use a registry of US government health data in order to track the fate of stem cells in organ transplant recipients.

His goal was to track the fate of stem cells after they have been implanted, via an organ transplant, into a new host. To this end, he created a clever method to keep track of donor and recipient stem cells. He realized that, in many cases, his team could determine the origin of a transplanted stem cell based on its sex. Cells derived from males carry an X and a Y chromosome, while the cells of females cells carry two X chromosomes.

This means that if a woman develops cancerous cells containing a Y chromosome after transplant surgery, the cells are derived from a male organ donor. Similarly, if a male develops a tumor after a transplant operation, and the cells contain only X chromosomes, they undoubtedly came from a female donor. In order to determine the sex of the stem cells examined, Barsky’s team labeled slices of recipient tumors with green fluorescent tags that bind to the X chromosome and red tags that bind to the Y. When tagged in this manner, cells of each sex glowed brightly in different colors when viewed using specific tools.

Barsky and team sifted through a patient registry of transplant recipients and identified 280 people who had undergone an organ transplant and later developed a solid tumor. In nearly half the cases, donor and recipient were of different sexes. In fact, the results turned up an abundant number of transplant-derived cancers: in 12% of cases, the sex of the tumor matched the donor rather than the recipient. For example, a 62-year-old man developed colon cancer ten years after receiving a kidney transplant from a female donor. The colon-cancer cells lacked a Y chromosome, meaning they had to be female in origin. In a separate instance, a 48-year-old woman developed skin cancer nine months after receiving a bone-marrow transplant from a man. Her tumor cells had a Y chromosome, making it clear that the cancer had arisen from donated bone marrow cells.

Closer examination of the DNA in the tumor cells and surrounding tissue showed that the tumors definitely did originate from the donor organs rather than those of the recipients. Dr. Barsky also found that if a tumor formed in the transplanted organ, it could be derived from either recipient or donor cells. In each of these cases, the tumor that formed resembled any other tumor that would form in that site. The 48-year-old woman’s looked like skin cancer, not cancer of the bone marrow. The 62-year-old man’s looked like colon cancer and not like a kidney tumor.

Naturally, Barsky came up with a hypothesis to explain his observations. He postulated that if donor stem cells migrate to a new site in an organ recipient, the cells can take on the behavior and appearance appropriate to that location—losing the identity they had once held in the donor’s body. Having reached a new location, they somehow “go awry”, leading to the formation of a tumor. The assumption that stem cells can migrate to new organs isn’t far fetched, as biologists have confirmed that stem cells in the bone marrow move into the blood stream.

And yet, the probability reigns high that Barsky’s hypothesis fails to include a major component of tumor formation and cancer pathogenesis in stem cell recipients and cancer patients in general. What’s the missing puzzle piece? You guessed it! Bacteria. The knowledge that the cells of cancer patients are likely teeming with chronic, intraphagocytic, metagenomic bacteria (often referred to as the Th1 pathogens) allows for other, likely more accurate, interpretations of Barsky’s data.

First off, it’s important to note that the presence of bacteria in cancer studies run high. For example, in 2006, D.L. Mager and team published a review article in the Journal of Translational Medicine called, “Bacteria and Cancer: Cause, or Cure?” According to Mager, “An overwhelming body of evidence has determined that relationships among certain bacteria and cancers exist.” In the paper, Mager details how research teams around the world have implicated Salmonella typhi in gallbladder cancer, Streptococcus bovis and E.coli in colon cancer, andChlamydia pneumoniae in lung cancer. According to Mager, the mechanisms by which bacterial agents may induce carcinogenesis include “chronic infection, immune evasion, and immune suppression.”

Not to mention the fact that numerous researchers have actually detected bacteria inside the cells of cancer patients, including Dr. Alan Cantwell, who used acid-fast staining to identify bacteria in patients with Hodgkin’s Disease, lymphoma, prostate cancer and other immunological diseases.

If the Th1 pathogens can infect the stem cells – and growing evidence indicates that they do – then in many cases, transplant recipients may simply be given organs in which the stem cells are infected with chronic bacterial forms. Under such circumstances, the stem cells themselves don’t contribute to tumors and the pathogenesis of cancer. Rather, the bacteria inside the stem cells spread from an infected donor organ to other areas of the body, where, after infecting the stem cells of the new organ, they proceed to cause the development of tumors and cancer in the new area of the body. Rather than the stem cells dividing rapidly, the bacteria spread rapidly, leading to a large number of infected cells.

Or, in a similar scenario, infected stem cells from a donor organ migrate to other areas of the body. Once at a new location, the stem cells transform into cells of the new organ. Meanwhile, the bacteria inside them spread to other cells of the organ, causing a clump of infected cells to develop that eventually turns into a tumor.

“In this second scenario, the donor tissues (containing infected stem cells) spread themselves, via the bloodstream, to the area which becomes cancerous,” argues Marshall.

So while Barsky argues that the new data support the idea that tumors arise from stem cells that have gone wrong, those familiar with the Marshall Pathogenesis realize that the reason the cells have “gone wrong” is almost certainly because they are infected with bacteria.

So there we have it. More evidence which suggests that the Th1 pathogens may infect the stem cells just as easily as they infect other cells types. And since the resiliency of the stem cells strongly contributes to the aging process, the possibility opens up a Pandora’s Box of possible aging-related phenomena. Thus, Barsky’s research not only allows for a better understanding of tumor development, it also brings us one step closer to understanding the processes that may hamper longevity and resiliency.