September 4th, 2007 by Dr. Val Jones in News
2 Comments »
I subscribe to Eureka Alert Breaking News – and although a lot of their press releases are on small studies of questionable relevance, I do think that some of the basic science research is provocative. Let’s see if I can pique your interest with the best of this week’s Petri dish news:
1. Tylenol may inhibit bone growth? A small study conducted at the University of Granada suggested that bone forming cells (called osteoblasts) were inhibited by a Tylenol bath. As far as pain killers are concerned, we’ve known for a while that non steroidal anti-inflammatory medications (NSAIDs) may indeed inhibit bone growth. But since Tylenol is not an NSAID, we were hoping that it would not adversely affect bone healing. Could this mean that Tylenol is not so great for bone surgery pain after all? That’s a stretch… but an interesting question.
2. Can you clean blood with a laser? Boy it sure would be nice to be able to kill all the potential viruses in blood used for transfusions. Apparently there’s a new pulsed laser technique that shows some promise in fracturing viruses with laser vibrations. So far, the laser was successful in reducing bacterial viruses by 1000x. Next up? Let’s see what the technique can do to Hepatitis C and HIV viruses.
3. Skinny people might have a “skinny gene.” Scientists have been studying a gene called Adipose (Adp) for over 50 years now. It was first discovered in fat fruit flies (I kid you not). Apparently if the Adp gene doesn’t work well, the flies become fat and “have difficulty getting around.” Worms, mice, and humans seem to have the same gene. Further analysis might unlock the secret to the genetics of thinness. Or maybe we should just eat less and exercise more?This post originally appeared on Dr. Val’s blog at RevolutionHealth.com.
March 26th, 2007 by Dr. Val Jones in Opinion
No Comments »
-Continued from previous post–
In contradistinction to these patients exposed to tumor cells who did not develop malignancies, other studies have shown that normal cells can become malignant in an environment where a malignancy had developed. One study, for example, followed two leukemia patients whose bone marrows were eradicated with radiotherapy and who subsequently received bone marrow transplants from normal donors. Two to four months following the procedure, the transplanted bone marrow donor cells were found to have become leukemic.(11)
Clearly, cellular environment plays a critical role in cancer development. Malignant cells infused into a normal environment may not produce a tumor while normal cells placed into an environment that had previously harbored a tumor can become malignant. We are no longer even sure from what cell type a particular cancer develops. Stomach cancer in mice has been shown to originate not from the lining cells of the stomach, as we had thought, but from bone marrow cells responding to experimentally-induced stomach inflammation.(12) The problem may be the environment not the “malignant” cell.(13)
Are we at least able to recognize clinically significant cancer? Can we confidently say, as one judge did when defining pornography, “I know it when I see it.?” Apparently not.
Autopsies on people who died of non-malignant causes have caused us to re-examine our definition of cancer. Patients with previously treated Hodgkins disease—showing no clinical evidence of tumor and thought to have been cured, who died of unrelated causes—were found on autopsy to have residual foci of the disease.(14) Although thyroid cancer is diagnosed in only 1 in 1000 adults between the ages of 50 and 70, on autopsy it has been found in 1 of 3 adults.(15) The prevalence of clinically apparent prostate cancer in men 60 to 70 years of age is about 1%; nevertheless, over 40% of men in their 60s with normal rectal examinations have been found to have histologic evidence of the disease,(16) and autopsy studies have found evidence of prostate cancer in 1 out of 3 men by age 50(17), a finding which rises to 7 out of 10 men by age 80.(18) Similarly, clinical breast cancer is diagnosed in 1 out of 100 women between the ages of 40 and 50;(19) on autopsy it was found in a startling 1 out of 2.5 women in this age group. Moreover, over 45% of the autopsied women had more than one focus of breast cancer and 40% had bilateral breast cancer.(20)
What, then, is cancer? What is responsible for the clinical behavior of cancer, sometimes lying dormant and undiagnosed because it causes no symptoms, sometimes progressing inexorably to death?
For the present, we don’t know the answers to these questions. We have developed treatment programs that offer the best current options for cure, but we should, and do, remain unsatisfied with these approaches. First, because they don’t always work and, second, because with rare exception, they are based on trial and error, not on an understanding of the disease process we are treating.
Once we identify the processes responsible for the accumulation of cells into tumors, we can treat these conditions more effectively, reduce or eliminate the side effects associated with many of our current “best practice” treatments, and remove the terror currently shadowing cancer the way terror used to shadow diseases like syphilis, tuberculosis, and pernicious anemia before we learned how they were caused and developed treatments directed at those causes. We are making progress. Stay tuned.
REFERENCES
1. Bennington JL. Cancer of the kidney – etiology, epidemiology and pathology. Cancer 1973;32:1017-29
2. Salvador AH, Harrison EG Jr, Kyle RA. Lymphadenopathy due to infectious mononucleosis: its confusion with malignant lymphoma. Cancer 1971;27:1029-40
3. Lukes RJ, Tindle BH, Parker JW. Reed-Sternberg-like cells in infectious mononucleosis. Lancet 1969;2:1003-4
4. Agliozzo CM, Reingold IM. Infectious mononucleosis simulating Hodgkin’s disease: a patient with Reed-Sternberg cells. Am J Clin Pathol 1971;56:730-5
5. Mirra JM, Kendrick RA, Kendrick RE. Pseudomalignant osteoblastoma versus arrested osteosarcoma. A case report. Cancer 1976;37:2005-14
6. Taubert HD, Wissner SE, Haskins AL. Leiomyomatosis peritonealis disseminata. Obstet Gynecol 1965;25:561-74
7. Croslend DB. Leiomyomatosis peritonealis disseminata: a case report. Am J Obstet Gynecol 1973;117:179-81
8. Mintz B, Illmensee K. Normal genetically mosaic mice produced from malignant teratocarcinoma cells. Proc Natl Acad Sci 1975;72(9):3585-9
9. Lanman JT, Bierman HR, Byron RL Jr. Transfusion of leukemic leukocytes in man. Hematologic and physiologic changes. Blood 1950;5:1099-1113
10. Greenwald P, Woodard E, Nasca PC, Hempelmann P, Dayton P, Maksymowicz G, Blando P, Hanrahan R jr, Burnett WS. Morbidity and mortality among recipients of blood from preleukemic and prelymphomatous donors. Cancer 1976;38:324-8
11. Thomas ED, Bryant JI, Bruckner CD, Clift RA, Fefer A, Neiman P, Ramberg RE, Storb R. Leukemic transformation of engrafted human marrow. Transpl Proc 1972;4:567-70
12. Houghton J, Stoicov C, Nomura S, Rogers AB, Carlson J, Li H, Cai X, Fox JG, Goldenring JR, Wang TC. Gastric cancer originating from bone marrow-derived cells. Science 2004;306:1568-71
13. Bluming AZ. Cancer: The eighth plague – A suggestion of pathogeneisis. Isr J Med Sci 1978;14:192-200
14. Dorfman RF. Biology of malignant neoplasia of the lymphoreticular tissues. J Reticuloendothelial Soc 1972;12:239-56
15. Harach HR, Franssila KO, Wasenius VM. Occult papillary carcinoma of the thyroid. A “normal” finding in Finland. A systematic autopsy study. Cancer 1985; 56 (3): 531-8
16. Montie JE, Wood DP Jr, Pontes E, Boyett JM, Levin HS. Adenocarcinoma of the prostate in cytoprostatectomy specimens removed for bladder cancer. Cancer 1989;63:381-5
17. Oottamasathien S, Crawford D. Should routine screening for prostate-specific antigen be recommended? Arch Intern Med 2003;163:661-2
18. Pienta KJ, Esper PS. Risk factors for prostate cancer. Ann Intern Med 1993;118:793-803
19. Feldman AR, Kessler L, Myers MH, Naughton MD. The prevalence of cancer, estimates based on the Connecticut Tumor Registry. N Engl J Med 1986; 315:1394-7
20. Nielsen M, Thomsen JL, Primdahl S, Dyreborg U, Andersen JA. Breast cancer and atypia among young and middle-aged women: a study of 110 medicolegal autopsies. (Br J Cancer 1987; 56:814-9
This post originally appeared on Dr. Val’s blog at RevolutionHealth.com.
March 21st, 2007 by Dr. Val Jones in News
No Comments »
As spring approaches, we can expect a new onslaught of pollen, bugs, and mud puddles. Mosquito eggs will hatch in stagnant water, and a new generation of hungry little disease vectors will be lurking in wooded areas, awaiting their first meal.
Luckily for those of us who live in North America, those annoying mosquito bites are unlikely to infect us with malaria.
A team of scientists committed to eradicating malaria (one of my personal favorite parasites) has taken a new approach to reducing transmission rates: creating a strain of malaria-immune mosquitoes.
I had been under the mistaken impression that mosquitoes lived in perfect harmony with malaria parasites, but apparently the organisms can make them quite ill as well. Not ill enough to die immediately (hence their ability to spread the disease) but ill enough to die prematurely.
So if we could create a malaria immune mosquito, we could give them a survival advantage over their peers, thus slowly influencing the mosquito population in favor of the new strain. This could result in a new population of mosquitoes who could not harbor malaria.
In humans, malaria parasites have learned how to attach themselves to red blood cell proteins and incubate inside the cells. In mosquitoes, the parasites latch on to a protein (called SM1) on the surface of epithelial cells of their gut lining. Through the miracle of genetic engineering, we’ve managed to alter the SM1 proteins in certain mosquitoes, making them immune to invasion by parasites they ingest through infected blood.
Although the immune mosquitoes are not ready for prime time release in malaria endemic countries (the research only showed that the scientists could genetically engineer resistance to one strain of malaria), it sure would be interesting to see if we could use mosquitoes themselves to fight a disease that claims the lives of over one million people per year.
This is a rare case of a problem becoming the solution!
This post originally appeared on Dr. Val’s blog at RevolutionHealth.com.
February 21st, 2007 by Dr. Val Jones in News
1 Comment »
Malaria is caused by a crafty little parasite that has become resistant to many medicines. But now researchers at Northwestern University have discovered a chink in its armor – a blood pressure medicine called propranolol. Who knew that a common beta-blocker used to treat hypertension might provide the death blow to such a scourge?
Usually, malarial parasites infect their host’s blood stream through a mosquito bite, and then congregate in the liver and pounce on red blood cells as they pass by. They have a way of adhering to the red blood cells via certain surface receptors (beta 2 adrenergic receptors linked to Gs proteins). They latch on to the red cells and then burrow into the cell and hijack it in order to reproduce inside it. Then, like the horror movie Alien, once they’re fully grown (into “schizonts”) they burst out of the cells and roam free to repeat the process all over again.
Now propranolol happens to block the Gs proteins, which effectively makes it impossible for the parasites to attach themselves to the red blood cells (which they need to use to reproduce themselves).
So what’s the caveat to of all this? Well, folks don’t know they have been infected with malaria until they have symptoms, and the symptoms include high fevers and low blood pressure… so giving someone a medicine that lowers their blood pressure even further might not be a good idea.
The other caveat is that propranolol works like a charm in the test tube, and in mice, but we haven’t yet tried it out in humans who have malaria.
Still, it seems to me that a little bit of propranolol might go a long way to preventing malarial infections in at risk populations. I’ll be interested to see what further studies show!
And if you’re interested, I’ll create a few more blog posts about parasites and other creepy crawly human invaders… Just let me know if you can handle more of this!
This post originally appeared on Dr. Val’s blog at RevolutionHealth.com.
