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Cancer: do we really understand it? Part 2

-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.


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

Spider saves man from cancer

In my last blog post I was describing how adversity can be used for good, and as I was reading the medical news this morning I found another great example. While gardening, a British man was bitten on the neck by a spider. Now, the report doesn’t say exactly what type of spider this was, but judging from the outcome it was probably not a black widow or brown recluse. I’m assuming that the insect was some sort of common garden spider, though it must have had “fangs.” (Imagine my sister recoiling in horror here.)

As it turned out, the spider bit the man right next to a growth on his neck that he hadn’t noticed before. When he went to the doctor’s office to have the bite inspected, they found the growth and decided to biopsy it. The growth was cancerous, and the medical team was able to remove it before it had spread anywhere.

The little spider inadvertently saved a man from cancer. As he weaves his web, nestled between the coarse, hairy leaves of turnip plants, this tiny creature may never understand his contribution to humanity. Small actions can have a positive ripple effect, and a seemingly bad experience can save a life.

This post originally appeared on Dr. Val’s blog at

Hope for accident prone kids

My mother had a good deal of trouble with me, but I think she enjoyed it.

–Mark Twain

Parenting is a difficult job – and one that few would sign up for given full advanced disclosure. I suppose my parents had their share of woes – my near-death experience as an infant, my being mauled by a vicious dog as a toddler, my getting lost in the woods (collecting poisonous toad stools) at age 4, my facial surgery after a bicycle accident, my head injury from a fall out of the tree house, my toboggan versus barbed wire fence encounter, my front teeth versus metal bar incident, my rib fractures and nearly ruptured spleen from another fall from a bunk bed, and my ski accident requiring knee reconstruction surgery… I guess you could call me accident prone.

Looking back it makes sense why my parents encouraged me not to play contact sports, but pursue academics. I took to jogging and tennis instead (yes, I managed to sprain my ankle and catch a racket to the eye nonetheless), and physical training in the gym. But my redirection towards reading and homework was probably a good thing – as it helped me to develop intellectual discipline, and at the very least kept me out of the ER.

So what is the moral of this story? I guess if you have a kid who’s physically challenged – or at least seems to be a magnet for high velocity metal objects, do not lose heart. With a little direction, he or she can grow up to become a doctor who helps other kids who injure themselves repeatedly in creative and unexpected ways.

Were you an accident prone kid, or do you have an accident prone kid? I’d like to hear some of your war stories!

This post originally appeared on Dr. Val’s blog at

Informed consent & the animal guessing game

Growing up in Canada, my family spent a lot of time in the car. While my European friends would tell me how they could drive through 4 countries in a matter of hours, in Canada I couldn’t get part of the way through our smallest province in the same time period. Canadians have to travel long distances to get anywhere, which is part of the reason why they’re such a tolerant and patient lot.

So on these long drives (long before the days of portable entertainment devices) my family would have to think of ways to pass the time. Our favorite game was inspired by “20 questions.” We called it “the animal guessing game.”

It basically worked like this – you thought of the most unusual animal you knew of (perhaps something you’d seen on Animal Kingdom or in an animal encyclopedia) and the rest of the family would ask yes and no questions until they guessed what it was, or all agreed to being stumped.

Now, most of us would systematically narrow the field of possibilities by asking typical questions related to size, territory, habitat, skin type (fur, scale etc.) and so on. But my younger sister would always begin by asking the same question:

“Does it have fangs?”

At the time I thought she was hopelessly silly and incapable of systematic analysis. So few animals, after all, would fall into that category. Surely that wasn’t a good lead question.

But as I reflect on my sister’s perseverance on fangs, I realize that she was using an emotive hierarchy. To her, animals with fangs were so frightening, that she wanted to get it out of the way first thing – to be sure that we weren’t going to be spending time reviewing the life cycle and eating habits of animals with sharp teeth.

You know, it may seem funny, but I think that when it comes to matters of medicine some patients feel the way my sister did about the animal guessing game. They’re in unfamiliar territory, they are afraid of a real or perceived threat of a painful test or procedure, and they are internally focused on that threat to the exclusion of the big picture.

Doctors have the natural tendency to be removed from the emotional priorities of patients. We think that the patient is most interested in the evidence behind certain tests, the statistics, the technical aspects of a procedure – but sometimes as they try to comprehend the details of your informed consent, they really have one burning question:

Does it have fangs?

This post originally appeared on Dr. Val’s blog at

Genetic engineering & mosquito bites

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

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