Archive for July, 2011
30 July 2011
Anne Kenworthy writes:
I was just turned onto this site by a friend. I am currently battling cancer. In April, My CEA (cancer marker) was at 22. Today, in the last week of July, it is at 1.9. My oncologist told me this was the “normal” range; was pleased and refused to enlighten me beyond that. What does it mean to have a “normal” cancer marker? Does this mean we all walk around with some level of “cancer” in our bodies and this is the acceptable level? What’s going on?
I am sorry to hear of your cancer battle, but I am pleased to hear that an experienced oncologist was pleased at your current biomarkers. However, I am not pleased that he was not willing to discuss exactly what that means. You hit on a very interesting topic that I would like to explore with two articles.
CEA, or Carcinoembryonic Antigen, is a protein that is normally produced during fetal development. Certain types of tumors can begin to produce CEA in adults, and it is useful as a tumor marker because the progress of cancer treatment can be tracked by levels of CEA. However, nothing is absolute in biology, and some level of CEA is not uncommon in healthy adults.
According to the website of the National Institutes of Health, normal levels of CEA in adults is 0 to 2.5 micrograms per liter. For smokers, the range is 0 to 5.0 ug/L. (1) Those numbers were derived from testing the blood of many, many healthy individuals, and it would be incorrect to say that a level of CEA in that range is necessarily indicative of cancer.
In a broader sense, tumor biomarkers are usually proteins that are absent or low in people without cancer. There are many tumor markers used for various types and subtypes of cancer, and they all have their nuances and limitations. A tumor biomarker is not the golden standard to whether or not someone has cancer. A tumor biopsy combined with a trained pathologist and a somewhat low-tech (but still very nice) microscope is actually the golden standard of diagnosis. But, that process still requires one to know where tumors are, and for the tumors to be large enough to get a needle biopsy.
The disease will never be cured for some cancer patients, but they will live for decades with the disease without quick progression. Some will eventually die with the disease, not of it, and live fairly normal lives thereafter.
But is it possible that all of us have some level of cancer? Yes. I will explore this paradox in next week’s article. Within the scientific community, cancer is being seen more and more as a “natural” hiccup of physiology.
Reference: National Institutes of Health
23 July 2011
The inspiration for this week’s article is not from one person, but from a culmination of many people asking me “dumb” questions about cancer and forcing myself and others to re-examine the assumed, the dogma, and the textbooks. If B leads to C, and C leads to D, and A hinders B, does A inhibit D?
It’s common knowledge that sunscreen helps prevent UV exposure to the skin. It’s well established that UV rays cause DNA damage. It’s also well established that DNA damage leads to carcinogenesis and cancer. But does sunscreen really prevent melanoma, the most dangerous and lethal of skin cancers?
Above: Sunscreen has been applied to the right half (left to us) of this man’s face. On the right is an image taken in the visible spectrum of light (what we see) and on the right is one taken with the ultraviolet spectrum. Image source: Wikipedia Commons
After all, common knowledge is meant to be questioned, and any assertion should be backed up by experimentation whenever possible. In biological systems, transitive theorems can run into trouble because of unforeseen confounding factors. Whenever possible, one needs to see if, say, A inhibits D.
I was surfing PubMed (link) the other morning and found this interesting study.
Here is the abstract:
Regular sunscreen use prevents cutaneous squamous cell carcinoma long term, but the effect on melanoma is highly controversial. We evaluated whether long-term application of sunscreen decreases risk of cutaneous melanoma. Participants and
In 1992, 1,621 randomly selected residents of Nambour, a township in Queensland, Australia, age 25 to 75 years, were randomly assigned to daily or discretionary sunscreen application to head and arms in combination with 30 mg beta carotene or placebo supplements until 1996. Participants were observed until 2006 with questionnaires and/or through pathology laboratories and the cancer registry to ascertain primary melanoma occurrence.
Ten years after trial cessation, 11 new primary melanomas had been identified in the daily sunscreen group, and 22 had been identified in the discretionary group, which represented a reduction of the observed rate in those randomly assigned to daily sunscreen use (hazard ratio [HR], 0.50; 95% CI, 0.24 to 1.02; P = .051). The reduction in invasive melanomas was substantial (n = 3 in active v 11 in control group; HR, 0.27; 95% CI, 0.08 to 0.97) compared with that for preinvasive melanomas (HR, 0.73; 95% CI, 0.29 to 1.81).
Melanoma may be preventable by regular sunscreen use in adults.
For those that do not speak sci-geek, please let me translate: During a four-year period in Queensland, Australia a group of 1600 volunteers were randomly split into two groups: test and control. The test group was told to use a UV-blocking sunscreen every day for four years. The control group was given a dummy sunscreen that looked and smelled like the real stuff but had no UV protection.
People in the control group had a 2X higher incidence of melanoma. Those that had UV-blocking sunscreen did not develop melanoma as frequently as the control group. Also, the most aggressive forms of melanoma were not as common among the UV-protected group as well. So, sunscreen lessens both the risk of melanoma, and further still lessens the risk of the more aggressive forms of melanoma.
However, some people who received the UV-protecting cream still had some incidence of melanoma. The rate of melanoma was reduced, but not ablated. This underscores the importance of regular check-ups and avoiding harsh, direct sunlight whenever possible. For instance, if you’re an athlete and love running, it’s still a good idea to avoid running in the middle of the day, even if you use sunscreen liberally.
16 July 2011
This week’s article was inspired by Hollis Cameron in San Diego, CA:
How did Lance Armstrong beat his cancer/cancers?
What an appropriate question for mid-July! We’re right in the midst of the Tour de France, arguably the most grueling endurance race on the planet. In fact, today’s stage ended at Plateau de Beille, an alpine ski resort in the French Pyrenees where Lance himself won en route to his 2002 overall victory at the Tour. (See photo to the right)
The Texan Lance Armstrong won the Tour de France seven times, more than any athlete before or since. He was one of the most dominant athletes of his generation and his influence spans more than his sport. He often claims that his hardest battle was not amidst the thin air of the jagged Alps, but in a hospital bed in Indiana. With the odds stacked against him, Lance Armstrong went on to beat his testicular cancer. Like all major victories, his battle was both part will and part luck.
I do not have access to Lance Armstrong’s medical records, but Sally Jenkins’s book on Armstrong It’s Not About the Bike describes in fairly good detail some of his experiences with cancer. Or I should say: good enough for this scientific apprentice to piece a thing or two together?
Armstrong only sought medical attention once he started coughing up blood. By this time his left testicle had swollen to the size of a grapefruit and had known that something was not right for a while. The cough was caused by metastatic tumors that had spread to his lungs. When he finally went to the doctor, x-rays revealed many tumors in his lungs, and further investigation revealed metastases in his brain.
The doctors immediately removed the offending testicle. Next, they attempted a surgical procedure to remove tumors from his brain. Armstrong was extremely fortunate in a sense that his brain tumors had already stared to die off on their own, and were relatively simple for the surgeon to remove.
His second major strike of luck was that his tumors responded really well to the then-new platinum-based chemotherapy. The drug? Cisplatin. It works by actually causing MORE damage to DNA in quickly dividing cells. It has some pretty serious side effects, including: hair loss, extreme weight loss, muscle atrophy, unexplained pain, and severe anemia. It’s a double-edged sword at best, but there is one type of cancer that it works really well against: testicular cancer. The reason why cisplatin works so well against testicular cancer and not other cancers is not known.
Armstrong’s tumors practically melted away with the drugs his doctors gave him. His recovery was greatly aided by the fact that he was in very good physical shape prior to his diagnosis, which many doctors speculate is what can help young patients survive cancer more often than their more mature counterparts. (I hope I don’t sound too much like a broken record when it comes to the importance of physical fitness to mitigate cancer risk)
His story underscores the importance of a good communication with your doctor. Although it is rare, cancer can affect young people, and no one is immune to cancer. That being said, it’s really not worth it to worry about such things unless one develops highly atypical symptoms that do not go away. An example would be a rapidly expanding testicle.
Reference: It’s Not About the Bike: My Journey Back to Life by Sally Jenkins, Lance Armstrong
See the Cancer for Dummies homepage for more articles!
9 July 2011
Craig Ricker of San Diego, CA writes:
What is the most painful type of cancer?
What an objective question for a tantalizingly subjective measure! I love it. Humanities meets Science!
Pain is hard to quantify and compare, and there are many type of cancer, as there are many types of pain. How would one say that one patient’s pain is worse than another? This is a question to which I do not know how to answer. Though with science, it’s very dangerous to say that it will never be answered or that it will never be quantified.
But for now, I will propose a candidate for such a dubious distinction: Bone Metastasis, or the spread of cancer to the bones, followed by the growth of tumors in the bone.
(Image above: the bone is rarely the site of primary tumor growth. Rather, tumors will often begin in another location and migrate to the bone. The two patients above have undergone a bone scan. The brighter spots indicate bone metastases)
Growing tumors will literally eat away at the bone, causing it to weaken and become brittle. I’ve heard cancer patients describe the pain as the worst cavity you’ve ever had, or like having fractures all over your body. The pain is unrelenting. It is so bad that morphine can often have no effect. Unchecked bone metastasis can actually cause fractures. Unlike fractures from blunt trauma, the bone will slowly chip away. It is akin to slowly removing a sticky bandage on a hairy forearm rather than quickly tearing it off, except it’s amplified on the pain scale of broken bones.
It’s a very morbid image, I admit. Cancer metastasis to the bone is my nomination for most painful “type” of cancer.
Cancer metastasis to the bone is not a specific type of cancer, but it is part of several late-stage cancers. Bone metastasis is particularly common in breast cancer, which accounts for close to one of every three cancers diagnosed in women in the US. (1) Despite continued efforts in early detection and screening, many women will develop metastases from their breast cancer, and the most common site of metastasis from breast cancer is bone (2). Bone metastasis can be exceptionally painful, affecting nearly 90% of patients with metastatic breast cancer (3).
So there you have it. I hope this helps to underscore a recurring theme in my scientific pulpit: It’s exceptionally important to catch cancer early before it spreads. Or, to prevent cancer and not get it at all.
For more topics, please visit the Cancer for Dummies main page!
1. American Cancer Society. Breast Cancer Facts and Figures 2003-2004. Atlanta, GA: American Cancer Society; 2003.
2. Hillner BE, Ingle JN, Berenson JR, et al. American Society of Clinical Oncology guideline on the role of biphosphonates in breast cancer. J Clin Oncol. 2000;18(6):1378-1391.
3. Diel IJ, Mundy GR. Biphosphonates in the adjuvant treatment of cancer: experimental evidence and first clinical results. Br J Cancer. 2000;82(8):1381-1386.
3 July 2011
As a prelude to writing about more specific topics, I thought it would be worthwhile to answer the following question that has indirectly come up from several sources:
What types of cancer are there?
“Cancer” is actually a broad term used to describe a class of over 200 diseases with overlapping symptoms, mechanisms, epidemiology, and therapy. The specific type of cancer is named according to the tissue and cell type of origin.
Carcinomas are cancers of epithelial cells, like skin, lining of throat, gut, and ductal tissues. Example: breast carcinoma.
Sarcomas are cancers of connective tissue such as bone, cartilage, fat tissues. Example: Osteosarcoma (bone).
Blastoma is a type of cancer derived from developmental precursor cells in unborn children. Not surprisingly, these most commonly become apparent in children. An example is Neuroblastoma, which arises from the neural crest, an embryonic structure in the third trimester.
Leukemia is cancer of the blood. (think: white blood cells) An example is Chronic Myleogenous Leukemia.
Teratoma is a type of cancer from pluripotent cells in testes or ovaries. Example: Testicular cancer.
In humans, the most common cancers, by far, are carcinomas. Breast cancer, prostate cancer, lung cancer, colon cancer, and pancreatic cancers usually derive from the epithelial cells that make up the organ, making them carcinomas. Epithelial cells usually line the outside of an organ, or line the inside of a lumen (enclosed space, like the inside of the gut). Epithelial cancers are likely common because they are the first tissues exposed to external insults. For instance, skin cells are the first to intercept UV rays. Epithelial cells in the lungs and the cells lining the throat and trachea are the first to see a cigarette’s smoke, etc…
Another reason why carcinomas are the most common type of cancer in humans is that epithelial tissues are constantly being re-made and have a relatively high turnover rate. Example: your skin cells are always flaking off. (A side note: did you know that a lot of indoor dust is actually dried up, exfoliated human skin cells?) While this is in itself a defense mechanism against cancer, epithelial tissues are also in a perpetual state of growth. Already being friendly to growing, many propose this as being one step closer to a tumor than other tissues.
Cancers are named for their tissue of origin, as are metastases. A woman battling recurrent breast cancer in her lungs is not the same as having lung cancer, though the symptoms may be very similar. The architecture of the tumors is different, and most importantly, the type of therapy that would have the most effect on the cancer is usually defined by the tumor of origin, not necessarily the tissue it’s in.
There are theoretically as many different kinds of cancer as there are cell types in the body. And of those types of cancer, scientists are beginning to discover discrete genetic pathways that can lead to further classification of subtypes of the same cancer origin. For instance, there are several types of breast carcinoma that arise from the same cell type. Some breast cancers rely on amplification of an oncogene called HER-2, some rely on a steady supply of estrogen to continue growing, etc. While that may seem somewhat esoteric, that knowledge has lead to significant breakthroughs in the way women with breast cancer are treated, reduced symptoms, and allowed for much less invasive therapy.
Source: Weinberg, The Biology of Cancer, 4th Edition
(See the Cancer for Dummies main page for more topics)