In a study of 600 patients, those with NSCLC survived an roughly six months longer with Alimta compared to those who received a placebo. A notable exception is the patient group that had the squamous cell subtype of NSCLCL. Unfortunately, Alimta had virtually no benefit on these patients.

Alimta works by disrupting metabolic processes involving folate, a vitamin essential to nucleotide production and consequently cellular reproduction.

Most of Alimta’s side effects can be attributed to damaged blood cells as folate is pivotal in producing healthy RBC’s.

Most traditional cancer treatments (ie, chemotherapy) have powerful side effects as they damage healthy tissue as well as cancerous cells; however, these new nano-cells are readily incorporated into transformed cell lines, and most significantly, they can be deployed in “waves” containing different drugs without meeting any resistance. This is effective since physicians can fill the first wave of nano-cells with drugs to disarm cancer cells thereby making them more susceptible to upcoming waves. Pretty neat stuff. Hopefully the human trials will continue to produce promising results!

Eliminating two methods of cellular repair sure does pose a threat to the propagation of cancer cells. Studies have shown that healthy cells remain relatively unscathed (since they have several options for self-repair), but cancer cells die. I surmise that future studies will encompass cancers not directly related to a mutation in the BRCA1 and BRCA2 genes.

This is one fork of the future of personalized medicine – using an individual’s own molecular weaknesses for positive results.

I love how fundamental concepts can be used in such radical ways. In this case, analyzing the difference between healthy cells and cancer cells, and exploiting any variations to damage the latter while preserving the former. Medicine really is a grand application of simple ideas.

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Now I’m going to keep my opinion short as I’m eager to read your comments, but I think religion inherently commands us to preserve life above all else. If conventional treatment (chemotherapy and radiation in Daniel’s case) has an 85% or better chance of eliminating the growing tumor (which experts are saying), I would accept that I’m violating my religion in favor of the scientific community… in favor of continuing life.

In the case of Daniel, though he and his family made his “no-treatment” wishes clear, a court order demanded that he receive the chemotherapy. The result? Daniel and his mom have fled to an unknown destination. As Daniel’s tumor continues to grow, he will gradually lose the ability to breath and ultimately suffocate. Was the court right in ordering the chemotherapy, or should the patient and his family have the last call?

Nonmelanoma skin cancer is the most prevalent form of cancer in humans, and if caught early, it’s very treatable. Skin cells which have been damaged by UV radiation pose a serious risk of transforming into a cancerous line due to mutations in their DNA. Fortunately, the body has mechanisms (namely the ATR protein) to address the cells before they can transform. Some will be targeted for apoptosis, but many others will attempt to heal. In this context, caffeine increases the number of damaged cells that undergo apoptosis.

It seems like a pretty simple concept. Skin cells are generated at a relatively high rate, so getting rid of any which may potentially result in cancer seems like a good choice.

Furthermore, researchers propose that caffeine may one day be utilized as a topical lotion of some kind to “spot treat” areas of damage. Since caffeine has a natural affinity to absorb radiation at approximately 270 nanometers (ultraviolet light), perhaps it can be combined with similar constituents in sunscreen (titanium dioxide, etc.) to form a more thorough layer of protection.

The overwhelming majority of our genome (the complete set of human genes) is actually “junk DNA” which doesn’t code for a specific protein. So why is it there to begin with? Well a big reason is it increases the likelihood that a spontaneous mutation somewhere in the genome will NOT harm our actual coding regions. Scientists also theorize that these non-coding regions participate in regulating the expression of genes. At the symposium, I finally had an opportunity to learn another role for these seemingly useless spans of DNA.

Now let me go back. It’s not appropriate to say that the aforementioned “non-coding” sequences code for nothing. In reality, they’re still transcribed into mRNA, but these transcripts doesn’t get translated into viable proteins. A select few of these transcripts will ultimately become microRNA (miRNA), but as soon as they’re transcribed, the resulting 21-23 bp transcript is known as pri-miRNA. The diagram illustrates how the pri-miRNA becomes mature miRNA through a series of enzymes (namely Drosha and Dicer). Oh, and if these enzymes sound familiar, it’s because they’re the same ones we discuss in the context of RNAi (RNA interference). Kind of cool how everything comes full circle.

So what’s the big deal with miRNA? Well, different families of miRNAs have been shown to have varying levels throughout embryonic development, and parallels have been drawn with the levels of miRNA found in cancer cell lines. The mature form of Let-7, a type of miRNA, has been shown to have reduced levels in cancerous cell lines compared to healthy cell lines. This made scientists wonder whether or not the maturation of Let-7 was being inhibited by something, thereby promoting oncogenesis. A protein known as Lin-28 has been shown to bind to Let-7 in its pre-miRNA form and prevents it from maturing.

Ta-da, there’s our competitive inhibitor. So now if we could prevent Lin-28 from binding to the pre-miRNA form of Let-7, then Let-7 could mature (just like it does in healthy cell lines). Researchers overcame the inhibition by introducing synthetic transcripts of Let-7. That’s enzyme kinetics 101: to overcome a competitive inhibitor, increase the level of substrate. Now, more of the Lin-28 was being sidetracked to the “dummy” transcripts, while Let-7 was finally able to mature. 

This therapy actually showed a decrease in the rate of cancer proliferation in murine models making its potential as a “cancer treatment” in humans increasingly favorable.

It doesn’t make sense how much we worry about cancer when we’re the ones, for the most part, who can prevent/postpone the onset. Breathing city air can cause cancer. Going outside can cause cancer. And for those who are content on breathing purified air while staying indoors, you’re out of luck too – aging causes cancer. It’s true that cancer is no laughing matter and prevention should be important (especially for seniors). However, this doesn’t mean we should compromise the luxuries of technology. Cell phones are routinely accused of emitting radiation directly to the brain therefore being a great threat to the user’s health.

Let’s use some simple logic. In our technological era, all electrical devices emit radiation of varying levels and types. Heck, the granite countertop in my kitchen may be emitting dangerous levels of radon gas (a known carcinogen) without me even knowing. It’s true that cell phones are far more prevalent than other “luxuries”, but there are measures that can be taken to minimize the amount of radiation one is exposed to. For example, purchase a phone based on documented radiation emissions. I use an LG Voyager which has a SAR (specific absorption rate) of 0.765 watts/kilogram. This is a moderate SAR rating compared to other phones. Hands free technology (ie, Bluetooth) will also reduce one’s exposure to the radiation. Imagine our phones having to transmit/receive signals from cell towers which may be miles away. That’s a pretty strong radio frequency compared to the signal given off by a Bluetooth headset from a few feet away. 

To conclude, just use some common sense when using your cell phone. Yes, they give off radiation, but there’s no scientific fact that conclusively states the connection between cell phones and any form of cancer. Experimental results have not been reproducible in laboratory animals. Regardless, in our pursuit of “minimizing the risk”, we have to cut exposure to radiation wherever possible. Reducing your cell phone usage and/or investing in hands-free devices may contribute to this effort.

Like most cancers, there are two forms of skin cancer – nonmelanoma and melanoma. About 95% of all skin cancers are of the nonmelanoma type, and as cancer biology nomenclature suggests, the cancer has not metastasized. In contrast, melanoma arises from the pigmented skin cells known as melanocytes and is far more dangerous since the cancer usually metastasizes before the tumor has been noticed. In either case, cancer is cancer. Fortunately in this case, the same preventative measures can be taken to reduce one’s chances for acquiring it.

So far, what amazes me is the utter ignorance when dealing with outdoor activities. In the summer time, it’s natural for people to enjoy recreational sports like swimming, tennis, biking, etc. Just keep in mind that your skin isn’t as forgiving as you wish it was. Now I’ll interject my biased opinion – the overwhelming majority of skin cancer cases can be linked to excessive exposure to UV light.

Why am I saying this? Well, quite frankly, the numbers speak for themselves. Some may argue that immunocompromised individuals (AIDS patients) or exposure to certain chemicals/radiation may increase one’s chances for getting skin cancer; however, how many public service announcements have you seen advocating the usage of sun screen? They’re not just saying that since it makes your skin look all shiny. There’s scientific evidence supporting their suggestion. The research behind UV light’s interaction with DNA, the formation of thymine dimers, the body’s innate repair response to fix damaged DNA and so on is more than enough to convince a semi-educated person about the dangers of UV light. Yet I ask, why do all of us take it for granted? “We have our youth! We’ll worry about skin cancer when we’re 50+ years of age.” Too bad for those people that even teenagers are routinely diagnosed with metastatic melanoma. And to those who have an insatiable desire to use a tanning bed on a weekly basis. What good is your beautiful, golden tan going to do when you’re unnecessarily being hospitalized later in life? Seriously, think about it.

What I advise is the following:

1. Wear sunscreen when you’re outdoors. Not only will your skin thank you in twenty years, but you’ll prevent premature skin aging and the wonderful signs it leaves behind (ie, wrinkles).
2. Make sure you wear enough sunscreen. A typical, small tube (roughly 5 ounces) should be used up within a weekend. An expensive, SPF 60 sunscreen is going to act more like an SPF 30 if not applied liberally.
3. Think about investing in sun-protective clothing for activities like swimming where prolonged sun exposure becomes a problem.
4. Roughly every few months, follow this self-checkup by Howcast. It outlines the famous “ABCD” method for diagnosing skin cancer.

Hopefully if we start to get into a good habit about this, we’ll begin to see cancer rates steadily decline over the next decade. (Source: Professor Lewis J. Kleinsmith)