CANCER'S CAUSE, CANCER'S CURE (8 page)
The mutational theory of cancer basically says that when mutations occur in genes that tell the cell to divide, regulation of this process may be lost and the cells may continue to divide and multiply out of control. Unregulated cell division is a characteristic of cancer-cell growth. That is why the search for significant mutations has long been considered the priority issue in cancer research and why studies of DNA and cancer have focused on the genetic aspect of DNA. Beljanski was well aware of the fact that cancer sometimes develops from mutations that occur in the DNA. However, he found through hundreds of hours of painstaking research that cancer can be caused by environmental carcinogens (substances that cause cancer) that don’t necessarily act as mutagens. He discovered that many carcinogens induce physical structural (not genetic) changes in the DNA, and in order to understand what thatmeans, we need to turn now to biology lesson number two on DNA, its primary and secondary structures, and how it replicates.
DNA Replication
As I noted above, when a cell replicates, it allows life to continue. When a cell replicates out of control, it is cancerous. The self-replication of DNA happens at the structural level, and there is a primary and a secondary part to that structure.
The sugar-phosphate side of the DNA ladder is bonded covalently to one of the groups of the two pairs of bases, or rungs, of the ladder (the TA/AT or CG/GC combinations). Covalent bonds hold the rungs to the sides in a chemical bond formed by the sharing of electrons (electron being the particle of an atom that is negatively charged). Covalent bonds are very strong because the negative particles of one molecule bond together with the positive particles of another molecule, thereby creating a stable balance of positive and negative forces.
Together, the sugar-phosphate sides and the nitrogenous bases or rungs of the ladder are called a nucleotide. The nucleotides in the double chain are considered the primary structure of the helix. Nucleotides are bound together in long chains, and while the structure of this is in fact quite complicated, what matters for our discussion here is mutations are any alteration of the primary molecular structure of DNA (most often when there is an unplanned change in one base to another).
The secondary structure of the DNA molecule is the middle part of the rung of the ladder. The two base pairs are held together by a hydrogen bond. Hydrogen bonds are much weaker than the covalent bonds that hold the rungs to the sides of the ladder.
This secondary structure of DNA is where Dr. Beljanski focused much of his attention because of what happens to that hydrogen bond in cancerous DNA.
The bases or rungs of the ladder held together by the hydrogen bonds I just mentioned act like the teeth of a zipper. When the DNA molecule is zipped up with all its hydrogen bonds intact, it is a very stable and unshakable molecule. It is hard to mess with it. But DNA is constantly replicating itself to make new cells in the body. To do that, it has to unzip itself, and that’s where all the trouble lies. Cells divide and replicate trillions of times in our body every day. It’s a normal process. It starts with the DNA making a copy of itself. Then the rest of the cell copies its parts. When the copy is complete, it splits off from the parent cell. The copied cell is then “all of a piece,” ready and able to do whatever job it’s meant to do.
DNA replication, the heart of cell replication, is really an enigma.
It is so small you have to use special microscopes to view it, but it is also unimaginably large in scope. It takes place at rates between fifty nucleotides per second in mammals to five hundred nucleotides per second in bacteria. To give you a sense of the scope of the amount of replication that is taking place in your body right now, do some simple math. Fifty nucleotides replicating per second means that one cell is duplicating itself around 4.3 million times a day. There is no consensus on how many cells are in a human body, but estimates range from 50 to 100 trillion (a trillion is a million million of something. It is almost impossible to conceive of such a large number). Another way to put it— the nucleotides in your cells reproduce more times in one hour than there are dollars missing in the U.S.’s national current deficit of fourteen trillion dollars. And that’s just in a healthy cell. Cancer cells divide and replicate themselves in an out-of-control fashion—far faster than a healthy cell.
How DNA Recreates Itself by Replication
Like every form of life, individual cells have a lifespan. Rather than measure lifespan as a length of time, the lifespan of a cell is measured by how many times it can replicate itself. An average number of replications of cells observed in laboratory experiments is fifty but is theorized to be at a maximum of eighty. When a cell is no longer able to replicate, apoptosis (self-induced cell death) is the result. Self-induced cell death is exceedingly important for the overall health of body tissues. Without apoptosis, every newborn organism would otherwise in reality be just one ongoing cancer with its physiological systems overrun by excessive numbers of growing cells.
Figure 7 shows DNA replication—the recreations of itself again and again.
There are a series of steps that it must go through:
1. The top of the illustration shows a “parental” DNA molecule. The rungs of the parental DNA (the bases bound together with a hydrogen bond) break apart and the sides of the ladder break off (the zipper unzips itself). The parent molecule floats off and the open-sided rungs of the ladder are ready to replicate.
2. Open, unbonded bases can now be acted upon by the DNA polymerase, the crucial enzyme that literally makes a new copy of these open, unbonded bases (the open half of the ladder). The copy the DNA polymerase makes is actually complementary to the existing half. If you look at the illustration, you will notice that the side of the ladder that’s from the parent DNA molecule has the A, the T, the C, and the G waiting for their proper mates. The DNA polymerase makes a strand that has the corresponding T, A, G, C bases ready to fuse with the existing half.
3. The existing half of the ladder then fuses with the replicated, complimentary half because the hydrogen bonds between the bases reform. The process continues until two identical molecules of DNA have been formed. This happens twice, once for each side of the ladder that was split from the parent DNA molecule. (One zipper is now two and both are zipped up.) In a healthy cell, this process continues in each cell until the cell reaches its maximum number of times it can divide, and its preprogrammed death, apoptosis, occurs.
This is a remarkably efficient system, and in a perfectly healthy body it runs along smoothly. However, the two strands are bound together by hydrogen bonds whose opening and closing are susceptible to internal and external influences. When the hydrogen bonds of the base pairs fail to rezip, the message that DNA delivers may be dramatically modified.
The hydrogen bonding is disrupted by many types of molecules that come from both inside the body and from outside substances such as pollutants that the body absorbs through air, food, water, or even through the skin. These modifications lead to the replication process malfunctioning, which brings on the appearance of various serious diseases such as cancer. It is this malfunctioning that Dr. Beljanski discovered and named DNA destabilization.
DNA Destabilization
DNA interacts with many types of molecules, and these interactions may affect the fate of the cell. DNA initiates the production of other cells, so ensuring the integrity of the DNA is of prime importance in maintaining the structural integrity of cells.
Structural integrity, however, can be compromised by damage either to the primary structure (the order and nature of the base pairs) or the secondary structure (the hydrogen bonding of the base pairs). To reiterate an important point I made above, primary structural damage is usually caused by a mutation of a base or the activation or deactivation of a base by its binding to another molecule. This is the prevailing idea of what happens to the DNA in a cancer cell.
What Beljanski discovered was that the secondary structure (the hydrogen bonding between the two nucleotides that form the base pairs) can be damaged when something interferes with the hydrogen bond reforming in the replication process.
Beljanski was able to conclude this discovery through a series of tests on the ability of the DNA cell to absorb ultraviolet light (in other words, to make a cell glow like a fluorescent light bulb). He was able to observe that sometimes the hydrogen bonds that have been unzipped for replication to occur do not zip back up. They are prevented from doing so by molecules of chemicals commonly known as carcinogens (cancer causing substances). Carcinogens disallow the hydrogen bonds to be reformed. And therein lies the problem.
Figure 8 shows DNA destabilization:
1. When a DNA parent molecule is closed, it cannot be acted upon by DNA polymerase to create copies of open-stranded DNA. However, once the DNA strand has split itself and the half of the ladder is open, the DNA polymerase that is always there does what it is supposed to do: it causes the open strand to replicate itself. It will continue to do this over and over until the two sides of the DNA ladder can zip themselves back up or until the open side of the ladder is somehow killed or is rendered inert.