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1 in 3 Will Get Cancer, and 1 in 4 Will Die: Why is Cancer So Hard to Kill?

The pursuit of cancer cures has taken the medical world decades, with little to show by way of positive results – because of the complications involved in the way cancer cells develop.

The Gist of It

  • Cancer cells are super difficult to destroy because they can clone themselves forever without showing any signs of aging / dying off.
  • Natural agents that prevent the cancer cells from duplicating could also be killing off regular cells.
  • If a cancer medication is too general, it can disrupt this self-recovery process and may even promote more cancerous cell developments instead.
Source: mylifeadviser.co.uk

Source: mylifeadviser.co.uk

Many people have difficulty trying to understand why just why it is so difficult to treat cancers. Sometimes, even the doctors themselves have the same trouble – as cancer cells often look the same as surrounding tissue when under the microscope.

When you peek into these cells using special microscopes however – to see the extra tiny genetic material of DNA (deoxyribonucleic acid) – the differences become clear. And the clues lie in the genetic building blocks called chromosomes, or more specifically, substances called telomeres.

What are telomeres?

Telomeres are super important to the life of the cell. They keep the ends of the various chromosomes in the cell from accidentally becoming attached to each other. This function is especially important for growth, which happens via cell division or mitosis.

What happens during mitosis?

When mitosis occurs, the basic genes become duplicated before separating into ‘daughter’ chromosomes. The daughter chromosomes then form the nuclei of the two new cells. When this occurs, each of the daughter chromosomes will have a shortened telomere.

Source: dartmouth.edu

Source: dartmouth.edu

Human telomeres lose about 100 base pairs from their telomeric DNA during each mitosis.

Why this happens is an important aspect of our growth. Telomeres are important in regulating cell growth cycles. Their steady shrinking with each mitosis might give cells a limited life span.

This is also why we age.

However, cancerous cells are different.

These cells are able to maintain the length of their telomeres with the help of an enzyme called telomerase. Telomerase is an enzyme that adds telomere repeat sequences to the end of DNA strands and lengthens the telomeres at the end of the chromosomes.

By lengthening this strand, DNA polymerase is able to complete the synthesis of the ‘incomplete ends’ of the opposite strand, which is shortened when mitosis occurs. As a result, cancer cells can divide indefinitely without ever showing any aging effects – effectively becoming immortal cells!

In other words, cancer cells are clones that outlive your other cells!

Source: cancer.ca

Source: cancer.ca

The cancer cells continue to remain fresh while the surrounding tissue ages and slowly loses its ability to fight off the enemy. No matter how many trillions of cells are present in the cancer, they are all descended from a single ancestral cell.

How to fight against cancer 

Cellular immortalisation is a crucial step during the development of human cancers. Hence, natural agents that prevent the expression of the gene for telomerase or prevent the action of the enzyme are important in cancer therapy.

But, the fight against cancer cells isn’t so simple. This is also because oxidants from the environment (food, breath intake, absorption via the skin, etc) can also damage the genetic molecule in normal cells, but this damage can be naturally fixed by our bodies.

If a cancer medication is too general, it can disrupt this self-recovery process and may even promote more cancerous cell developments instead.

How cancer happens

The key to this self-repair process is a tumour suppressor gene called p53 that stops the cell cycle when damage has occurred to the DNA. It also stimulates repair enzymes to repair the DNA. This triggers the production of a special protein that prevents the cell from dividing and allowing the damaged DNA to spread. If the DNA cannot be repaired, the p53 protein stimulates apoptosis or cell death.

Cancer happens when tumour-suppressor genes don’t function properly. When they are not able to prevent abnormal cell division in mutated cells, you could end up with cancer. The most frequent cause of new cancer is a mutation in the p53 gene.

A mutated p53 gene is involved in an estimated 60% of all cancers including cancers of the breast, lung, liver, skin, prostate, bladder, cervix, and colon. Breast cancer prognosis is associated with a tumour suppressor gene called p27. It is obvious that there are many factors that lead to the uncontrolled growth and proliferation of cancer cells.

Complications of viruses could lead to cancer as well

Then, there’s the additional complication of viruses which can cause cancerous cell development. Viruses that cause human cancers include:

  • Hepatitis B virus (liver cancer)
  • Human papillomavirus (cervical and other anogenital cancers)
  • Epstein-Barr virus (Burkitt’s lymphoma and nasopharyngeal carcinoma)
  • Kaposi’s sarcoma-associated herpesvirus (Kaposi’s sarcoma)
  • Human T-cell lymphotropic virus (adult T-cell leukaemia)

The search for effective cancer cures needs to be accelerated as the spread of cancers is growing rapidly. For example, the cancer rate in the US in 1900 was three out of one hundred. Today, one in three people will get cancer and one in four will die from it. This amounts to over one million people yearly in the US alone, killing some 520,000 of people annually.

What about in Malaysia? We’re not doing much better ourselves. In 2008, we had 32,000 new cases of cancer. In 2012, it rose to 37,400 cases.  Cancer deaths rose from 20,100 deaths in 2008 to 21,700 deaths in 2012, according to the International Agency for Research on Cancer (IARC) Globocan of the World Health Organisation (WHO).

This is why it’s very important to get checked up annually to ensure you catch cancer in its early stages.

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Edited by The HealthWorks Team
source: HealthWorks' Content Provider - Only Health
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