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6 Differences Between Cancer Cells and Normal Cells

Louis is a practicing physician who writes on various health topics. He focuses on case studies of patients and unusual complications.

six-differences-of-cancer-cells-compared-to-normal-cells

What Is Cancer?

For many, cancer is a very vague term that encompasses a type of disease that a) has no cure; and b) eventually causes misery and death. Many people believe that a cancer diagnosis is a sure death sentence.

How do people get cancer in the first place? What causes normal cells to form a “malignancy”? What do scientists, researchers, and oncologists know about these cells?

"Cancer" is a term used to describe a group of diseases rather than a single disease. There are myriad forms of cancer that can affect different body organs. In simple terms, a cancer is a new growth; it is a part of an organ that has changed or formed in a way that it should not have.

Old English, from Latin, ‘crab or creeping ulcer,’ translating Greek karkinos, said to have been used to name such tumors because the swollen veins around them resembled the limbs of a crab. Canker was the usual form until the 17th century.

Old English, from Latin, ‘crab or creeping ulcer,’ translating Greek karkinos, said to have been used to name such tumors because the swollen veins around them resembled the limbs of a crab. Canker was the usual form until the 17th century.

Cancer Classes and Nomenclature

There are several ways to classify tumors. One is by location; cancer can grow in any part of the body since every single part of the body is made up of cells. Hence, we have several types dedicated to each organ, i.e., lung cancer, breast cancer, colorectal cancer, etc.

Another way of organizing them is the specific subtype of growth rather than the specific organ. For example, there is adenocarcinoma, rhabdomyosarcoma, etc.

To sum up the nomenclature, the organ involvement and the subtype is usually used to label it—lung adenocarcinoma is cancer in the lungs, while colorectal carcinoma is a similar histologic subtype but found in the digestive system. From here, we can deduce the wide range of diseases when one mixes and matches; all that is covered by the umbrella term cancer.

All types of new growth in the body may be called a neoplasm. These types of growth may be classified as either benign or malignant. The change in cells and proliferation of mutation to cancer are known as tumorigenesis. Everything else gets interesting from here.

A benign neoplasm may not be considered as dangerous as that of a malignant one. There is no clear-cut differentiation, but common differences are that benign tumors grow more slowly, do not invade other tissues, have self-limited growth, and have no ability to travel to other body parts.

Nonetheless, it is not always this categorization that is important but its clinical picture. If a person will have a benign growth near the neck, and it grows so much that it eventually obstructs the esophagus or the windpipe- it still probably needs to be resected even though it lacks the characteristics of being a “malignancy”.

The most common cancers in 2016 are projected to be breast cancer, lung and bronchus cancer, prostate cancer, colon and rectum cancer, bladder cancer, melanoma of the skin, non-Hodgkin lymphoma, thyroid cancer, kidney and renal pelvis cancer, leukemia, endometrial cancer, and pancreatic cancer

— National Cancer Institute, 2016

Characteristics of Cancer Cells

In order to understand how cancer develops, it is important to note that in an ordinary manner, there is a specific predetermined way cells in the body mature, grow, and function. Each cell is pre-programmed to undergo a series of events that lead to its target state. At some point in its cycle, it starts out as an immature cell, then changes to a mature form; it may multiply and specialize later on; when it reaches its target form, it carries out its function.

Eventually, it may be damaged and repaired and will, later on, be scheduled for replacement and will be decommissioned to die. Every single type of specialized cell in the body works the same way. Cancer cells, on the other hand, have found a way to release themselves from this predestined cyclical way that nature has programmed cells.

Over several decades, researchers have tried to find a way and focus on how these cells eventually lead to random growth. In order for clinicians to be able to find a cure, the specific mechanisms for changes are being determined. The six main hallmarks of cancer were proposed early at the turn of the millennium.

Uncontrolled cell growth

Uncontrolled cell growth

1. Self-Sufficiency in Growth Signals

Every cell has a destiny. As mentioned above, there are specific ways a cell matures and is specialized to perform its intended function. There are several growth signals which indicate and serve as foremen to supervise these tasks of cell growth. Here is an example to illustrate the point: when a person does intense exercise, several muscle cells die. In order to replicate and re-grow, there are signals which inform the need hence new cells grow from the previous cell line. When the intended effect or purpose is served, the signals stop. This happens when the old cells are regenerated, and the muscle tissue comes back to its optimal form.

Cancer cells, on the other hand, have properties wherein the signal for growth keeps continuing. This leads to a continuous growth pattern which causes the expression of more and more proteins that make up cancer cells. These are called growth factors (GF). Research also reveals that these cells are more responsive to GF. What does this imply? This simply means that once there is a signal, there is more reaction to cells leading to more multiplied growth, further influencing the cell behavior.

Currently, it is proposed that the growth-promoting signals come from the main stroma or the main bulk of the tumor cells. The signal is also passed to the neighboring cells and will eventually cause a multiplicative effect.

Immortalized cell proliferation

Immortalized cell proliferation

2. Insensitivity to Anti-growth Signals

Concurrent to the increased capacity of cancer cells for growth, they are also insensitive to inhibitory or anti-growth signals. Cells typically have signals to stop the multiplication of their components. It is important to note that they have small organs which play a role in their sustenance; these are called organelles. These provide machinery for transport, movement, and production and the process of energy and resources, which are products of the cell. Insensitivity to control mechanisms leads to proliferation and rapid increase, not only in cell size but also in the small organs. One can imagine a cell abomination that is formed in this case.

Nature has provided people with control mechanisms that are programmed for control and management of aging and disabled cells. These are called tumor-suppressor genes. Their main function is to detect damage in cells, usually in the nuclear material. Most of these are spontaneous mutations that may lead to problems later on. Hence, these cells are then marked for retirement.

Liver cells blebbing and undergoing apoptosis

Liver cells blebbing and undergoing apoptosis

3. Evading Apoptosis

Normal cells have to eventually die or retire at some point. Apoptosis is a term used to describe the process of programmed cell death. This is the time when senescence has reached its toll, and the cell will either eventually be (1) programmed for decommission or (2) forced to retire. In this normal process, the cells will autodigest themselves with very little remnant or effect on other cells if it was programmed to die. There are apoptosis signals which function to target these cells. There are also instances when a proliferative cell is changed in a functional but quiescent stage. It will just form a structure but will no longer be part of the cell pool which is actively dividing and functioning.

These signals are not effective on cancer cells. The cancer cells develop means to decrease the effect of these signals or even block it altogether. Cancer cells become immortal. They continue to grow, which is only limited by their resources, blood, and oxygen supply.

The evasion of apoptosis is proposed as the capacity to skip parts in the normal cell cycle proliferation. Simply put, it skips the steps which check the cell if it is already due to death and apoptosis. Normally, the body has defense mechanisms to avoid continuous cell growth by having checkpoints at every cell cycle. Those cells which are damaged beyond repair or show signs of mutation are programmed to be destroyed. Cancer cells skip these checkpoints leading to uncontrolled growth.

One famous type of cell growth evasion mechanism for cancer is seen in cases of cervical cancer. Many know that HPV is a type of virus that may cause cervical cancer. It is proposed that the virus causes changes in the E7 apoptosis pathway, which causes a decrease in signal for cell death. This causes the uncontrolled proliferation of cancer cells.

Lymphoma Cell Dividing

Lymphoma Cell Dividing

4. Limitless Replicative Potential

Cells normally stop dividing when they reach a certain stage. Different studies conclude that, typically, cells stop dividing and proliferating once they reach a certain number of cell cycles. This is coined senescence. It is observed in human cells that it only takes 50 to 70 doublings before it stops dividing. This property is not present in some cancer cells. These cells break through the mortality barrier and cause almost unlimited potential.

Like apoptosis, the replication barrier serves as a defense mechanism for the body. It should be noted that there is no perfect replication of cells. It is observed that every time a cell does replicate, it produces two more copies of itself but not every single piece of nucleotide and protein is copied exactly. There are some minor mutations here and there that may or may not cause cell changes. The block in replication up to a certain point ensures that a cell’s lineage will stop its division and avoid further proliferation of natural and spontaneous mutations.

The property of cancer cells to avoid the cell checks leads to more mutations along the way. When coupled with the inability to be targeted by apoptosis is added to the mix, this leads to more mutations on top of mutations leading to more damage at the end of the road.

Angiogenesis in action

Angiogenesis in action

5. Sustained Angiogenesis

So far, it has been discussed that there is an increase in multiplied growth, decreased anti-growth, and evasion of culling of mutated cells. When all these factors are considered, we end up with the thought of multiple large unregulated badass mutant cells laying waste in the very foundation of tissues. There is no stopping these cells aside from one thought—their resources. How can they grow so much without nutrients and oxygen supply?

Cancer cells developed the capacity to form their own signals for growth. These growth signals not only function for their own components but more so to target other cell types, including cells that form blood vessels. The formation of blood vessels is known as angiogenesis. Angiogenesis leads to the formation and repair of blood vessels which are usually utilized by the body in times of inflammation. For instance, if one gets bruised, it is expected that there is damage to muscle cells leading to a mounted inflammatory response. More blood vessels are being recruited in the process to serve as pathways for increased delivery of nutrition in the affected tissues, delivery of inflammatory cells for defense against microbes, and more cells for repair.

This function is utilized by cancer cells to divert more nutrients to the growing tumor cells to meet their demand for more resources. This leads to an unprecedented proliferation and uncontrolled growth of the mutated cells.

Invading cell

Invading cell

6. Tissue Invasion and Metastasis

Earlier it was described that some of the defining characteristics of malignant as compared to benign cells include the capacity to invade other tissues and metastasize. Cells form tissues, and these are bordered by structures such as sheaths which compartmentalize them. Borders include basement membranes which function as the delineation of different types of tissues. Benign tumors, despite their increased growth, are usually unable to breach these membranes. The contrary is true for malignant cells; this causes not only uncontrolled growth but also damage to the functional capacity of tissues. Partly, this is due to their capacity to produce more proteases; these are protein enzymes that have the capacity to eat through normal barriers. Some have acidic components which assist in their capacity to breach borders and invade local tissues.

Metastasis is a commonly used term whenever one hears of cancer. It pertains to the movement of the tumor from its original location to another distant location. For instance, if a person has breast cancer, the cells may metastasize and start seeding on the adjacent lung and cause metastatic tumors in the lungs. At this stage, the tumor is usually considered advanced. There are also instances wherein the metastasis causes the demise of the patient rather than the original tumor itself.

Given the six properties discussed above, it must be emphasized that each type of cancer is unique.

The sequence of how they utilize this pathway may differ from one type of cancer to another, and it is also dependent on the natural environment where the tumor is growing. Ultimately, all of these unique characteristics lead to the difference between normal cells and malignant cells.

References

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  2. De Palma, M., & Hanahan, D. (2012). The biology of personalized cancer medicine: Facing individual complexities underlying hallmark capabilities. Molecular Oncology, 6(2), 111–127. doi:10.1016/j.molonc.2012.01.011
  3. Hanahan, D., & Weinberg, R. A. (2000). The Hallmarks of Cancer. In Cell (Vol. 100). doi:10.1007/s00262-010-0968-0
  4. Hanahan, D., & Weinberg, R. A. (2011). Hallmarks of cancer: The next generation. Cell, 144(5), 646–674. doi:10.1016/j.cell.2011.02.013
  5. Negrini, S., Gorgoulis, V. G., & Halazonetis, T. D. (2010). Genomic instability--an evolving hallmark of cancer. Nature Reviews. Molecular Cell Biology, 11(3), 220–228. doi:10.1038/nrm2858
  6. Szachowicz-Petelska, B., Dobrzynska, I., Sulkowski, S., & Figaszewski, Z. (2010). Characterization of the cell membrane during cancer transformation. Journal of Environmental Biology, 31(5 SUPPL.), 845–850. doi:10.5772/29559
  7. Valastyan, S., & Weinberg, R. A. (2011). Tumor metastasis: Molecular insights and evolving paradigms. Cell, 147(2), 275–292. doi:10.1016/j.cell.2011.09.024

This content is accurate and true to the best of the author’s knowledge and does not substitute for diagnosis, prognosis, treatment, prescription, and/or dietary advice from a licensed health professional. Drugs, supplements, and natural remedies may have dangerous side effects. If pregnant or nursing, consult with a qualified provider on an individual basis. Seek immediate help if you are experiencing a medical emergency.

© 2016 LM Gutierrez

Comments

LM Gutierrez (author) on February 09, 2016:

MsDora, thanks for taking time to read. I preferred to write on this topic since I've seen many patients have all farfetched notions about many broad health topics. Cancer is one on the list.

Dora Weithers from The Caribbean on February 09, 2016:

Very informative and helpful and well-presented. Thanks for doing this research and presenting the details. Your article gives a much clearer picture of the cancer process, than I previously had.