Know the characteristics of cancer cells, as stock in a chemopreventive study the potential anti-tumor compounds
Written: Dyah Ratna Budiani
(S3 students of Biotechnology, Gadjah Mada University /
Lecturer of Pathology, FK UNS)
Study of anti-cancer potential of natural materials has been widely implemented by various research centers, laboratories, and universities from all over the world. Methodologically the analysis is varied and evolved over time. However, most types of analysis used to test a potential anti-cancer compounds simply and solely aimed to determine the molecular point negate or minimize the signs or characters of cancer cells (The Hallmark of cancer). Before we design a study testing a potential anti-tumor compounds, so it's good we get to know first what is meant as "The Hallmark of Cancer." What and how the characteristics of a cell are said to be a cancer cell? so then we can design the type of test or analysis that can be used in accordance with the purposes of research, we can finally get the results we expect with that is: knowing where the path of anti-tumor potential of these compounds work. From here we can test the next and subsequent danselanjutnya that these compounds could eventually be used as chemopreventive agents in cancer clinical penatalaksanakan in the future.
The six hallmark of cancer (six characters of cancer cells) (Pecorino, 2005) are as follows:
1. Growth signal Autonomy:
• normal cells require external signals for growth and pembelahannya
• Cancer cells are able to produce growth factors and growth factor receptors themselves.
• In proliferasinya cancer cells is not dependent on normal growth signals.
• Mutations that has allowed cancer cells to shorten the growth factor pathways.
2. Growth inhibitory signals Evasion:
• normal cells respond to growth inhibitory signals to achieve homeostasis. So there is a specific time for normal cell proliferation and rest.
• Cancer cells do not recognize and did not respond to growth inhibitory signals.
• The situation is much due to mutations in several genes (proto-oncogene) in cancer cells.
3. Evasion of Apoptosis Signals:
• normal cells will be reduced in number with the mechanisms of apoptosis, when there is DNA damage that can no longer be repaired.
• Cancer cells are not sensitive to apoptotic signals (when cancer cells carry DNA acumulative errors that are irreversible)
• Failure of cancer cells in response to apoptotic signals is due to mutations of genes and the apoptosis regulator genes apoptotic signal.
4. Unlimited replicative potential:
• normal cells to recognize and be able to stop cell division when it reaches a certain amount and reach maturation. Pengitungan cell number was determined by the shortening of telomeres in the chromosomes that will take place whenever there is DNA replication.
• Cancer cells have a specific mechanism for maintaining telomere length and equipment, allowing to keep dividing.
• Disability in the regulation of telomere shortening is what allows cancer cells have unlimited replicative potential.
5. Angiogenesis (formation of blood vessels):
• normal cell has a dependency on blood vessels to supply oxygen and nutrients needed for life. However, the architecture of the blood vessels more seherhana normal cells or cells was constant until adulthood.
• Cancer cells could induce angiogenesis, ie growth of new blood vessels around cancer tissues. The formation of new blood vessels is required for cancer cell survival and expansion into other parts of the body (metastases).
• Disability in the balance settings angiogenik inducer, and inhibitor can activate angiogenic switch.
6. Invasion and metastasis:
• Normal cells are not thinking about compliance to move to another location in the body.
• Switching the location of the cancer cells from primary to secondary or tertiernya location is the main factor of death due to cancer
• Mutation enables enhanced enzyme-enzyme activity involved the invasion of cancer cells (MMPs)
• Changes also allow reduction or loss of adhesion between cells by the addition of molecules, cells, increased attachment, and migration degragasi
In experiments in vitro, the difference in character between normal and cancer cells are as follows:
• normal cells will grow as a layer of cells (monolayer) if dibiakan in petridish, all of this because of the sensitivity to contact inhibition by neighboring cells (when normal cells have touched the neighboring cells, the growth will stop).
• Transformed cells (cancer cells) have a phenotype as follows:
o Growing continue without knowing the contact inhibitory signals, grew up not accumulate sebgai monolayer.
o Able to grow in low serum conditions (serum / FBS (fetal bovine exclaimed) contains many growth factors, cancer cells are able to meet the needs of growth factors alone.
o cancer cells more rounded morphology with a relatively larger core (because the active splitting).
Apart from the things above is still associated with an important feature of cancer cells is the TSA (Tumor specific antigen) and TAA (Tumor Associated Antigen).
1. TSA (Tumor specific antigen) is:
a. Tissue-specific shared antigens.
b. Antigen Resulting from mutation
c. Viral antigen (for malignancy associated viral oncogenic denganinfeksi).
2. TAA (tumor-associated antigen) are:
a. Tissue specific antigen (MUC-1 specific instance in colon adenocarcinoma).
b. Over-expressed antigens
c. Onco-fetal antigen (eg CEA
d. Differentiations antigen.
Hopefully what we write briefly could be useful for readers, especially for beginning observers of Chemo-preventive research. Happy studying, researching and good luck because the results of your findings will be useful for cancer patients worldwide.
Reference:
1. Vinay Kumar, K. Abbul Abas, Nelson Foustro, 2005, Bassic of Dissease Pathology, Elsevier Inc.., International ed.
2. Lauren Pecorino, 2005, Molecular Biology of Cancer mechanism, target, and Therapeutics, Oxford University Press.
Written: Dyah Ratna Budiani
(S3 students of Biotechnology, Gadjah Mada University /
Lecturer of Pathology, FK UNS)
Study of anti-cancer potential of natural materials has been widely implemented by various research centers, laboratories, and universities from all over the world. Methodologically the analysis is varied and evolved over time. However, most types of analysis used to test a potential anti-cancer compounds simply and solely aimed to determine the molecular point negate or minimize the signs or characters of cancer cells (The Hallmark of cancer). Before we design a study testing a potential anti-tumor compounds, so it's good we get to know first what is meant as "The Hallmark of Cancer." What and how the characteristics of a cell are said to be a cancer cell? so then we can design the type of test or analysis that can be used in accordance with the purposes of research, we can finally get the results we expect with that is: knowing where the path of anti-tumor potential of these compounds work. From here we can test the next and subsequent danselanjutnya that these compounds could eventually be used as chemopreventive agents in cancer clinical penatalaksanakan in the future.
The six hallmark of cancer (six characters of cancer cells) (Pecorino, 2005) are as follows:
1. Growth signal Autonomy:
• normal cells require external signals for growth and pembelahannya
• Cancer cells are able to produce growth factors and growth factor receptors themselves.
• In proliferasinya cancer cells is not dependent on normal growth signals.
• Mutations that has allowed cancer cells to shorten the growth factor pathways.
2. Growth inhibitory signals Evasion:
• normal cells respond to growth inhibitory signals to achieve homeostasis. So there is a specific time for normal cell proliferation and rest.
• Cancer cells do not recognize and did not respond to growth inhibitory signals.
• The situation is much due to mutations in several genes (proto-oncogene) in cancer cells.
3. Evasion of Apoptosis Signals:
• normal cells will be reduced in number with the mechanisms of apoptosis, when there is DNA damage that can no longer be repaired.
• Cancer cells are not sensitive to apoptotic signals (when cancer cells carry DNA acumulative errors that are irreversible)
• Failure of cancer cells in response to apoptotic signals is due to mutations of genes and the apoptosis regulator genes apoptotic signal.
4. Unlimited replicative potential:
• normal cells to recognize and be able to stop cell division when it reaches a certain amount and reach maturation. Pengitungan cell number was determined by the shortening of telomeres in the chromosomes that will take place whenever there is DNA replication.
• Cancer cells have a specific mechanism for maintaining telomere length and equipment, allowing to keep dividing.
• Disability in the regulation of telomere shortening is what allows cancer cells have unlimited replicative potential.
5. Angiogenesis (formation of blood vessels):
• normal cell has a dependency on blood vessels to supply oxygen and nutrients needed for life. However, the architecture of the blood vessels more seherhana normal cells or cells was constant until adulthood.
• Cancer cells could induce angiogenesis, ie growth of new blood vessels around cancer tissues. The formation of new blood vessels is required for cancer cell survival and expansion into other parts of the body (metastases).
• Disability in the balance settings angiogenik inducer, and inhibitor can activate angiogenic switch.
6. Invasion and metastasis:
• Normal cells are not thinking about compliance to move to another location in the body.
• Switching the location of the cancer cells from primary to secondary or tertiernya location is the main factor of death due to cancer
• Mutation enables enhanced enzyme-enzyme activity involved the invasion of cancer cells (MMPs)
• Changes also allow reduction or loss of adhesion between cells by the addition of molecules, cells, increased attachment, and migration degragasi
In experiments in vitro, the difference in character between normal and cancer cells are as follows:
• normal cells will grow as a layer of cells (monolayer) if dibiakan in petridish, all of this because of the sensitivity to contact inhibition by neighboring cells (when normal cells have touched the neighboring cells, the growth will stop).
• Transformed cells (cancer cells) have a phenotype as follows:
o Growing continue without knowing the contact inhibitory signals, grew up not accumulate sebgai monolayer.
o Able to grow in low serum conditions (serum / FBS (fetal bovine exclaimed) contains many growth factors, cancer cells are able to meet the needs of growth factors alone.
o cancer cells more rounded morphology with a relatively larger core (because the active splitting).
Apart from the things above is still associated with an important feature of cancer cells is the TSA (Tumor specific antigen) and TAA (Tumor Associated Antigen).
1. TSA (Tumor specific antigen) is:
a. Tissue-specific shared antigens.
b. Antigen Resulting from mutation
c. Viral antigen (for malignancy associated viral oncogenic denganinfeksi).
2. TAA (tumor-associated antigen) are:
a. Tissue specific antigen (MUC-1 specific instance in colon adenocarcinoma).
b. Over-expressed antigens
c. Onco-fetal antigen (eg CEA
d. Differentiations antigen.
Hopefully what we write briefly could be useful for readers, especially for beginning observers of Chemo-preventive research. Happy studying, researching and good luck because the results of your findings will be useful for cancer patients worldwide.
Reference:
1. Vinay Kumar, K. Abbul Abas, Nelson Foustro, 2005, Bassic of Dissease Pathology, Elsevier Inc.., International ed.
2. Lauren Pecorino, 2005, Molecular Biology of Cancer mechanism, target, and Therapeutics, Oxford University Press.
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