Oncogene have an operator gene and tumor suppressor gene. The tumor suppressor gene is always turn-on and an operator gene is turn-off. There are several factors to create tumor suppressor to turn of by a mutation in the P53 protein to play oncogenesis.
I am not sure, if I understand your question correctly.
However, all humans have proto-oncogenes. They are normal genes that could become an oncogene due to mutations or increased expression.
Proto-oncogenes code for proteins that help to regulate cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products. Upon acquiring an activating mutation, a proto-oncogene becomes a tumor-inducing agent, an oncogene. This mutation can happen directly within a proto-oncogene, or within a regulatory region, for example the promoter.
Other ways of turning a proto-oncogene into an oncogene would be chromosomal aberrancies like gene duplication or chromosomal translocations.
Basically every increase in the amount of the encoded protein turns an proto-oncogene into an oncogene. However, the resaon must not always be a regulatory defect of the operator gene / region. There are also less common reasons, e.g. increase of protein (mRNA) stability, prolonging its existence and thus its activity in the cell.
Hope, that helps.
Bests
I am not sure, if I understand your question correctly.
However, all humans have proto-oncogenes. They are normal genes that could become an oncogene due to mutations or increased expression.
Proto-oncogenes code for proteins that help to regulate cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products. Upon acquiring an activating mutation, a proto-oncogene becomes a tumor-inducing agent, an oncogene. This mutation can happen directly within a proto-oncogene, or within a regulatory region, for example the promoter.
Other ways of turning a proto-oncogene into an oncogene would be chromosomal aberrancies like gene duplication or chromosomal translocations.
Basically every increase in the amount of the encoded protein turns an proto-oncogene into an oncogene. However, the resaon must not always be a regulatory defect of the operator gene / region. There are also less common reasons, e.g. increase of protein (mRNA) stability, prolonging its existence and thus its activity in the cell.
Hope, that helps.
Bests
Hi Musthtak,
by chance we all on earth share the same genomics, indeed we therefore have all oncogenes, proto-oncogenes and anti-oncogenes...the only changes that can differ from one to one is the presence of variants (CNV, SNV and real variants). some of them will induce morphological differences (height, skin, eyes..), pathways changes and pathologies, while the other won't. see craig venter who was surprised to see that his genome differs from the reference genome with about 6 millions variations....
hope this helps
fred
I think you have an incorrect view about the interrelation between oncogene and oncosuppressor genes. You said " Oncogene have an operator gene and tumor suppressor gene. The tumor suppressor gene is always turn-on and an operator gene is turn-off "
In the first place usually there is no such a thing as an oncogene, but as Dominik said we have proto-oncogenes that under certain circumstances may become oncogenes.
Oncogenes do not have an operator gene and a tumor suppressor gene. Tumor suppressor genes usually have no relation with protooncogenes. It is not an "on/off" process.
For example Akt is almost always operational, in normal and pathological tissues. But in cancer Akt may be hyperactive through phosphorylation and in normal cells it is just active.
mTORC1 is always operative but it may be "more" operative in cancer.
Tumor suppressor genes may be completely off for example p53 in cancer which may be mutated or silenced by epigenetic mechanisms. On the other hand there are genes in which the loss of one allele makes the gen insufficient: that is the case of PTEN. Even if one of the alleles is still operative it is insufficient to downregulate the PI3K-Akt pathway.
Proto-oncogenes do not always cause cancer. But yes, we all have these oncogenes, they are helper cells(cell growth and division), until the time they start growing out of control(mutation). Then they can transform a cell into a tumor.
Hi there! With respects to how the above researchers have clearly explained the differences between proto-oncogenes and oncogenes, I hope you understand how to clearly differentiate the two know.
As proto-oncogenes are found in DNA that produce proteins which stimulate normal cell growth and division, they can mutate into "cancer-causing" oncogenes by the following ways:
1) Translocation or transposition
Unnatural increase in expression of a gene (extra promoter) - Growth stimulating proteins are produced in excess
2) Gene amplification
Unnatural increase in number of copies of a gene - Growth stimulating proteins are produced in excess
3) Point mutation
Two types - within the gene or within a control element. They lead to production of hyperactive or degradation-resistant proteins and increase in number of protein molecules released in respective order.
A more detailed explanation is that missense mutations in codons 12, 13 and 61 alter gene product activity, leading to unregulated MAP kinase cascade, causing increased cell proliferation.
I hope this helps, thanks!
Yes, everyone has his harmful genes which are oncogene genes. These genes make part of our genome and can be activated in certain circumstances including mutations, environmental external factors (pollution, food elements, ........) or internal factors produced under continuous stress.
As outlined by Dominik I think many people share this idea that oncogenes are "bad" genes. The truth is that proto-oncogenes are "good" genes involved in many normal biological processes, including cell cycle control. It is only when a mutation or a chromosomal rearrangement comes to disrupt their normal expression pattern or protein structure that they unravel a hidden oncogenic "bad" side participating to uncontrolled cell proliferation: a kind of "Dr Jekkyl and Mr Hyde" story.
I agree with the other experts. Proto-oncogenes are present in all of us. The constitutive activation causes the problem.
Amended on 28 August 2018
I have searched for oncogene (gene responsible for cancer)-related proteins in our human protein database (please see file; HepG2 Fucoidan).
Conclusion; Oncogene (gene responsible for cancer??)-related proteins are unexpectedly not directly linked to the cancer at all, but are related to infection of Picornavirus, HPV, and possibly non-enveloped phages of Rickettsia.
Fetal hepatocyte Hc has Protein regulator of cytokinesis 1/PRC1 at 13.8 μg/mg cell protein.
Hepatoma HepG2 (cultured without fucoidan) has SH2 (Src homology 2) domain-containing protein 4A at 0.9, and Serine/threonine-protein kinase Nek5/Never in mitosis A-related kinase 5 at 1.1 μg/mg cell protein, respectively.
Healed hepatocyte HepG2 (cultured with fucoidan) has Serine/threonine-protein kinase Krs-1/Serine/threonine-protein kinase 3 at 0.28 μg/mg cell protein.
Normal liver (with Pseudo-liver cancer) has Ras GTP-activating protein nGAP/RAS protein activator like 1 at 6.8, Mas-related G-protein coupled receptor member X3 at 1.6 μg/mg tissue protein, respectively.
LC tissue (with leprosy) has GTPase KRas at 0.33, Serine/threonine-protein kinase A-raf/A-RAF proto-oncogene serine/threonine-protein kinase at 3.7, Serine/threonine-protein kinase B-raf/B-Raf proto-oncogene serine/threonine-protein kinase/P94 at 1.4, and Mas-related G protein-coupled receptor MRG/MAS-R at 0.88 μg/mg tissue protein, respectively.
HCC tissue (with PBC) has Receptor tyrosine-protein kinase erbB-2/Erb b-2 receptor protein-tyrosine kinase at 5.7, and Tyrosine-protein kinase ABL1/Proto-oncogene c-Abl/Abelson murine leukemia viral oncogene homolog 1 at 7.2 μg/mg tissue protein, respectively.
LC tissue (named to be No.6) has Ras-like protein TC10/Rho-related GTP-binding protein RhoQ/Ras-like protein family member 7A at 0.23, ENL protein/YEATS domain-containing protein 1 at 1.7, and Mas-related G protein-coupled receptor MRG at 5.1 μg/mg tissue protein, respectively.
HCC tissue (No.6) has Serine/threonine-protein kinase A-Raf/Proto oncogene Pks2 at 0.53, Tyrosine protein kinase LYN at 1.30, and Tyrosine-protein kinase BTK at 0.35 μg/mg tissue protein, respectively.
Serum of 7mo1w healthy boy has Rho-related protein HP1/Rho-related GTP-binding protein RhoD at 12.3 μg/mg serum protein.
Serum of 1y girl (with biotin deficiency) has Guanine nucleotide exchange factor DBS at 19.4 μg/mg serum protein.
The serum of the above girl (healthy; 1y4mo) has Abl interactor 2 at 9.5 μg/mg serum protein.
The serum of the above girl (1y11mo; with excess biotin) has V-maf musculoaponeurotic fibrosarcoma oncogene homolog B at 2.9, and Ras-interacting protein 1 at 4.0 μg/mg serum protein, respectively.
Serum of 8mo girl (with gastritis) has Rho GTPase-activating protein 29 at 1.4, and Myc box-dependent-interacting protein 1/Amphiphysin II/Box-dependent myc-interacting protein 1 at 2.8 μg/mg serum protein, respectively.
Serum of the above girl (12mo; with common cold) has Rab effector Noc 2 at 12.7, and Rabenosyn-5/RAB effector RBSN at 5.8 μg/mg serum protein, respectively.
Serum of 22y female (with light Gait disorder) has Proto-oncogene TRE-2/Ubiquitin carboxyl-terminal hydrolase 6 at 2.8 μg/mg serum protein.
Serum of healthy male (33y) has GRB2-related adapter protein 2/Hematopoietic cell-associated adapter protein GrpL at 8.1 μg/mg serum protein.
It is very interesting that non-envelope type Picornavirus (HAV, Human poliovirus/PV, Foot-and-mouth disease virus/FMDV, and ECHOvirus/Enteric Cytopathic Human Orphan virus), HPV, and possibly non-envelope type phages of Rockettsias seem to up-regulate these oncogene-related proteins.
Only 4 biological specimens (serum of Gait disorder, GSD-1b, one male with biotin deficiency, and one healthy female (52y)) among 13 serum do not have oncogen-related proteins, and they also do not have non-envelope type Picornavirus (HAV, Human poliovirus/PV, Foot-and-mouth disease virus/FMDV, and ECHOvirus/Enteric Cytopathic Human Orphan virus), HPV, and Rickettsia.
Therefore, we have safely and validly declared that the Hepatocellular carcinoma (HCC) of humans is caused by the co-infection of Gag-Pol polyprotein gene of HIV-1 and peptidase-containing Genome polyprotein gene of HCV (please see page 32 of the file; The Fascio effect).
By using similar proteomics, we estimated that co-infection of HCoV and HIV-1 is the cause of Pancreatic cancer.
We also estimated that co-infection of HIV-1 and Animal Coronavirus (Murine coronavirus/MCoV, Canine coronavirus/CCoV, or Avian infectious bronchitis virus/IBV/Avian cornavirus/ACoV) is the cause of Cervical cancer, and HPV (dsDNA, no envelope) can not the origin of Cervical cancer (our unpublished results).
Thus, I am now considering that the excess injections (vaccine and drugs) at the hospital and excess stresses such as taking of nitrosoamine, X-ray, MIR, CT, asbest or asbestos, vitamin D, UV-light, radio wave, mental stress, etc. should be reduced, and the adequate taking of nutritions such as biotin and metal is recommended in order not to become the cancer (please see file; Feed by Measure).
Hi everybody
we are sharing all the same genes, at different stage in fonction of sexe, age and environment. all these genes have key role in body life but sometime cells are loosing their capacity to run usually (exposed to chemicals, rays...) and are developing in a selective pressure manner (the stronger, the faster, the alive cells).
fred
Yes, following the multi-step theory of carcinogenesis ("Mehrschritt Theorie der Karzinogenese") a "mutation" is an inducing event in different steps potentially leading/beeing associated with inhibition of p53 (repair mechanisms) and activation of proto-oncogenes to oncogeneses (e.g. c-Myc) leading to increased proliferation and reduced repair, allowing tumor proliferation and propagation and potentially further leading to metastasis etc.
Moreover, most organisms (eukaryotes) possess and express tumorsupressors and proto-oncogenes.
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