Oncological diseases: causes and risk factors

Oncological diseases: causes and risk factors

Part 1: Molecular and cellular base of oncogenesis

Genetic instability and mutations:

1.1. The role of DNA in the cellular functioning: DNA, deoxyribonucleic acid, is a carrier of genetic information that determines the structure, function and development of the body. It consists of two complementary circuits folded into a double spiral, and contains genes encoding proteins necessary for cellular processes. The accuracy of DNA replication, that is, copying genetic information before dividing the cell, is critical to maintain the stability of the genome.

1.2. DNA damage mechanisms: DNA is constantly exposed to various damaging factors, both endogenous (internal) and exogenous (external). Endogenous factors include DNA replication errors, oxidative stress caused by free radicals, and spontaneous chemical modifications of nucleotides. Exogenous factors include the effects of ultraviolet (UV) radiation, ionizing radiation, chemical carcinogens and viruses.

1.3. Mutations: random changes in the genetic code: Mutations are constant changes in the DNA sequence. They can occur spontaneously during replication or be induced by the effects of mutagenes. Mutations can be pointed (replacing one nucleotide by another), deeds (loss of DNA), inerts (insertion of the DNA section), inversions (DNA coup) or translocations (moving the DNA section from one chromosome to another).

1.4. Types of mutations and their effect on cellular processes: Not all mutations lead to cancer. Many mutations are neutral and do not have a significant effect on the function of the cell. However, some mutations can change the activity of genes that regulate cell growth, division and differentiation. There are two main types of genes, mutations in which play a key role in the development of cancer: oncogenes and tumors-genes.
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1.4.1. **Онкогены:** Онкогены – это гены, которые в нормальных условиях регулируют клеточный рост и деление. Мутации в этих генах могут приводить к их гиперактивации, что вызывает неконтролируемое размножение клеток. Онкогены часто возникают из протоонкогенов, нормальных клеточных генов, путем приобретения мутаций, усиливающих их активность.

1.4.2. **Гены-супрессоры опухолей:** Гены-супрессоры опухолей – это гены, которые в нормальных условиях подавляют клеточный рост и деление, а также способствуют апоптозу (программированной клеточной смерти) в случае повреждения ДНК. Мутации, инактивирующие эти гены, снимают торможение клеточного роста и позволяют клеткам с поврежденной ДНК выживать и размножаться.
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1.5. The accumulation of mutations and multi -stage oncogenesis: Cancer development is a multi -stage process that requires the accumulation of several mutations in the cell. Usually it is necessary that both oncogenes (activated) and the tumor-genes are affected (inactivated). Each mutation provides the cell with a selective advantage, allowing it to grow and share faster, ignoring normal control mechanisms. Over time, the cell accumulates more and more mutations, which leads to the development of a malignant tumor.

Epigenetic changes:

2.1. Determination of epigenetics: Epigenetics studies changes in genes expression that are not associated with changes in the sequence of DNA. Epigenetic changes can affect which genes are active or inactive in the cage, and, therefore, to its behavior.

2.2. The main epigenetic mechanisms: The main epigenetic mechanisms are DNA methylation, histone modifications and regulation to non -pounding RNA.

2.2.1. **Метилирование ДНК:** Метилирование ДНК – это добавление метильной группы к цитозину (одному из нуклеотидов ДНК). Метилирование ДНК обычно связано с репрессией генов, то есть с их выключением.

2.2.2. **Модификации гистонов:** Гистоны – это белки, вокруг которых обернута ДНК, образуя хроматин. Модификации гистонов, такие как ацетилирование и метилирование, могут изменять структуру хроматина и, следовательно, влиять на доступность ДНК для транскрипционных факторов, которые регулируют экспрессию генов.

2.2.3. **Некодирующие РНК:** Некодирующие РНК – это молекулы РНК, которые не кодируют белки, но выполняют важные регуляторные функции в клетке. Некоторые некодирующие РНК, такие как микроРНК, могут связываться с мРНК и подавлять их трансляцию, то есть синтез белка.

2.3. Epigenetic changes in oncogenesis: Epigenetic changes play an important role in the development of cancer. They can lead to inactivation of genes of tumors or to activate oncogenes. For example, hypermethylization of promotional regions of tumor tumor genes is often observed in cancer cells and leads to their shutdown.

2.4. The reversibility of epigenetic changes and therapeutic potential: Unlike mutations, epigenetic changes are potentially reversible. This opens up opportunities for the development of new therapeutic strategies aimed at restoring the normal expression of genes in cancer cells.

Violation of the cell cycle:

3.1. Normal cell cycle and its regulation: The cell cycle is a sequence of events taking place in a cell leading to its division and the formation of two subsidiaries. The cell cycle is regulated by a complex system of control points, which ensure the correctness of DNA replication and cell division. The main stages of the cell cycle: G1 (cell growth), S (DNA replication), G2 (preparation for division) and M (mitosis).

3.2. Control points of the cell cycle: Control points of the cell cycle are mechanisms that stop the progression of the cell cycle if any errors or damage are detected. For example, the control point G1/S checks the presence of DNA damage before replication. If DNA is damaged, the cell cycle stops to give the cell the ability to correct damage.

3.3. Violation of control points in cancer cells: In cancer cells, the control points of the cell cycle are often disturbed, which allows cells with damaged DNA to survive and multiply. This can be caused by mutations in genes encoding proteins involved in the regulation of the cell cycle, such as P53, RB and Cyclin-dependent kinase (CDK).

3.4. Proliferation and apoptosis: Proliferation is the process of cell reproduction. Apoptosis is a programmed cell death that plays an important role in the removal of damaged or unnecessary cells from the body. Normally, there is a balance between proliferation and apoptosis. In cancer cells, this balance is disturbed: the proliferation is increased, and apoptosis is suppressed.
The role of tumor micro -infection:

4.1. The composition of the tumor micro -angle: Micro -anguing of the tumor is a complex environment surrounding cancer cells. It consists of various types of cells, such as fibroblasts, immune cells, endothelial cells (lining blood vessels) and extracellular matrix (ECM).

4.2. The effect of micro -inflection on the growth and metastasis of the tumor: Micro -angry of the tumor plays an important role in growth, progression and metastasis of cancer. Fibroblasts, for example, can distinguish growth factors that stimulate the proliferation of cancer cells. Immune cells can both suppress and stimulate tumor growth, depending on the type of immune cells and the characteristics of the tumor. Endothelial cells are involved in angiogenesis, that is, in the formation of new blood vessels that provide the tumor with nutrients and oxygen. ECM can provide structural support of the tumor and participate in the regulation of cell migration.

4.3. Angiogenesis and neo -perhaps: Angiogenesis is the process of the formation of new blood vessels from existing ones. Angiogenesis is necessary for the growth of a tumor, since the tumor needs nutrients and oxygen for its growth and metastasis. Cancer cells distinguish factors that stimulate angiogenesis, such as vascular endothelium factor (VEGF).

4.4. The interaction of cancer cells with the immune system: The immune system plays an important role in the control of cancer development. Immune cells, such as T-lymphocytes and NK cells (natural killers), can recognize and destroy cancer cells. However, cancer cells can develop mechanisms that allow them to evade the immune response. For example, they can express proteins that suppress the activity of immune cells, or hide from the immune system, changing the expression of antigens on their surface.

Part 2: Risk factors for the development of oncological diseases

Genetic factors:

1.1. Hereditary predisposition: The hereditary predisposition to cancer means that a person has an increased risk of cancer due to the presence of mutations in certain genes inherited from parents. About 5-10% of all cases of cancer are associated with a hereditary predisposition.

1.2. High risk genes (for example, BRCA1/2): BRCA1 and BRCA2 genes are tumors-tumor genes that play an important role in DNA reparation. Mutations in these genes significantly increase the risk of developing breast cancer, ovarian cancer and other types of cancer. Women with mutations in BRCA1 or BRCA2 have a much higher risk of developing breast cancer during life compared to women without these mutations. Other high-risk genes include TP53 (Lee-Franeum syndrome), PTEN (COUDENNI syndrome) and MLH1/MSH2 (linch syndrome).

1.3. Genetic testing and counseling: Genetic testing allows you to identify the presence of mutations in genes associated with an increased risk of cancer. Genetic counseling helps people understand the results of genetic testing and make informed decisions on the prevention and treatment of cancer.

1.4. Family history and risk assessment: Family history, that is, information about cases of cancer in the family, is an important factor in assessing the risk of cancer. If the family has several cases of cancer, especially at a young age, this may indicate a hereditary predisposition.
Life lifestyle factors:

2.1. Smoking: Smoking is one of the most significant risk factors for cancer. It is associated with the development of lung cancer, laryngeal cancer, cancer of the oral cavity, esophagus cancer, bladder cancer, pancreatic cancer, kidney cancer and other types of cancer. Tobacco smoke contains more than 7000 chemicals, many of which are carcinogens. Smoking causes DNA damage, which can lead to cancer.

2.2. Alcohol: The use of alcohol is associated with an increased risk of developing oral cancer, throat cancer, esophagus cancer, liver cancer, breast cancer and colon cancer. Alcohol can damage DNA and increase the risk of cancer. The risk of cancer is increased with an increase in the amount of alcohol consumed.

2.3. Inal meals: Incorrect nutrition, including insufficient consumption of fruits, vegetables and fiber, as well as excessive consumption of red and treated meat, is associated with an increased risk of developing colon, breast cancer, prostate cancer and other types of cancer. Obesity, which is often associated with malnutrition, is also a risk factor for cancer.

2.4. Obesity: Obesity is associated with an increased risk of breast cancer (after menopause), colon cancer, endometrial cancer, kidney cancer, esophagus cancer (adenocarcinoma), pancreatic cancer and liver cancer. Obesity can lead to chronic inflammation, which contributes to the development of cancer.

2.5. Insufficient physical activity: Insufficient physical activity is associated with an increased risk of developing colon cancer, breast cancer and endometrial cancer. Physical activity can reduce the risk of cancer, improving the immune function, reducing the level of hormones and helping to maintain healthy weight.
Environmental factors:

3.1. Ultraviolet radiation (UV): UV radiation emanating from the sun and solariums is the main risk factor for the development of skin cancer, including melanoma, basal cell cancer and flat cell cancer. UV radiation damages DNA of skin cells, which can lead to cancer.

3.2. Ionizing radiation: Ionizing radiation, for example, from x -rays, computed tomography (CT) and nuclear accidents, can increase the risk of cancer, especially leukemia, thyroid cancer and bone cancer.

3.3. Air pollution: Air pollution, especially with solid particles (PM2.5), is associated with an increased risk of lung cancer. Air pollution can damage DNA and cause inflammation, which contributes to the development of cancer.

3.4. Exposure to chemicals (for example, asbestos, benzene): The impact of certain chemicals, such as asbestos, benzene, vinyl chloride and polychlorined biphenilles (PHB), is associated with an increased risk of cancer. Asbest, for example, increases the risk of developing lung cancer and mesothelioma (pleural cancer). Benzole increases the risk of leukemia.
Infectious agents:

4.1. Viruses (for example, HPV, hepatitis B and C, Epstein-Barr, HTLV-1 virus): Some viruses are associated with an increased risk of cancer. The human papilloma virus (HPV) is the cause of cervical cancer, cancer of the anal canal, cancer of the penis, vaginal cancer, vulva cancer and oropharynx cancer. Hepatitis B viruses increase the risk of liver cancer. Epstein-Barr (VEB) virus is associated with the development of Hodgkin lymphoma, Berkitt lymphoma and nasopharynx cancer. The HTLV-1 virus is associated with the development of T-cell leukemia/adult lymphomas.

4.2. Bacteria (for example, Helicobacter pylori): Helicobacter pylori (H. pylori) is a bacterium that infects the gastric mucosa and can cause an ulcer of the stomach and duodenum. H. Pylori is also associated with an increased risk of developing stomach cancer.

4.3. Parasites (for example, Schistosoma haematobium): Schistosoma haematobium is a parasite that causes a schistosomosis, an infectious disease common in Africa and the Middle East. Schistosoma haematobium infection is associated with an increased risk of developing bladder cancer.
Age:

5.1. Age as a risk factor: The risk of developing many types of cancer increases with age. This is due to the fact that mutations in DNA accumulate with age and the effectiveness of DNA reparation mechanisms decreases.
Other factors:

6.1. Chronic inflammation: Chronic inflammation is associated with an increased risk of developing many types of cancer. Chronic inflammation can damage DNA and stimulate cell proliferation, which contributes to the development of cancer.

6.2. Immunodeficiency: People with a weakened immune system, for example, due to HIV infection or taking immunosuppressive drugs, have an increased risk of developing certain types of cancer, such as Kaposhi lymphoma and sarcoma.

Part 3: Prevention and early diagnosis of oncological diseases

Primary prevention:

1.1. Refusal of smoking: Refusal of smoking is one of the most effective ways to reduce the risk of cancer.

1.2. Moderate alcohol consumption: Moderate drinking of alcohol or refusal of it can reduce the risk of cancer.

1.3. Healthy nutrition: Healthy diet, including sufficient consumption of fruits, vegetables and fiber, as well as restriction of red and treated meat consumption, can reduce the risk of cancer.

1.4. Maintaining a healthy weight: Maintaining a healthy weight can reduce the risk of cancer.

1.5. Regular physical activity: Regular physical activity can reduce the risk of cancer.

1.6. UV protection protection: Protection against UV radiation, for example, with the help of sunscreen, clothing and avoiding solariums, can reduce the risk of skin cancer.

1.7. Vaccination (for example, against HPV and hepatitis B): Vaccination against HPV and hepatitis B can reduce the risk of cancer caused by these viruses.
Secondary prevention (screening):

2.1. Screening goal: Screening is a test of people without symptoms of cancer for the presence of signs of a disease at an early stage. The purpose of screening is to identify cancer at an early stage when treatment is most effective.

2.2. Types of screening (for example, mammography, colonoscopy, papa test, psa test): There are various types of screening for cancer, depending on the type of cancer. Mammography is used for screening for breast cancer. Colonoscopy is used for screening for colon cancer. The papa test is used to screening for cervical cancer. PSA test is used for screening for prostate cancer.

2.3. Recommendations for screening, depending on the age and risk factors: Recommendations for cancer screening may vary depending on age, gender and risk factors. It is important to discuss with a doctor which types of screening are suitable for you.
Treetic prevention:

3.1. Rehabilitation and supportive therapy: Tertiary prevention is aimed at improving the quality of life of people who have suffered cancer. It includes rehabilitation that supports therapy and relapse prevention.

Part 4: Prospects for research and developments in the field of oncology

Immunotherapy:

1.1. Immunotherapy mechanisms: Immunotherapy is a type of cancer treatment that uses its own immune system of the body to combat cancer cells. There are various types of immunotherapy, including inhibitors of immune control points, Car-T cell therapy and oncolytic viruses. Inhibitors of immune control points block proteins that suppress the activity of immune cells, allowing the immune system to more effectively attack cancer cells. Car-T-cell therapy includes the genetic modification of the patient’s T-lymphocytes so that they can recognize and destroy cancer cells. Oncolytic viruses are viruses that selectively infect and destroy cancer cells.
Target therapy:

2.1. Identification of molecular targets: Targeted therapy is a type of cancer treatment that is aimed at certain molecules involved in the growth and spread of cancer. To develop targeted therapy, it is necessary to identify molecular targets that play a key role in the development of cancer.

2.2. Development and use of targeted drugs: After detecting molecular targets, targeted drugs are developed that block the activity of this target. Targeted drugs can be more effective and less toxic than traditional chemotherapy.
Genomic sequencing and personalized medicine:

3.1. The role of genomic sequencing in oncology: Genomic sequencing is a process of determining the complete sequence of human DNA. Genomic sequencing can be used to detect mutations that lead to cancer development, and to determine the most effective treatment for a particular patient.

3.2. Personalized approach to cancer treatment: Personalized medicine is an approach to cancer treatment, which takes into account the genetic characteristics of the patient and tumor. A personalized approach can improve the results of cancer treatment.
Development of new diagnostic and treatment technologies:

4.1. Liquid biopsy: Liquid biopsy is a cancer diagnosis method that uses blood samples to detect cancer cells or tumor DNA. Liquid biopsy can be less invasive than traditional tissue biopsy.

4.2. Nanotechnology in oncology: Nanotechnology is the use of materials and devices the size of nanometers (billions of meters). Nanotechnologies can be used to deliver drugs directly to cancer cells, to improve cancer diagnosis and to develop new cancer treatment methods.

4.3. Artificial intelligence (AI) in oncology: Artificial intelligence (AI) is the ability of computers to perform tasks that usually require human intelligence. AI can be used to analyze medical images to predict the risk of cancer and to develop new cancer treatment methods.

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