A list of terms used on this website and their definitions. 


It is a benign tumor made of glandular epithelium.


This is a process characterized by the overgrowth of glandular tissue.


 A disorder of malignant tumor cell differentiation with a change in structure and biological properties. A distinction is made between biological anaplasia (loss of all functions, except for reproduction), biochemical (loss of enzyme systems, which leads to metabolic disorders) and morphological (changes in intracellular structures, shape and size of cells).


A malignant tumor made of glandular epithelium.


This is a process of new blood vessels forming in an organ or tissue. In a normal organism angiogenesis processes proceed with a moderate intensity and only during regeneration of damaged tissues, thrombus canalization, elimination of inflammation foci, scar formation and similar recovery processes, as well as during growth and development of the organism. A separate field of study of physiological angiogenesis is gynecology, since A. is an integral part of cyclic transformations in ovaries. Angiogenesis is necessary for normal growth of embryonic and postnatal tissues, endometrial proliferation, ovarian follicle and corpus luteum maturation, wound healing, collateralization stimulated by ischemia. It has been established that endothelial cells produce cytokines that stimulate not only the proliferation and migration of endothelial cells themselves, but also the proliferation of tumor cells. Sometimes these autocrine and paracrine factors are secreted by the tumor itself

A plasma cell

An antibody-producing cell that is the final stage of B-lymphocyte differentiation.

Apoptosis and malignancies

Formation of any malignant tumor involves disruption of apoptosis mechanisms (programmed cell death) controlled by the p53 protein. Its normal functioning prevents uncontrolled division of malignant cells. If damage to the DNA molecule occurs in a cell as a result of any exposure (radiation, chemicals), the p53 protein will stop the cell from dividing until the damage is repaired, or will activate its programmed death before it has time to divide.This mechanism works as long as the TR53 gene has a normal structure. When mutations occur in it, the mutant protein accumulates in the cell and cannot perform its primary function. This disrupts apoptosis activation mechanisms, which manifests itself in the development of neoplasms, and if they exist, contributes to the resistance of tumor cells to the ongoing chemotherapy.


A molecule capable of combining with a biochemical receptor on a cell and initiating the same response as occurs naturally


A subpopulation of leukocytes including lymphocytes and monocytes.


A substance that enhances the immune response to antigens.


A form of immune tolerance in which the antigen-specific lymphocyte remains functionally inactive despite antigen recognition.


 A substance or forms of a substance that, when introduced into the internal environment of the body, is capable of inducing an immune response to itself in the form of the production of specific antibodies and/or immune T-lymphocytes.

Antigenic determinant

A portion of an antigen molecule that directly interacts with the immunoglobulin receptors of B-lymphocytes.Antigen-presenting cells - cells that primarily recognize the pathogen, recycle its antigens and present them in a form that can be recognized by the T-helper.

Antigen presentation

 A mechanism of transferring information about the nature of an antigen from innate immunity cells (or B-lymphocytes) to T-helper cells; the antigen-recognition receptor on the T-lymphocyte side and the histocompatibility class II molecule-immunogenic peptide complex on the antigen-presenting cell side are directly involved in the antigen presentation. Antigen-recognition receptors are receptors of lymphocytes that can specifically interact with a particular antigen; they provide the fundamental property of the immune response - specificity, i.e. directed exclusively against a particular antigen.


Glycoproteins produced by plasma cells during the immune response that specifically recognize an antigen; secretory antigen-recognizing receptors of B-lymphocytes.

Antibody-dependent cell-mediated cytotoxicity

An immune response of destruction by leukocytes containing Fc-receptors (natural killer cells, macrophages, neutrophils, eosinophils) of a variety of target cells coated with antibodies.


It is a specific form of cell death resulting from the implementation of a genetic self-destruct program and is caused by enzymatic cleavage of DNA.


This is an IgE-mediated mast cell degranulation reaction in response to an allergen; in the case of immune response against helminths, such reaction is protective and quite physiological.


Immune reactions against its own antigens; such reactions are not always pathological in nature, as it has been established that autoimmunity is an important component of the antigenic homeostasis system of the human body.


A degree of affinity between the antigen-recognition receptor (immunoglobulin, B-lymphocyte immunoglobulin receptor and T-cell antigen-recognition receptor) and its specific ligand (antigen).


A chemical that acts within the body to reduce the physiological activity of another chemical substancei.e. opposing the action of a drug or a substance occurring naturally in the body by combining with and blocking its receptor

Beta Interferon

A protein released by connective tissue cells in response to a viral infection. The protein can be synthesised and used in the treatment of multiple sclerosis

Breakdown Products

Products that result from the disintegration or decomposition of a substance in the body

Basal cell cancer (BCC)

This  is a tumor that grows from skin cells located in the basal layer of the epithelium. The tumor is prone to infiltrative growth and can grow into surrounding tissues, causing destruction and metastasis. However, this process is very slow and may take years, which is why basalioma is called a semi-small tumor.Forms of BCC : Nodular ulcerative form of basalioma.   The disease begins with the formation of dense, well-defined and elevated above the skin surface areas - nodules. They may be gray, pink or yellowish. Gradually they increase, the skin above them thinning and becomes as if pearly. They then merge with each other to form a plaque with raised edges and a depression inside. Gradually, this depression is transformed into an ulcer, which is covered with a crust. It, in turn, also proliferates, infiltrating and destroying the underlying tissue, as a result of which the plaque begins to resemble a crater with very dense edges that resemble cartilage. As the neoplasm grows, there is destruction of the underlying tissue. Large-nodule basalioma. This type develops from a single nodule, which, increasing in size, takes the form of a hemisphere up to 3 cm in diameter or more. Its surface may be smooth, but scales may be present. As a basalioma grows, its surface begins to deteriorate - an ulcer appears, which oozes oozing. 

Infiltrative form. It is characterized by the most malignant course, because it initially grows "inside" the tissue, destroying it. Clear boundaries of this form of basalioma are very difficult to define. 

Papillomatous or wart-like form of basaloma is characterized by neoplasms that resemble papillomas in appearance.

Superficial basalioma. At its initial stage, it looks like a pink spot. Gradually it grows, thickens, and is transformed into a plaque. Nodules are formed along its edges, which also increase in size and form a roll when merged. The center of the neoplasm "subsides" and changes color to a darker color. The tumor is not prone to infiltrative growth, but at large sizes, infiltration into the underlying tissues is still possible.

Scleroderma-like basalioma. This type of tumor manifests as a yellowish or whitish plaque. As it grows, its edges are eroded and crusted. When they separate, an inflammatory reaction occurs. Cysts filled with calcinates may also develop in the thickness of the tumor.

Fibrous basalioma. This tumor begins with the formation of a nodule, which transforms into a plaque as its size increases. Its surface layer becomes thin and blood vessels can be seen through it.


A subpopulation of B-lymphocytes secreting natural antibodies (polyreactive IgM) and expressing CD5 molecules on their surface.


This is the main subpopulation of B-lymphocytes, providing synthesis and secretion of antigen-specific antibodies of various classes.

BRCA1 and BRCA2 mutations (BReast CAncer gene)  

 BRCA1 and BRCA2 by themselves do not cause cancer. They are present in the cells of any healthy person and serve important functions. The risk of malignancy increases when the function of these genes is disrupted by mutations.

Normally, the proteins that code for these genes are needed to repair damaged DNA. If defects occur in them, this function is impaired, the damaged DNA is not repaired properly, genetic breakdowns accumulate in the cell, and it can become cancerous.

According to statistics, mutations in the BRCA1 and BRCA2 genes occur in one in 300-800 people. Carriers have an increased risk of cancer of the breast, ovaries, fallopian tubes, peritoneum, prostate, pancreas, stomach, gallbladder and bile ducts, and melanoma. If a person inherits some mutations from both parents, he or she develops Fanconi anemia and has an increased risk of developing some malignant tumors and acute myeloid leukemia.


A group of identical cells derived from a single progenitor cell.


A system of serum proteins that recognize template molecules of microorganisms or antibodies that induce inflammation, enhance phagocytosis and destroy objects (microorganisms and compromised own cells) by osmotic lysis.

Costimulatory molecules

A group of membrane molecules of antigen-presenting cells that supply antigen-specific T-lymphocytes with a second activation signal during antigen presentation (confirming the foreign nature of the antigen).

Cross reactivity

Ability of two different antigens to induce similar immune reactions due to the partial similarity of their antigenic determinants; this phenomenon has an important role in the induction of autoimmune reactions during infections.


A broad group of diverse substances that contribute to the directed movement of leukocytes to the focus of inflammation.


A group of specialized cytokines that regulate the directional movement of leukocytes to the focus of inflammation.


A large family of low molecular weight soluble proteins involved in the regulation of cell activity involved in the immune response; mediators of the immune response.

Cytotoxic T-lymphocytes

Cytotoxic T-lymphocytes that express CD8 molecules and perform a killer function by destroying target cells upon recognition of the immunogenic peptide - class I histocompatibility molecule complex on their surface.


Potential to cause cancer

 Central Nervous System

 System of nerves of the brain and spinal cord


A disease or condition of long duration or frequent recurrence; in some instances, it may slowly become more serious over time

 Clinical Trials

The development of human therapeutic products is a highly regulated process. Evaluation and testing for safety and efficacy proceed through laboratory (research), animal (pre-clinical) and human (clinical) stages of development.

 These guidelines cover the manufacture of the drug substance, the manufacture of the dosage form, and the safety testing that must be conducted before evaluation in humans can proceed.

Clinical testing involves a three-phase process.

In Phase I, clinical trials are conducted with a small number (typically 10-50) of healthy subjects to determine the early safety profile and pharmacokinetic profile (pattern of drug distribution and metabolism).

In Phase II, clinical trials are conducted with groups of patients with a specified disease (typically 100-200) to determine preliminary effectiveness, optimal dosages and expanded evidence of safety. This is intended to show that the drug is effective in different patient populations under a variety of doses.

In Phase III, the company conducts large-scale (typically >1,000), multi-centre, comparative clinical trials with patients with the target disease to provide sufficient data to statistically evaluate the effectiveness and safety of the product. During these clinical studies, the manufacture of the drug will be refined and an optimal formulation will be selected. Additional safety studies will be required, including long-term toxicology studies (possibly of 12 months' duration) and carcinogenicity studies. The company also undertakes a detailed study of the pharmacology of the drug to identify any breakdown products and the routes of excretion from the body.


 Any of the steroid hormones produced by the adrenal cortex or their synthetic equivalents. Corticosteroids are used clinically for hormonal replacement therapy, for suppression of adrenocorticotrophic hormone (ACTH) secretion by the anterior pituitary, as anti-cancer and anti-allergic and anti-inflammatory agents and to suppress the immune response. They may be injected, taken as pills, inhaled via a puffer or rubbed on to the skin.


This is a disorder in the structure of body tissues, with simplification of their structure, deformation of cells and their constituent parts. Congenital dysplasia due to genetic causes usually has manifold manifestations, often multiple and in different systems.

Mucosal dysplasias are locally linked to a particular organ, such as the stomach, intestines, or cervix. Unlike all other dysplasias, this type of dysplasia is not inherited and not caused by a global genetic failure, but is caused by the vital activity of pathological microflora.             Types of dysplasia                                                                                                                               Dysplasia is very diverse and heterogeneous, congenital and acquired dysplasia are essentially very different processes, some involve several systems, others - only areas of the mucosa.

Congenital dysplasias are manifested by developmental abnormalities - abnormalities in the structure, which do not interfere with normal functioning, and malformations - these abnormalities already disturb the functioning of the anatomical area.

Mucosal dysplasias do not form malformations and abnormalities, but they can lead to malignant processes. Absolutely different manifestations of dysplasia do not allow to create a unified classification, each researcher of the problem offers his own systematization of heterogeneous pathology, which is not free from flaws.

Congenital dysplasia are formed in the intrauterine period, clinical manifestations affect the covering tissues and the musculoskeletal system, their division is very conditional.

They are divided into:

 Dysplasia of the ectoderm, the surface tissue of the embryo, from which the outer covers are formed: skin with nails and hair and oral mucosa with teeth. The pathology can appear at any age, in any set of signs and with any severity. It can be just dry skin with small patches of atrophy and almost complete absence of teeth, or nesting baldness with no nails and with moon-shaped defects of dental enamel with a full set of teeth. It is also possible to simply have a reduced number of sweat glands in the skin, leading to rapid overheating as early as infancy and the danger of sudden death.

In the vast majority of sufferers of genetic connective tissue dysplasia there can be disorders of all body systems from minor to life-threatening and with any set of signs: neurological disorders, heart valve defects, skeletal changes, vascular aneurysms, softening of tracheal rings, renal prolapse, as well as leading to sudden death combined lesions of cardiovascular and respiratory systems. The most active burst of manifestations is noted in adolescence, when, for example, scoliosis and flat feet sharply progress, cardiac arrhythmia and myopia appear.   

 Joint dysplasia is manifested by congenital malformations of the large - hips and knees, as well as the small joints of the hand and foot, and can be considered as the same connective tissue dysplasia, but in a separate joint system. As a rule, the pathology is detected in an infant, but in its minimal form can go unnoticed, which is stated during the examination for accidental injury to the leg.

Fibrous dysplasia is manifested by single and multiple cysts in the bones. Some people live a healthy life to a ripe old age and find out about the genetic pathology in the form of a small cyst by chance during an X-ray for another reason. Others suffer chronic pain and limb deformity, often with shortening, due to multiple cystic cavities in the bone tissue.

Dysplasia of the mucous membranes of the internal organs is "earned" in the course of life. In most cases, the process is asymptomatic or has uncharacteristic and unstable minimal signs, found by microscopy of a piece of tissue. Dysplasia can progress from mild, through moderate and severe, up to stage zero cancer - and that is its main danger. Severe dysplasia is difficult, if not impossible, to reliably distinguish from non-invasive cancer in situ.

Gastric dysplasia can clinically manifest as gastric abnormalities, and it is not uncommon for a patient to have a Helicobacter infection. The pathology consists of a simplification of the cellular structure - reduced differentiation, changes in cell nuclei and other intracellular structures. Mild dysplasia not only progresses to moderate, but also regresses, similarly proceeds moderate, and severe is considered a precancerous process and is subject to serious treatment and monitoring. Gastric dysplasia is significantly less common than metaplasia, which is the formation of areas of cells very similar to those of the colon or small intestine in the mucosa. On microscopy around any dysplasia, areas of intestinal metaplasia are necessarily found, and this is also a precancerous process.

Primary urothelial dysplasia is an infrequent pathology that manifests as irritable bladder with frequent and painful urge to urinate. This variant of dysplasia is not commonly divided into grades, the probability of developing cancer on dysplastic background is just over 15% and it takes 4 to 8 years to pass to the null stage of cancer. 

Cervical mucosal dysplasia or cervical dysplasia is a very common pathology, because its leading cause is infection with the human papilloma virus. It is impossible to kill the virus itself - it is resistant to any medication, but it is lethal and in the vast majority of women cures itself within the next two to three years.

 Dendritic cells

 Antigen-presenting cells present in the skin and mucous membranes that form the first barrier to antigen entry; these cells capture antigen with their long processes and then migrate to regional lymph nodes where they present antigen peptide to T lymphocytes, thereby inducing the development of an immune response.

 Dose Responsive Curve

 A dose response curve illustrates the relation between the amount of a drug or other chemical administered to a person or an animal and the degree of response it produces.


 An endothelial cell layer refers to the layer of cells that lines the blood vessels and airways

 Epithelial mast cells

 Mast cells are a variety of Leukocytes or white blood cellscontaining granules which store a variety of inflammatory mediators including histamine and serotonin. Mast cells play a central role in inflammatory and immediate allergic reactions. The extracellular release of the mediators is known as degranulation and may be induced by the presence of a specific antigen (allergen). Epithelial mast cells are those found in the epithelium (the membranous tissue composed of one or more layers of cells separated by very little intercellular substance and forming the covering of most internal and external surfaces of the body and its organs. Skin and the lung linings are two examples of epithelium.)

Flare or Flare-up

 Period of worsening symptoms


A subpopulation of white blood cells including neutrophils, basophils, and eosinophils.

HRR mutation

 A group of genes that encode proteins responsible for reparation ("repair") of damaged DnA by homologous recommendation. Thus, these genes belong to the suppressors of tumor growth. They "store" genetic material and prevent mutations that can lead to malignant cell transformation. Unfortunately, sometimes mutations occur in these genes themselves. The result is genomic instability and an increased risk of cancer. HRR mutation assays help detect the carrier of inherited mutations in healthy people and take preventive measures in a timely manner. Evaluate the molecular genetic characteristics of cancer cells and predict their sensitivity to certain anti-tumor drugs.Choose the most effective treatment regimen.


HER2 is a receptor protein embedded in the cell membrane that regulates cell division. It is a member of the epidermal growth factor receptor (EGFR for short) family.The HER2 gene and protein play an important role in oncology. In some malignant tumors, particularly gastric, breast, and ovarian cancers, the gene is amplified - the number of its copies increases. It becomes overactive: in medical language it is called amplification of expression, or overexpression. Accordingly, the amount of protein also increases, and the cell multiplies faster. Because of this, the oncological disease has a more aggressive course.


A term referring to all non-cellular immune factors contained in extracellular biological fluid, including serum and lymph.

Head-to-head trial

 A clinical trial in which a test compound is evaluated against another compound

 Hypertonic Saline

 A solution with a higher salt concentration than in normal cells of the body and the blood. A salt solution containing more than 0.9% salt is hypertonic.


Interferons are a multigenic family of inducible cytokines with diverse functions, including antiviral, antiproliferative, antitumor, and immunomodulatory. More than 20 interferons are currently known, differing in structure, biological properties, and the predominant mechanism of action. IFNs are subdivided into three types:

Type I - known as viral interferon, includes IFN-a (leukocytic, synthesized by activated monocytes and B-lymphocytes), IFN-b (fibroblast, synthesized by fibroblasts and epithelial cells, macrophages), IFN-w, IFN-k;

Type II - known as immune, includes IFN-y (synthesized by activated T-lymphocytes and NK-cells);

Type III - was discovered later than type I and type II, information about it indicates the importance of IFN type III in certain types of viral infections.

Type I (IFN-a, IFN-b) have mainly antiviral and antiproliferative effects, to a lesser extent immunomodulatory effects. They are produced directly after meeting with the pathogen, their action is aimed at localizing the pathogen and preventing its spread in the body. The main effect of IFN-b is local, aimed at preventing the spread of the infectious agent from the site of its introduction. If the infectious agent is not inactivated at the site of infiltration and circulates in the body, its contact with lymphocytes and macrophages induces IFN-a production. The latter rapidly spreads through the bloodstream and penetrates into the surrounding tissues, as its main function is to protect distant organs. These interferons carry out early and nonspecific protection of the body against the infectious agent.The main action of type 2 interferons (IFN-y) is to participate in immune reactions. It begins to be produced during the subsequent stages of the infectious process by already sensitized T-lymphocytes and actively participates in the cascade of the specific immune response. IFNs have not only antiviral but also immunomodulatory effects by influencing the expression of the major histocompatibility complex (MHC) receptors. IFNs increase the expression of MNS class 1 molecules on all cell types, thereby improving the recognition of infected cells by cytotoxic T lymphocytes (CTLs). In addition, IFN-y enhances the expression of MNS class 2 molecules on antigen-presenting cells, resulting in improved presentation of viral antigens to CD4+ lymphocytes and activation of natural killer (NK) cells. IFNs also stimulate phagocytosis.

Antiproliferative and antitumor effects

The antiproliferative and antitumor effects of IFN are explained by the following mechanisms:

-Activation of cytotoxic cells;

-Enhancement of expression of tumor-associated antigens;

-modulation of antibody production;

-Inhibition of the action of tumor growth factors;

-Inhibition of RNA and protein synthesis by tumor cell;

-Deceleration of the cell cycle with transition to the "resting" phase;

-stimulation of tumor cells to maturation;

-restoration of inhibitory control of proliferation;

-inhibition of new vessel formation in the tumor;

-inhibition of metastasis;

-biomodulation of cytostatic activity: changes in metabolism and decreased clearance;

-overcoming drug resistance through inhibition of multiple drug resistance genes.


a physiological protective reaction triggered by innate immunity factors in response to the arrival of foreign objects that disrupt the body's antigenic homeostasis.

Immune memory

 A fundamental property of the immune system to develop a quantitatively and qualitatively more efficient response upon repeated intake of the same antigen.

 The immune system

A set of lymphoid organs, tissues and cells that provide biochemical, structural and functional individuality of the body by eliminating carriers of alien genetic information from it.

 Immune tolerance

 A fundamental property of the immune system not to develop a specific response when recognizing certain antigens (first of all, we are talking about the body's own molecules).

Incurable stage

Disease means the abandonment of specific treatment of the malignant process in favor of palliative care, because a cure of the disease is no longer possible. Incurable is not the refusal of medical care at all, but the transition to another stage of treatment - symptomatic and supportive, aimed at alleviating the patient's condition.   Inevitably, often in the first two years of malignant disease detection, the patients whose tumor was detected already in the metastatic stage 4 reach incurability. Patients who have undergone all the stages of radical treatment of the primary tumor and therapy for disease progression, whose metastases no longer respond to anti-tumor treatment, do not pass this stage.

Incurable does not mean denial of medical care to a person suffering from a fatal disease. An incurable patient has no prospects of recovery from cancer, but the need for medical care remains, because the unstoppable progression of the malignant process exhausts the body, causing pain, frequent vomiting, and disruption of the functions of all critical organs and systems.

Immune complex

A product of the antigen-antibody reaction, which may also contain components of the complement system; the formation of immune complexes is the most important defense mechanism against infections and toxins.


An ability to induce an immune response mediated by T- and B-lymphocytes.

Immunogenic peptide

 A peptide derived from an antigen that is presented by an antigen-presenting cell in complex with a class III histocompatibility molecule for recognition by T-helpers.

Immunodeficiency disease

 A disease that is based on immunodeficiency, i.e., a defect or deficiency of one or another immune factor.

Immunologically privileged areas of the body are tissues or organs that elicit a weak immune response to antigens, in particular protected from the transplant rejection reaction (CNS, anterior chamber of the eye, sex glands, thyroid gland).

In Vitro

 In an artificial environment, outside the living body e.g. in a test tube

 In Vivo

 In the living body of a plant or animal, or in real life


 Immune cells; white blood cells


 A type of white blood cell found in the body's lymph, a clear fluid that flows through the body and has an important function in defending the body against disease

 Langerhans cells

An antigen-presenting skin cell that migrates to regional lymph nodes upon antigen recognition, where it turns into dendritic cells and initiates an immune response.

Memory cells are long-lived T- and B-lymphocytes, which are formed as a result of previous contact with the antigen and ensure the formation of a secondary immune response upon its reintroduction.

The effector cells

These are the lymphocytes and phagocytes that directly damage the pathogen during the immune response.


This is the process that leads to the transformation of benign cells into malignant cells. In essence, it is the transformation of healthy tissue into tumor tissue, resulting in malignant cells. It is worth noting that absolutely any tissue or organ can be affected.

The main differences between a malignant tumor and a benign one are as follows:

The level of differentiation (maturation) of cells decreases.Their morphological properties change - cells differ from healthy cells, for example, they may have larger nuclei. In undifferentiated tumors it is difficult to determine which tissue they originated from. Functional activity is impaired. Pathologically altered tissue can not perform the functions assigned to it. For example, in lympholeukemia the number of lymphocytes increases dramatically, but they do not perform their protective function, so such patients often suffer from severe infections.Uncontrolled cell multiplication occurs and, as a consequence, tumor growth and metastasis formation.


 Mannitol is a naturally occurring sugar used variously as a food additive, a therapeutic product, and a sweetener.

   Natural antibodies

 A polyreactive antibody that is synthesized by

B1-lymphocytes a priori (even before the antigen enters the body) and are a humoral factor of innate immunity.

Natural killer

 A lymphocyte that destroys damaged or compromised cells in response to disrupted expression of class I histocompatibility molecules.

class I molecules on their surface.


 Disease-causing microorganism

 PIK3CA mutations

 A gene that encodes the p110 alpha protein, a subunit (component) of a larger protein, phosphatidylinositol 3-kinase (PI3K). It is a link in a cascade of biochemical reactions that regulate important processes in cells. Genetic disorders can alter the function and structure of this protein. Pathological activation of the signaling pathway occurs, and cells begin to proliferate uncontrollably.

These mutations are found in many malignant tumors. For example, they are often found in hormone-positive and HER-negative breast cancer. Such malignancies are resistant (resistant) to hormonal therapy. Thus, the analysis for PIK3CA mutations in certain cases helps the oncologist to assess the sensitivity of a malignant tumor to certain drugs and choose the optimal treatment tactics.

Primary immune response

An immune response that develops upon first contact with a certain antigen; it takes about 5-7 days to materialize and is less effective than the secondary response, which develops in an organism already immunized to the antigen.

Prostate specific antigen (PSA)

 An organ-specific protein of the prostate that is an oncomarker; its content in the serum is used in the diagnosis and monitoring of prostate cancer and adenoma of the prostate (benign prostatic hyperplasia, BPH).


 This protein is a product of the TR53 gene located on chromosome 17 and is an anti-oncogene, i.e. it prevents the development of malignant tumors. It is a central component of an intracellular defense system whose main function is to prevent the multiplication of cells with damaged DNA in the body. For this reason this gene is called "guardian of the genome".

TR53 mutations are one of the most frequent events in malignant cells. According to various data, from 50 to 80% of solid tumors have various damages of DNA in this gene, about 90% of which are missense mutations, i.e. lead to changes in protein structure

 Pharmacokinetic Profile

 How a drug interacts in the body in terms of its absorption, distribution, metabolism, and excretion


 An inert or innocuous substance used especially in controlled experiments to test and compare the efficacy of another, active, substance


 Prior to being administered to volunteers or patients


 An enzyme that breaks the internal bonds of a protein

 RAS mutations

 A family of proteins that are important links in the transmission of molecular signals within the cell. Their main role is to regulate cell division. Some mutations lead to their constant activation, and this contributes to the growth, metastasis of malignant tumor. RAS stands for Retrovirus Associated DNA Sequences. The Ras genes were so named because their role was first studied in malignant tumors that developed after infection with a sarcoma virus from the retrovirus family.                                                                                                                             By now, scientists have known for more than 30 years that RAS mutations occur in nearly one-third of human cancers. For example, their frequency is high in colorectal, pancreatic, and lung cancers.

Regulatory T lymphocytes

A subpopulation of T-lymphocytes that limits the intensity of the immune response to an antigen, thereby preventing the development of autoimmune damage; a distinction is made between constitutional and acquired regulatory T cells, with the latter also referred to as type 3 T-helper cells. Spontaneous cell-mediated cytotoxicity is an effector response of the immune system mediated by natural killer cells and occurs without antibodies.

ROS1 mutations

Encodes a receptor with tyrosine kinase activity that is embedded in the cell membrane and causes some effects when activated. As a result of some mutations, it can lead to uncontrolled cell proliferation and contribute to the development of a malignant tumor. Thus, ROS1 is classified as a proto-oncogene. In particular, mutations in it are present in 1-2% of cases of non-small cell lung cancer.


 A recurrence of symptoms of a disease after a period of improvement or remission


 Period when the symptoms of the patient's disease are not present

 Respiratory Failure

 A clinical term used to define the inability of the lungs to function

 Respiratory Insufficiency

 A clinical term used to define a failure to adequately provide sufficient oxygen to the body, or remove excess carbon dioxide


 The study of the flow of materials that behave in an interesting or unusual manner

 Safety Profile

 Evidence gathered that indicates a substance is safe to be administered to people

 Secondary immune response

 A more efficient and rapidly developing immune response upon repeated contact with a specific antigen; conditioned by the formation of long-lived memory cells after an infection.


this is the most severe, generalized form of the infectious process, which develops either when the pathogenic agent is highly pathogenic or when the body's defense systems respond inadequately. The international consensus recommends the following definition: sepsis is life-threatening internal organ dysfunction caused by dysregulation of the body's response to infection. In sepsis, there is a general intoxication syndrome, thrombohemorrhagic syndrome (hemorrhage) and internal organ damage


These molecules of certain pathogens are capable of stimulating T-lymphocytes by interaction with constant sites of their antigen-recognition receptors; this leads to polyclonal activation of T-cells and loss of the fundamental property of the immune response - specificity.


A subpopulation of T-lymphocytes that expresses CD4 molecules and antigen-recognition receptors capable of specific interaction with the histocompatibility molecule class ²² complex - immunogenic peptide on the surface of antigen-presenting cells; the main regulatory cell of the immune response.


 Numerous natural or synthetic compounds that contain a 17-carbon 4-ring system and can modify reactions in the body

 Synthesis, Synthetic Compound

 A substance that is made by a series of chemical or biochemical reactions

  Tumor differentiation  

Malignant tumors look different under the microscope. In some cases they resemble normal tissue, and in other cases they are very different from it.

Depending on this, pathologists and doctors conventionally divide malignant neoplasms into two types:

Highly differentiated tumors retain many features of normal cells and tissues. They sprout into neighboring organs and metastasize quite slowly.

Low differentiated tumors contain cells and tissues that are very different from normal. They behave much more aggressively, spreading faster through the body.

In other words, the degree of differentiation of a tumor is how much of its tissue and individual cells have lost the features of normal cells.

The degree of differentiation of a cancer determines how quickly it is able to spread through the body. And this, in turn, directly affects the prognosis for the patient. In addition, low-differentiated tumors respond less well to radiation therapy and chemotherapy. The oncologist takes this into account when designing a treatment program.

 Tumor invasion

This is the process of spreading cancer cells by means of tumor invasion through the basal membrane.

Invasion determines the ability of tumors to give rise to metastases - secondary foci of the cancer process away from the mother tumor, arising due to the migration of cancer cells. An obligatory condition for metastasis is the presence of the tumor's own capillary network. It is formed when the number of neoplastic cells reaches 103 (1-2 mm).

Stages of invasion:

Breaking of intercellular connections connecting cancer cells to each other; Attachment of tumor cells to the basal membrane; Destruction of the basal membrane by lysing (cleaving) enzymes; Migration of cells to adjacent tissues and organs.                                       Cancer cells in the process of invasion are more resistant to radiation and chemotherapy than stationary cells. This is largely due to the temporary loss of the ability of migrating cells to divide. Also, migrating tumor cells show increased activity of anti-apoptotic genes (genes that prevent programmed cell death - apoptosis). And, because chemotherapeutic drugs aim to stimulate apoptosis, their resistance to treatment increases. Invasive tumor growth not only promotes its spread throughout the body, but also provides cancer cells with intensive nutrition. Therefore, it can be said that invasion is a factor in the "rooting" of the neoplasm.

T790M mutations

Mutation designation that occurs in the epidermal growth factor receptor (EGFR) gene. This protein is a receptor embedded in the cell membrane. When it is activated, a cascade of biochemical reactions is triggered in the cell and it begins to multiply uncontrollably.

 Toxicology Study

 Investigation into the adverse effects of a substance in an animal or human

 T-helper type 1

 A subpopulation of T-helpers that secrete cytokines IL-2,

γ-IFN, TNF-α and -β, etc., thereby directing the immune response predominantly to the cellular pathway with activation of cytotoxic T lymphocytes.

 Type 2 T-helpers

 A subpopulation of T-helpers secreting IL-4, IL-5, IL-6, etc., thereby directing the immune response mainly to the humoral channel with production of specific antibodies.                       T-helpers of the 3rd type.                                                                                                                   A subpopulation of T-helpers that secrete cytokines IL-10 and TDF-β, thereby suppressing the immune response process.


A process of selective absorption and digestion of various objects (microbes, foreign particles, damaged cells, etc.) by leukocytes.

Tumor necrosis factor alpha

A so-called "master cytokine", i.e., the main proinflammatory cytokine that can induce the production of other immune mediators that mediate the development of an inflammatory reaction.