Cancer is genetic because it is caused by changes in dna but not usually inherited, Modificările funcţionale ale celulelor canceroase în raport cu celulele normale


The human body is composed of trillions of cells, which constantly grow, divide and die. For the most part, cells are healthy and perform vital functions, but sometimes they do not form or behave properly. Cancer begins when an abnormal cell grows and does not stop dividing. Cancer cells also do not obey the laws of contact inhibition, which means that cancerous cells propagate when they touch another cell normal cells stop dividing when this happens.

This proliferation of cancerous cells enables the disease to quickly form tumors and spread throughout the body. Keywords cancer, cell cycle, type of tumors, genetics of cancer Rezumat Scopul acestui articol este de a explica ce modificări funcţionale apar atunci când celulele normale se transformă în celule can­ceroase. Organismul uman este alcătuit din trilioane de celule care cresc, se divid şi mor. Majoritatea celulelor sunt sănătoase şi îndeplinesc funcţii vitale, dar uneori celulele nu se comportă corespunzător.

Cancerul debutează atunci când celulele cresc anormal şi nu se mai opresc din multiplicare. Celulele can­ce­roase nu se supun regulii cancer is genetic because it is caused by changes in dna but not usually inherited de contact, ceea ce în­seam­nă că ele se vor multiplica chiar dacă vor fi în contact cu alte celule celulele normale se opresc din divi­ziu­ne atunci când sunt în contact cu o altă celulă.

Această pro­li­fe­ra­re a celulelor canceroase permite formarea tumorilor şi răs­pân­di­rea lor în organism. Cuvinte cheie cancer ciclu celular tipuri de tumori genetică oncologică Introduction Why does a normal cell suddenly become a foreign for the body, breaking the rules, dividing recklessly, invading other tissues, usurping resources, and in some cases eventually killing the body in which it lives?

To understand how and why cells rebel, papillomavirus come curarlo need to understand the normal functions of cell growth and reproduction. Research in cell biology, biochemistry and molecular biology has provided astonishingly detailed information about the molecules and processes that allow cells to divide, grow, differentiate and perform their essential functions.

This basic knowledge of cell biology has also led to practical discoveries about the mechanisms of cancer. Specific molecules that control the progression of a cell through the cell cycle regulate cell growth. An understanding of normal cell cycle processes and how those processes go awry provides key information about the mechanisms that trigger cancer. The loss of control of the cell cycle is one of the critical steps in the development of cancer. Although cancer cancer is genetic because it is caused by changes in dna but not usually inherited at least different diseases, all cancer cells share one important characteristic: they are abnormal cells in which the processes regulating normal cell division are disrupted.

That is, cancer develops from changes that cause normal cells to acquire abnormal functions. These changes are often the result of inherited mutations or are induced by environmental factors such as UV light, X-rays, chemicals, tobacco products and viruses.

All evidence suggests that most cancers are not the result of one single event or factor. Rather, around four to seven events are usually required for a normal cell to evolve through a series of premalignant stages into an invasive cancer.

Often many years elapse between the initial event and the development of cancer. The development of molecular biological techniques may help in the diagnosis of potential cancers in the early stages, long before tumors are visible.

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What is cancer? Cancer results from a series of molecular events that fundamentally alter the normal properties of cells. In cancer cells, the normal control systems that prevent cell overgrowth and the invasion of other tissues are disabled. These altered cells divide and grow in the presence of signals that normally inhibit cell growth, therefore they no longer require special signals to induce cell growth and division.

As these cells grow, they develop new characteristics, including changes in cell structure, decreased cell adhesion and production of new enzymes.

Functional changes of cancerous cells in relation to normal cells

These heritable changes allow the cell and its progeny to divide and grow, even in the presence of normal cells that typically inhibit the growth of nearby cells. Such changes allow the cancer cells to spread and invade other tissues.

The abnormalities in cancer cells usually result from mutations in protein-encoding genes that regulate cell division. Over time, more genes become mutated. This is often because the genes that make the proteins that normally repair DNA damage are themselves not functioning normally because they are also mutated.

Consequently, mutations begin to increase in the cell, causing further abnormalities in that cell and the daughter cells. Some of these mutated cells die, but other alterations may give the abnormal cell a selective advantage that allows it to multiply much more rapidly than the normal cells.

This enhanced growth describes most cancer cells, which have gained functions repressed in the normal, healthy cells. As long as these cells remain in their original location, they are considered benign; if they become invasive, they are considered malignant.

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Cancer cells in malignant tumors can often metastasize, sending cancer cells to distant sites in the body where new tumors may form. Genetics of cancer Alterations in the same gene are often associated with different forms of cancer. These malfunctioning genes can be broadly classified into three groups: The first group, called proto-oncogenes, produces protein products that normally enhance cell division or inhibit normal cell death.

The mutated forms of these genes are called oncogenes.

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The second group, called tumor suppressors, makes proteins that normally prevent cell division or cause cell death.

The third group contains DNA repair genes, which help prevent mutations that lead to cancer. Controlled cell growth is maintained by regulation of proto-oncogenes, which accelerate growth, and tumor suppressor genes, which slow cell growth. Mutations that produce oncogenes accelerate growth, while those that affect tumor suppressors prevent the normal inhibition of growth. In either case, uncontrolled cell growth occurs. In normal cells, proto-oncogenes code for the proteins that send a signal to the nucleus to stimulate cell division.

These signaling proteins act in a series of steps called signal transduction cascade or pathway.

Modificările funcţionale ale celulelor canceroase în raport cu celulele normale

This cascade includes a membrane receptor for the signal molecule, intermediary proteins that carry the signal through the cytoplasm and transcription factors in the nucleus that activate the genes for cell division. In each step of the pathway, one factor or protein activates the next; however, some factors can activate more than one protein in the cell.

Cancer is genetic because it is caused by changes in dna but not usually inherited are altered versions of the proto-oncogenes that code for these signaling molecules.

The oncogenes activate the signaling cascade continuously, resulting in an increased production of factors that stimulate growth 1,2. Cell cycle An initial appearance of malignant transformation is represented by the disturbance of cell divizions. Normal cells grow and divide in accordance with the cell cycle. Mutations in proto-oncogenes or in tumor suppressor genes allow a cancerous cell to grow and divide without the normal controls imposed by the cell cycle.

The major events in the cell cycle are described in Figure 1.

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Figure 1. Cell cycle The cell cycle is an ordered process of events that occurs in four stages. During the two gap phases, G1 and G2, the cell is actively metabolizing, but not dividing. In S synthesis phase, the chromosomes duplicate as a result of DNA replication. During the M mitosis phase, the chromosomes separate in the nucleus and the division of the cytoplasm cytokinesis occurs. There are checkpoints in the cycle at the end of G1 and G2 that can prevent the cell form entering the S or M phases of the cycle.

Cells that are not in the process of diving are in the G0 stage, which includes most adult cells. Several proteins control the timing of the events in the cell cycle, which is tightly regulated to ensure that cells divide only when necessary.

Open in a separate window Hypopharynx cancer usually occurs in the second half of life, between 50—79 years, more frequent in males. There have been described pharyngeal cancers in children. An increased incidence of post—cricoid cancer has been encountered in women with Plummer—Vinson syndrome from anglo—saxon countries. Some authors Wahlberg by analyzing statistics from — period in Sweden noticed a rate of 1.

The loss of this regulation is the hallmark of cancer 3. Major control switches of the cell cycle are cyclin-dependent kinases.

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Each cyclin-dependent kinase forms a complex with a particular cyclin, a protein that binds and activates the cyclin-dependent kinase. The kinase part of the complex is an enzyme that adds a phosphate to various proteins required for tratament pentru paraziti of a cell through the cycle.

These added phosphates alter the structure of the protein and can activate or inactivate the protein, depending on its function. Cancer cells do not stop dividing, so what stops a normal cell from dividing? In terms of cell division, normal cells differ from cancer cells in at least four ways: Normal cells require external growth factors to divide. When synthesis of these growth factors is inhibited by normal cell regulation, the cells stop dividing.

Cancer cells have lost the need for positive growth factors, so they divide whether or not these factors are present.

Consequently, they do not behave as part of the tissue — they have become independent cells. Normal cells show contact inhibition; that is, they respond to contact with other cells by ceasing cell division.

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Therefore, cells can divide to fill in a gap, but they stop dividing as soon as there are enough cells to fill the gap. This characteristic is lost in cancer cells, which continue to grow after they touch other cells, causing a large mass of cells to form.

Normal cells age and die, and are replaced in a controlled and orderly manner by new cells. Apoptosis is the normal, programmed death of cells. Normal cells can divide only about fifty times before they die. This is related to their ability to replicate DNA only a limited number of times.

The epidemiology of hypopharynx and cervical esophagus cancer

Each time the chromosome replicates, the ends telomeres shorten. In growing cells, the enzyme telomerase replaces these lost ends. Adult cells lack telomerase, limiting the number of times the cell can divide. However, telomerase is activated in cancer cells, allowing an unlimited number of cell divisions. Normal cells cease to divide and die when there is DNA damage or when cell division is abnormal.

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