Neoplasia is an abnormal and excessive type of tissue growth. The growth of neoplasia is not coordinated with normal surrounding tissue, and it keeps growing abnormally, even if the original trigger is removed. This abnormal growth usually (but not always) forms a mass. When forming a mass, it can be called a tumor .
ICD-10 classifies neoplasms into four major groups: benign neoplasms, in situ neoplasms, malignant neoplasms, and uncertain or unknown behavioral neoplasms. Malignant neoplasms are also known as cancer and are the focus of oncology.
Before abnormal tissue growth, such as neoplasia, cells often experience abnormal growth patterns, such as metaplasia or dysplasia. However, metaplasia or dysplasia does not always develop into neoplasia. The word comes from Ancient Greek ???? - neo "new" and ?????? plasma "formation, creation".
Video Neoplasm
Jenis
Neoplasms can be benign, potentially malignant, or malignant (cancer).
- Benign tumors include uterine fibroids, osteophytes and melanocytic nevi (skin mole). They are restricted and localized and do not turn cancerous.
- Malignant neoplasms include carcinoma in situ. They are localized, non-invasive and devastating but in time, may turn cancerous.
- Malignant neoplasms are commonly called cancers. They attack and destroy the surrounding tissue, can form metastasis and, if left untreated or unresponsive to treatment, will be fatal. Secondary neoplasm refers to one class of cancerous tumors that are the metastatic branches of the primary tumor, or seemingly unrelated tumors that increase the frequency after certain cancer treatments such as chemotherapy or radiotherapy.
- There is rarely a metastatic neoplasm of unknown primary cancer sites and this is classified as an unknown primary origin cancer
Clonality
Neoplastic tumors are often heterogeneous and contain more than one cell type, but initiation and continued growth usually depend on a population of neoplastic cells. These cells are considered clonal - that is, they are from the same cell, and all carry the same genetic or epigenetic anomaly - as evidenced by clonality. For lymphoid neoplasms, eg. lymphoma and leukemia, clonalities are evidenced by amplification of a single rearrangement of their immunoglobulin genes (for B cell lesions) or T cell receptor genes (for T cell lesions). Clonality demonstrations are now considered necessary to identify lymphoid cell proliferation as neoplastic.
It is very tempting to define neoplasms as clonal cell proliferation, but clonality demonstrations are not always possible. Therefore, cloning is not required in the definition of neoplasia.
Neoplasia vs. tumor
Tumors (English English) or tumors (English English), Latin for swelling , one of the signs of cardinal inflammation, any form of swelling, neoplastic or not. Current English, however, both medical and non-medical, uses tumors as synonyms for neoplasms (cystic or solid fluid lesions that may or may not be formed by abnormal growth of neoplastic cells) are visible enlarges in size. Some neoplasms do not form tumors; These include leukemia and most forms of carcinoma in situ. Tumor is also not identical with cancer . Although cancer is malignant, tumors can be benign, precancerous, or malignant.
The terms mass and nodule are often used synonymously with tumors . In general, however, the term tumor is used in general, without reference to the physical size of the lesion. More specifically, the term mass is often used when the lesion has a maximum diameter of at least 20 millimeters (mm) in the largest direction, whereas the term nodule is usually used when the lesion size is less than 20 mm in its largest dimension (25.4 mm = 1 inch).
Maps Neoplasm
Cause
Neoplasm can be caused by abnormal tissue proliferation, which can be caused by a genetic mutation. Not all types of neoplasms cause tumorous overgrowth, but (such as leukemia or in situ carcinoma) and similarities between neoplasmic growth and regenerative processes, eg, de-differentiation and rapid cell proliferation have been demonstrated.
More recently, tumor growth has been studied using mathematics and continuum mechanics. Vascular tumors (formed from blood vessels) are thus viewed as an amalgam of a solid framework formed by sticky cells and organic fluids filling the space in which cells can grow. Under this type of model, mechanical stress and strain can be handled and its effect on tumor growth and surrounding tissue and blood vessels are described. Recent findings from experiments using this model indicate that tumor active growth is confined to the outer edge of the tumor, and that the underlying normal stiff tissue inhibits tumor growth as well.
Benign conditions that are not associated with abnormal proliferation of tissue (such as sebaceous cysts) may also appear as tumors, but have no malignant potential. Breast cysts (as occurs generally during pregnancy and at other times) are other examples, such as encapsulated gland encapsulation (thyroid, adrenal gland, pancreas).
Encapsulated hematomas, encapsulated necrotic tissue (from insect bites, foreign objects, or other harmful mechanisms), keloids (excessive overgrowth of scar tissue) and granulomas may also appear as tumors.
Discrete localized enlargement of normal structures (ureter, blood vessels, intrahepatic or extrahepatic biliary ducts, pulmonary inclusions, or gastrointestinal duplications) due to outflow or narrowing obstruction, or abnormal connections, may also appear as tumors. Examples are arteriovenous fistulas or aneurysms (with or without thrombosis), biliary fistulas or aneurysms, sclerosis cholangitis, cysticercosis or hydatid cysts, intestinal duplication, and pulmonary inclusions as seen in cystic fibrosis. It can be dangerous to biopsy a number of tumor types where the leakage of the contents has the potential to be catastrophic. When such types of tumors are encountered, diagnostic modalities such as ultrasound, CT scan, MRI, angiogram, and nuclear drug scans are used before (or during) surgical biopsy or excision in order to avoid these severe complications.
The nature of the tumor is determined by imaging, by surgical exploration, or by a pathologist after tissue examination of a biopsy or surgical specimen.
Malignant neoplasms
DNA damage
DNA damage is considered a major cause of malignant neoplasms known as cancer. Its main role in progression to cancer is illustrated in the figure in this section, in the box near the top. (The main features of DNA damage, epigenetic changes and imperfect DNA repair in progression to cancer are shown in red.) DNA damage is very common. The naturally occurring DNA damage (largely due to cellular metabolism and the properties of DNA in water at body temperature) occurs at a rate of over 60,000 new, average, per human, per day damage [also seen DNA article damage (occurring naturally) )]. Additional DNA damage may result from exposure to exogenous agents. Tobacco smoke causes an increase in exogenous DNA damage, and DNA damage is a possible cause of lung cancer from smoking. UV rays from solar radiation cause important DNA damage in melanoma. Helicobacter pylori infection produces high levels of reactive oxygen species that damage DNA and contribute to stomach cancer. Bile acids, at high levels in the intestines of humans consume foods high in fat, also cause DNA damage and contribute to colon cancer. Katsurano et al. shows that macrophages and neutrophils in the inflamed colonic epithelium are the source of the reactive oxygen species that causes DNA damage that initiates colonic tumorigenesis. Some sources of DNA damage are shown in the box at the top of the image in this section.
Individuals with germ line mutations that cause deficiency in one of 34 DNA repair genes (see article on DNA deficiency repair) are at increased risk of cancer. Some mutations of germ lines in DNA repair genes cause up to 100% chance of a lifetime of cancer (eg, p53 mutation). These germ line mutations shown in the box to the left of the image with arrows indicate their contribution to the lack of DNA repair.
About 70% of malignant neoplasms have no hereditary component and are called "sporadic cancer". Only a small percentage of sporadic cancers have a deficiency in DNA repair due to mutations in DNA repair genes. However, the majority of sporadic cancers have a deficiency in DNA repair due to epigenetic changes that reduce or silence the expression of DNA repair genes. For example, of 113 sequential colorectal cancers, only four had missense mutations in the MGMT DNA repair genes, while the majority had reduced MGMT expression due to methylation of the promoter region of MGMT (epigenetic change). Five reports present evidence that between 40% and 90% of colorectal cancers have reduced the expression of MGMT due to MGMT region promoter methylation.
Similarly, out of 119 cases of colorectal cancer that did not improve mectatch improvements that did not have expression of PMS2 gene gene repair, PMS2 deficiency at 6 due to mutations in the PMS2 gene, while in 103 cases PMS2 expression deficiency because the partner pair MLH1 is suppressed due to promoter PMS2 is unstable in the absence of MLH1). In the other 10 cases, the loss of PMS2 expression is likely due to epigenetic overexpression of the microRNA, miR-155, which decreases-regulates MLH1.
In further examples, epigenetic defects are found at frequencies ranging from 13% -100% for DNA repair genes BRCA1, WRN, FANCB, FANCF, MGMT, MLH1, MSH2, MSH4, ERCC1, XPF, NEIL1 and ATM. This epigenetic defect occurs in different types of cancer (eg breast, ovary, colorectal and head and neck). Two or three deficiencies in the expression of ERCC1, XPF or PMS2 occur simultaneously in most of the 49 colon cancers evaluated by Facista et al. Epigenetic changes that cause reduced expression of DNA repair gene are indicated in the center box at the third level of the upper portion of the image in this section, and the resulting DNA repair deficiency is indicated at the fourth level.
When the expression of the DNA repair gene decreases, DNA damage accumulates in cells at a higher than normal level, and this excessive damage leads to increased frequency of mutations or epimutation. Mutation rates are greatly increased in damaged cells in inappropriate DNA repair or in homologous recombination repair (HRR).
During repair of double strand DNA damage, or repair of other DNA damage, repair sites that are not repaired can cause silencing of epigenetic genes. Improved DNA deficiency (level 4 in the image) leads to an increase in DNA damage (level 5 in the image) resulting in an increase in somatic mutation and epigenetic changes (level 6 in the figure).
Field deformity, normal tissue that appears with some changes (and is discussed in the section below), is a common precursor to the development of irregular clonal tissue and reproduces incorrectly in malignant neoplasms. Such field defects (the second level from below the image) may have many epigenetic mutations and changes.
Once the cancer is formed, it usually has genomic instability. This instability may be caused by reduced DNA repair or excessive DNA damage. Because of these instabilities, the cancer continues to evolve and produce sub clones. For example, kidney cancer, sampled in 9 areas, has 40 mutations everywhere, indicating tumor heterogeneity (ie in all areas of the cancer), 59 mutations held by some (but not all areas), and 29 private mutations "only. present in one area of ​​cancer.
Field disabled
Various other terms have been used to describe this phenomenon, including "field effect", "field of cancer", and "field carcinogenesis". The term "field of cancer" was first used in 1953 to describe an area or "plane" of the epithelium that has been preconduced by (at the time) most of the unknown process so as to affect the development of the cancer. Since then, the terms "cancer field" and "field defects" have been used to describe pre-malignant tissue where new cancer is likely to emerge.
An important field deformity in development becomes cancerous. However, in most cancer studies, as shown by Rubin "Most studies in cancer research have been conducted on well-defined tumors in vivo, or in the discrete neo-plastic focus of in vitro, but there is evidence that more than 80% of the mutations somatik found in the human phenotype human color tumor mutator occurred before the onset of clonal expansion of the terminal. Similarly, Vogelstein et al showed that more than half of the somatic mutations identified in the tumors occurred in the pre-neoplastic phase (in the field defects), during the growth of the cells which seems normal. Thus, epigenetic changes present in the tumor may have occurred in pre-neoplastic field defects.
The expanded view of the field effect has been called the "field etiological effect", which includes not only molecular and pathological changes in pre-neoplastic cells but also the influence of exogenous environmental factors and molecular changes in local micro-environments on neoplastic evolution from tumor initiation to patients. Dead.
In the colon, field defects may arise by the natural selection of mutant cells or cells that are epigenetically altered between the stem cells at the base of one of the intestinal crypts on the inner surface of the colon. Epigenetically modified mutant or epigenetic stem cells can replace other stem cells adjacent to natural selection. Thus, abnormal tissue patches may appear. The figure in this section includes a recently resected and open-faced colon photo segment showing colon cancer and four polyps. Below this photo there is a schematic diagram of how a large patch of mutant cells or epigenetically modified cells has been formed, shown by large yellow areas on the diagram. In the first major patch in the diagram (large clone of a cell), such a second mutation or epigenetic change may occur so that the given host cell benefits from other stem cells in the patch, and this altered stem cell may expand. clonally forming a secondary patch, or sub-clone, inside the original patch. This is shown in the diagram by four smaller patches of different colors in the large yellow original area. In these new patches (sub-clones), the process can be repeated several times, indicated by smaller patches in four different clonal (clonally different colored diagrams) of secondary patches until stem cells appear that produce little polyp or Malignant neoplasms (cancer).
In the photograph, the visible field defects of this large intestine segment have produced four polyps (labeled with polyps, 6mm, 5mm, and two of 3mm, and about 3cm in the longest dimension). This neoplasm is also shown, on the diagram beneath the photo, by 4 small brown circles (polyps) and larger red areas (cancer). Cancer of the photo occurs in the area of ​​the colon cecal, where the large intestine joins the small intestine (labeled) and where the appendix occurs (labeled). The fat in the photo is outside the outer wall of the large intestine. In the colon segment shown here, the large intestine is cut open longitudinally to expose the inner surface of the colon and to display cancer and polyps that occur within the epithelial lining of the colon.
If a common process in which sporadic colon cancer arises is the formation of pre-neoplastic clones that spread through natural selection, followed by the formation of internal sub-clones in the early clones, and sub-clones therein, colon cancer should generally be associated with, and preceded by, areas of increased abnormality that reflect the succession of pramalign events. The most widespread abnormality areas (yellow outer yellow areas in the diagram) will reflect the earliest events in the formation of malignant neoplasms.
In the experimental evaluation of DNA specific deficiency defects in cancer, many specific DNA repair deficiencies have also been shown to occur in field defects around the cancer. The table, below, provides examples for where the deficiency of DNA repair in a cancer is shown to be caused by epigenetic changes, and a somewhat lower frequency that causes the same lack of DNA repair to be found in the surrounding field defects.
Some small polyps on the field defect shown in the open colon photo segment may be relatively benign neoplasms. Polyps less than 10mm in size, found during colonoscopy and followed by repeated colonoscopy for 3 years, 25% unchanged in size, 35% regression or shrinking in size while 40% increased.
Genomic Instability
Cancer is known to show genomic instability or mutator phenotype. DNA coding of proteins in the nucleus is about 1.5% of total genomic DNA. In this protein-coding DNA (called exome), the average cancer of the breast or colon can have about 60 to 70 mutations that convert proteins, of which about 3 or 4 may be a "driver" mutation, and what remains may be "Passengers However, the average number of DNA sequence mutations across the genome (including non-protein-coding regions) in breast tissue samples is about 20,000. In the average melanoma tissue sample (where melanoma has a higher mutation mutation frequency) the total number of DNA sequence mutations is about 80,000. This is proportional to the very low mutation frequency of about 70 new mutations across the genomes across generations (parent to child) in humans.
The high frequency of mutations in total nucleotide sequences in cancer suggests that frequent early changes in field defects that cause cancer (eg, yellow areas in the diagram in this section) are deficient in DNA repair. Large field defects around colon cancer (extending to about 10 cm on each side of the cancer) are demonstrated by Facista et al. often have epigenetic defects in 2 or 3 DNA repair proteins (ERCC1, XPF or PMS2) in all areas of the field defect. Deficiencies in DNA repair lead to an increase in the rate of mutation. Deficiencies in DNA repair, in itself, can allow accumulated DNA damage, and the synthesis of transceptions that are prone to error passing through some of the damage can lead to mutations. In addition, a faulty repair of the accumulation of DNA damage can cause epimutation. This new mutation or epimutation can provide proliferative benefits, resulting in a defective field. Although mutations in DNA repair genes do not, in themselves, provide selective benefits, they can be brought together as passengers in cells when cells receive additional mutations/epimutations that provide proliferative benefits.
Etymology
The term 'neoplasm' is a synonym of "tumor". 'Neoplasia' denotes the process of neoplasm/tumor formation, a process called a 'neoplastic' process. 'Neoplastic' itself comes from the Greek 'neo' - new and 'plastic' - formed, formed.
The term tumor is derived from the Latin word "tumor" "swelling" eventually from the verb tum? Re "swell". In the Commonwealth, spelling "tumors" are commonly used, whereas in the US it is usually spelled "tumor".
In its medical sense it traditionally means abnormal swelling of the flesh. The Roman medical encyclopedic expert Celsus (ca 30 BC-38 AD) described four cardinal signs of acute inflammation as tumors ,
In contemporary English, the word tumor is often used as a synonym for cystic growth (fluid-filled) or solid neoplasms (cancer or non-cancer), with other forms of swelling often referred to as swelling .
Commonly related terms in the medical literature, in which the noun tumefaction and tumescence (derived from the adjective tumefied), are the current medical term for non-neoplastic swelling. This type of swelling is most often caused by inflammation caused by trauma, infection, and other factors.
Tumors can be caused by conditions other than the growth of neoplastic cells that are too fast. Cysts (such as sebaceous cysts) are also called tumors, although they do not have neoplastic cells. This is the standard in medical billing terminology (especially when billing for growth whose pathology has not been determined).
See also
- Somatic evolution in cancer
- List of biological developmental disorders
- Cancer epidemiology
References
External links
Source of the article : Wikipedia
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