If you have a lump on your butt cheek what can that mean?


The lump could be a tumor, the name for a neoplasm or a solid lesion formed by an abnormal growth of cells (termed neoplastic) which looks like a swelling. The lump could also be a mosquito or spider bite. If it doesn't go away soon, show a doctor.

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In medical parlance, swelling, turgescence or tumefaction is a transient abnormal enlargement of a body part or area not caused by proliferation of cells. It is caused by accumulation of fluid in tissues. It can occur throughout the body (generalized), or a specific part or organ can be affected (localized). Swelling is considered one of the five characteristics of inflammation; along with pain, heat, redness, and loss of function. In a general sense, the suffix "-megaly" is used to indicate a growth, as in hepatomegaly, acromegaly, and splenomegaly. A body part may swell in response to injury, infection, or disease. Swelling, especially of the ankle, can occur if the body is not circulating fluid well. Generalized swelling, or massive edema (also called anasarca), is a common sign in severely ill people. Although slight edema may be difficult to detect to the untrained eye, especially in an overweight person, massive edema is very obvious. Congenital swellings are present since birth, e.g., hemangioma, meningocele, etc. Some congenital swellings may not appear since birth, but later in life, e.g., branchial cyst, dermatoid cyst, thyroglossal cyst. Traumatic swellings develop immediately after trauma, e.g., hematoma, dislocation. Inflammatory swelling: It may be either acute or chronic variety. The presentations of acute swellings are redness, local fever, pain and impairment of function of the affected organ. The related lymph nodes will be affected and will show signs of acute lymphadenitis. Chronic inflammatory swellings will show the signs of acute inflammatory swellings, but in subdued form. In this case, edema might not occur. Such swellings can be differentiated from neoplastic swellings by the fact that neoplastic swellings never recede in size, but inflammatory swellings may show occasional diminution. Causes of generalized swelling: Some possible causes of a swollen limb include: While it is possible for mild swelling to go away on its own, several things can be done to relieve the symptoms or hasten the process. The RICE first aid method of rest and protecting the affected area has long been taught as a short term solution. The application of oxygen is known to assist in the reduction of swelling. An effective option for extrinsic treatment of swelling and it's reduction is Kinesio Tape (KT). By strategically cutting and placing Kinesio Tape above the area of swelling it assists in the removal of edema (swelling) by directing the exudates toward lymphatic ducts. This is aided by KT's inherent property of lifting the epidermis away from the dermis creating a larger area for blood flow and lymphatic movement.][ M: INT, SF, LCT anat/phys/devp noco (i/b/d/q/u/r/p/m/k/v/f)/cong/tumr (n/e/d), sysi/epon proc, drug (D2/3/4/5/8/11) M: SKA anat/phys/devp noco/cong/tumr, sysi/epon proc, drug (D10)
Carcinoma in situ (CIS) is an early form of cancer that is defined by the absence of invasion of tumor cells into the surrounding tissue, usually before penetration through the basement membrane. In other words, the neoplastic cells proliferate in their normal habitat, hence the name "in situ" (Latin for "in its place"). For example, carcinoma in situ of the skin, also called Bowen's disease, is the accumulation of neoplastic epidermal cells within the epidermis only, that has failed to penetrate into the deeper dermis. For this reason, CIS will usually not form a tumor. Rather, the lesion is flat (in the skin, cervix, etc.) or follows the existing architecture of the organ (in the breast, lung, etc.). Some CIS, however, do form tumors, such as in the colon (polyps), in the bladder (pre-invasive papillary cancer), or in the breast (more properly called ductal carcinoma in situ). Many forms of invasive carcinoma (the most common form of cancer) originate after progression of a CIS lesion. Therefore, CIS is considered a precursor or incipient form of cancer that may, if left untreated long enough, transform into a malignant neoplasm. When explaining a laboratory report to a patient, most doctors will refer to CIS as "pre-cancer", not cancer. However, because most forms of CIS have a high probability of progression into invasive carcinoma, doctors will usually recommend that the lesion be completely removed. Therefore, CIS is usually treated in much the same way as a malignant tumor. In the TNM classification, carcinoma in situ is reported as TisN0M0 (Stage 0). These terms are related since they represent the three steps of the progression toward cancer: Carcinoma in situ is, by definition, a localized phenomenon, with no potential for metastasis unless it progresses into a "true" cancer. Therefore, its removal eliminates the risk of subsequent progression into a life-threatening condition. This concept is in some ways analogous to uprooting a tree - easy when a young sapling, and much more difficult later. Some forms of CIS (e.g. colon polyps and polypoid tumours of the bladder) can be removed using an endoscope, without conventional surgical resection. Dysplasia of the uterine cervix is removed by excision (cutting it out) or by burning with a laser. Bowen's disease of the skin is removed by excision. Other forms require major surgery, the best known being intraductal carcinoma of the breast (also treated with radiotherapy). One of the most dangerous forms of CIS is the "pneumonic form" of bronchioloalveolar carcinoma of the lung, which can require extensive surgical removal of large parts of the lung. When too large, it often cannot be completely removed, with eventual disease progression and death of the patient. M: NEO tsoc, mrkr tumr, epon, para drug (L1i/1e/V03)
Neoplasm (from ancient Greek νεο- neo-, "new" + πλάσμα plasma, "formation", "creation") is an abnormal mass of tissue as a result of neoplasia. Neoplasia is the abnormal growth or division of cells. Prior to neoplasia, cells often undergo an abnormal pattern of growth, such as metaplasia or dysplasia. However, metaplasia or dysplasia do not always progress to neoplasia. The growth of neoplastic cells exceeds, and is not coordinated with, that of the normal tissues around it. The growth persists in the same excessive manner even after cessation of the stimuli. It usually causes a lump or tumor. Neoplasms may be benign, pre-malignant (carcinoma in situ) or malignant (cancer). In modern medicine, the term tumor means a neoplasm that has formed a lump. In the past, the term tumor was used differently. Some neoplasms do not cause a lump. A neoplasm can be benign, potentially malignant (pre-cancer), or malignant (cancer). Because neoplasia includes very different diseases, it is difficult to find an all-encompassing definition. The definition of the British oncologist R.A. Willis is widely cited: "A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues, and persists in the same excessive manner after cessation of the stimulus which evoked the change." This definition is criticized because some neoplasms, such as nevi, are not progressive. Neoplastic tumors often contain more than one type of cell, but their initiation and continued growth is usually dependent on a single population of neoplastic cells. These cells are presumed to be clonal – that is, they are descended from a single progenitor cell. Sometimes, the neoplastic cells all carry the same genetic or epigenetic anomaly that becomes evidence for clonality. For lymphoid neoplasms, e.g. lymphoma and leukemia, clonality is proven by the amplification of a single rearrangement of their immunoglobulin gene (for B cell lesions) or T-cell receptor gene (for T cell lesions). The demonstration of clonality is now considered to be necessary to identify a lymphoid cell proliferation as neoplastic. It is tempting to define neoplasms as clonal cellular proliferations but the demonstration of clonality is not always possible. Therefore, clonality is not required in the definition of neoplasia. Tumor (Latin for swelling, one of the cardinal signs of inflammation) originally meant any form of swelling, neoplastic or not. Current English, however, both medical and non-medical, uses tumor as a synonym of neoplasm. Some neoplasms do not form a tumor. These include leukemia and most forms of carcinoma in situ. DNA damage is considered to be the primary underlying cause of malignant neoplasms (cancers). Its central role in progression to cancer is illustrated in the figure in this section, in the box near the top. (The central features of DNA damage, epigenetic alterations and deficient DNA repair in progression to cancer are shown in red.) DNA damage is very common. Naturally occurring DNA damages (mostly due to cellular metabolism and the properties of DNA in water at body temperatures) occur at a rate of more than 10,000 new damages, on average, per human cell, per day [see article DNA damage (naturally occurring) ]. Additional DNA damages can arise from exposure to exogenous agents. Tobacco smoke causes increased exogenous DNA damage, and these DNA damages are the likely cause of lung cancer due to smoking. UV light from solar radiation causes DNA damage that is important in melanoma. Helicobacter pylori infection produces high levels of reactive oxygen species that damage DNA and contributes to gastric cancer. Bile acids, at high levels in the colons of humans eating a high fat diet, also cause DNA damage and contribute to colon cancer. Katsurano et al. indicated that macrophages and neutrophils in an inflamed colonic epithelium are the source of reactive oxygen species causing the DNA damages that initiate colonic tumorigenesis. Some sources of DNA damage are indicated in the boxes at the top of the figure in this section. Individuals with a germ line mutation causing deficiency in any of 34 DNA repair genes (see article DNA repair-deficiency disorder) are at increased risk of cancer. Some germ line mutations in DNA repair genes cause up to 100% lifetime chance of cancer (e.g. p53 mutations). These germ line mutations are indicated in a box at the left of the figure with an arrow indicating their contribution to DNA repair deficiency. About 70% of malignant neoplasms have no hereditary component and are called "sporadic cancers". Only a minority of sporadic cancers have a deficiency in DNA repair due to mutation in a DNA repair gene. However, a majority of sporadic cancers have deficiency in DNA repair due to epigenetic alterations that reduce or silence DNA repair gene expression. For example, for 113 sequential colorectal cancers, only four had a missense mutation in the DNA repair gene MGMT, while the majority had reduced MGMT expression due to methylation of the MGMT promoter region (an epigenetic alteration). Five reports present evidence that between 40% and 90% of colorectal cancers have reduced MGMT expression due to methylation of the MGMT promoter region. Similarly, out of 119 cases of mismatch repair-deficient colorectal cancers that lacked DNA repair gene PMS2 expression, PMS2 was deficient in 6 due to mutations in the PMS2 gene, while in 103 cases PMS2 expression was deficient because its pairing partner MLH1 was repressed due to promoter methylation (PMS2 protein is unstable in the absence of MLH1). In the other 10 cases, loss of PMS2 expression was likely due to epigenetic overexpression of the microRNA, miR-155, which down-regulates MLH1. In further examples [tabulated in the article Epigenetics (see section “DNA repair epigenetics in cancer”)], epigenetic defects were found at frequencies of between 13%-100% for the DNA repair genes BRCA1, WRN, FANCB, FANCF, MGMT, MLH1, MSH2, MSH4, ERCC1, XPF, NEIL1 and ATM. These epigenetic defects occurred in various cancers (e.g. breast, ovarian, colorectal and head and neck). Two or three deficiencies in expression of ERCC1, XPF and/or PMS2 occur simultaneously in the majority of the 49 colon cancers evaluated by Facista et al. Epigenetic alterations causing reduced expression of DNA repair genes is shown in a central box at the third level from the top of the figure in this section, and the consequent DNA repair deficiency is shown at the fourth level. When expression of DNA repair genes is reduced, DNA damages accumulate in cells at a higher than normal level, and these excess damages cause increased frequencies of mutation and/or epimutation. Mutation rates strongly increase in cells defective in DNA mismatch repair or in homologous recombinational repair (HRR). During repair of DNA double strand breaks, or repair of other DNA damages, incompletely cleared sites of repair can cause epigenetic gene silencing. DNA repair deficiencies (level 4 in the figure) cause increased DNA damages (level 5 in the figure) which result in increased somatic mutations and epigenetic alterations (level 6 in the figure). Field defects, normal appearing tissue with multiple alterations (and discussed in the section below), are common precursors to development of the disordered and improperly proliferating clone of tissue in a malignant neoplasm. Such field defects (second level from bottom of figure) may have multiple mutations and epigenetic alterations. Once a cancer is formed, it usually has genome instability. This instability is likely due to reduced DNA repair or excessive DNA damage. Because of such instability, the cancer continues to evolve and to produce sub clones. For example, a renal cancer, sampled in 9 areas, had 40 ubiquitous mutations (i.e. present in all areas of the cancer), 59 mutations shared by some (but not all areas), and 29 “private” mutations only present in one of the areas of the cancer. The term “field cancerization” was first used in 1953 to describe an area or “field” of epithelium that has been preconditioned by (at that time) largely unknown processes so as to predispose it towards development of cancer. Since then, the terms “field cancerization” and “field defect” have been used to describe pre-malignant tissue in which new cancers are likely to arise. Field defects are important in progression to cancer. However, in most cancer research, as pointed out by Rubin “The vast majority of studies in cancer research has been done on well-defined tumors in vivo, or on discrete neoplastic foci in vitro. Yet there is evidence that more than 80% of the somatic mutations found in mutator phenotype human colorectal tumors occur before the onset of terminal clonal expansion…” Similarly, Vogelstein et al. point out that more than half of somatic mutations identified in tumors occurred in a pre-neoplastic phase (in a field defect), during growth of apparently normal cells. Likewise, epigenetic alterations present in tumors may have occurred in pre-neoplastic field defects. In the colon, a field defect probably arises by natural selection of a mutant or epigenetically altered cell among the stem cells at the base of one of the intestinal crypts on the inside surface of the colon. A mutant or epigenetically altered stem cell may replace the other nearby stem cells by natural selection. Thus, a patch of abnormal tissue may arise. The figure in this section includes a photo of a freshly resected and lengthwise-opened segment of the colon showing a colon cancer and four polyps. Below the photo there is a schematic diagram of how a large patch of mutant or epigenetically altered cells may have formed, shown by the large area in yellow in the diagram. Within this first large patch in the diagram (a large clone of cells), a second such mutation or epigenetic alteration may occur so that a given stem cell acquires an advantage compared to other stem cells within the patch, and this altered stem cell may expand clonally forming a secondary patch, or sub-clone, within the original patch. This is indicated in the diagram by four smaller patches of different colors within the large yellow original area. Within these new patches (sub-clones), the process may be repeated multiple times, indicated by the still smaller patches within the four secondary patches (with still different colors in the diagram) which clonally expand, until stem cells arise that generate either small polyps or else a malignant neoplasm (cancer). In the photo, an apparent field defect in this segment of a colon has generated four polyps (labeled with the size of the polyps, 6mm, 5mm, and two of 3mm, and a cancer about 3 cm across in its longest dimension). These neoplasms are also indicated, in the diagram below the photo, by 4 small tan circles (polyps) and a larger red area (cancer). The cancer in the photo occurred in the cecal area of the colon, where the colon joins the small intestine (labeled) and where the appendix occurs (labeled). The fat in the photo is external to the outer wall of the colon. In the segment of colon shown here, the colon was cut open lengthwise to expose the inner surface of the colon and to display the cancer and polyps occurring within the inner epithelial lining of the colon. If the general process by which sporadic colon cancers arise is the formation of a pre-neoplastic clone that spreads by natural selection, followed by formation of internal sub-clones within the initial clone, and sub-sub-clones inside those, then colon cancers generally should be associated with, and be preceded by, fields of increasing abnormality reflecting the succession of premalignant events. The most extensive region of abnormality (the outermost yellow irregular area in the diagram) would reflect the earliest event in formation of a malignant neoplasm. In experimental evaluation of specific DNA repair deficiencies in cancers, many specific DNA repair deficiencies were also shown to occur in the field defects surrounding those cancers. The Table, below, gives examples for which the DNA repair deficiency in a cancer was shown to be caused by an epigenetic alteration, and the somewhat lower frequencies with which the same epigenetically caused DNA repair deficiency was found in the surrounding field defect. References in the table are given here: 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, Some of the small polyps in the field defect shown in the photo of the opened colon segment may be relatively benign neoplasms. Of polyps less than 10mm in size, found during colonoscopy and followed with repeat colonoscopies for 3 years, 25% were unchanged in size, 35% regressed or shrank in size while 40% grew in size. Cancers are known to exhibit genome instability or a mutator phenotype. The protein-coding DNA within the nucleus is about 1.5% of the total genomic DNA. Within this protein-coding DNA (called the exome), an average cancer of the breast or colon can have about 60 to 70 protein altering mutations, of which about 3 or 4 may be “driver” mutations, and the remaining ones may be “passenger” mutations However, the average number of DNA sequence mutations in the entire genome (including non-protein-coding regions) within a breast cancer tissue sample is about 20,000. In an average melanoma tissue sample (where melanomas have a higher exome mutation frequency) the total number of DNA sequence mutations is about 80,000. These high frequencies of mutations in the total nucleotide sequences within cancers suggest that often an early alteration in the field defects giving rise to a cancer (e.g. yellow area in the diagram in this section) is a deficiency in DNA repair. The large field defects surrounding colon cancers (extending to at about 10 cm on each side of a cancer) were shown by Facista et al. to frequently have epigenetic defects in 2 or 3 DNA repair proteins (ERCC1, XPF and/or PMS2) in the entire area of the field defect. Deficiencies in DNA repair cause increased mutation rates. A deficiency in DNA repair, itself, can allow DNA damages to accumulate, and error-prone translesion synthesis past some of those damages may give rise to mutations. In addition, faulty repair of these accumulated DNA damages may give rise to epimutations. These new mutations and/or epimutations may provide a proliferative advantage, generating a field defect. Although the mutations/epimutations in DNA repair genes do not, themselves, confer a selective advantage, they may be carried along as passengers in cells when the cell acquires an additional mutation/epimutation that does provide a proliferative advantage. M: NEO tsoc, mrkr tumr, epon, para drug (L1i/1e/V03)
Fibroadenomas of the breast are lumps composed of fibrous and glandular tissue. Because breast cancer can also appear as a lump, doctors may recommend a tissue sample (biopsy) to rule out cancer in older patients. Unlike typical lumps from breast cancer, fibroadenomas are easy to move, with clearly defined edges. Fibroadenomas are sometimes called breast mice or a breast mouse owing to their high mobility in the breast. The typical case is the presence of a painless, firm, solitary, mobile, slowly growing lump in the breast of a woman of child-bearing years. In the male breast, fibroepithelial tumors are very rare, and are mostly phyllodes tumors. Exceptionally rare case reports exist of fibroadenomas in the male breast, however these cases may be associated with antiandrogen treatment. A fibroadenoma is usually diagnosed through clinical examination, ultrasound or mammography, and often a needle biopsy sample of the lump. Fibroadenomas arise in the terminal duct lobular unit of the breast.][ They are the most common breast tumor in adolescent women. They also occur in a small number of post-menopausal women. Their incidence declines with increasing age, and, in general, they appear before the age of thirty years. Fibroadenomas are partially hormone-dependent and frequently regress after menopause. They are hypovascular compared to typical (especially malignant) neoplasms. Higher intake of fruits and vegetables, higher number of live births, use of oral contraceptives and moderate exercise are associated with lower frequency of fibroadenomas. The diagnostic findings on needle biopsy consist of abundant stromal cells, which appear as bare bipolar nuclei, throughout the aspirate; sheets of fairly uniform-size epithelial cells that are typically arranged in either an antler-like pattern or a honeycomb pattern. These epithelial sheets tend to show typical metachromatic blue staining on DiffQuick staining. Foam cells and apocrine cells may also be seen, although these are less diagnostic features. The gallery images below demonstrate these features. Approximately ninety percent of fibroadenomas are less than three centimetres in diameter. The vast majority of the remaining ten percent that are four centimetres or larger occur mostly in women under twenty years of age. The tumor is round or ovoid, elastic, and nodular, and has a smooth surface. The cut surface usually appears homogenous and firm, and is grey-white or tan in colour. The pericanalicular type (hard) has a whorly appearance with a complete capsule, while the intracanalicular type (soft) has an incomplete capsule. Fibroadenoma of the breast is a benign tumor composed of two elements : epithelium and stroma. It is nodular and encapsulated, included in breast. The epithelial proliferation appears in a single terminal ductal unit and describes duct-like spaces surrounded by a fibroblastic stroma. Depending on the proportion and the relationship between these two components, there are two main histological features : intracanalicular and pericanalicular. Often, both types are found in the same tumor. A) Intracanalicular fibroadenoma : stromal proliferation predominates and compresses the ducts, which are irregular, reduced to slits. B) Pericanalicular fibroadenoma : fibrous stroma proliferates around the ductal spaces, so that they remain round or oval, on cross section. The basement membrane is intact The gallery image below demonstrates both morphological subtypes. Most fibroadenomas are left in situ and monitored by a doctor, or the patient in question. Some are treated by surgical excision. They are removed with a small margin of normal breast tissue if the preoperative clinical investigations are suggestive of the diagnosis. A small amount of normal tissue must be removed in case the lesion turns out to be a phyllodes tumour on microscopic examination. Because needle biopsy is often a reliable diagnostic investigation, some doctors may decide not to operate to remove the lesion, and instead opt for clinical follow-up to serially observe the lesion over time using clinical examination and mammography to determine the rate of growth, if any, of the lesion. A growth rate of less than sixteen percent per month in women under fifty years of age, and a growth rate of less than thirteen percent per month in women over fifty years of age have been published as safe growth rates for continued non-operative treatment and clinical observation. Some fibroadenomas respond to treatment with ormeloxifene. Fibroadenomas have not been shown to recur following complete excision or transform into phyllodes tumours following partial or incomplete excision. There are also natural treatments being touted to diminish fibroadenomas, such as Fibrosolve, but no definite studies have been made as to prove their effectiveness. Europe recently recognized an alternative treatment that is called echotherapy and that uses high-intensity focused ultrasound to treat breast fibroadenoma. This method is non-invasive and relies on tissue heating to destroy fibroadenoma cells. Focused ultrasounds have been used for a long time in the treatment of different tumors such as prostate, liver or uterus, where they proved their efficacy. A French company, Theraclion, develops an echotherapy device for benign tumors treatment especially breast fibroadenoma. The FDA has approved cryoablation (the use of extreme cold to destroy tissue) of a fibroadenoma as a safe, effective and minimally-invasive alternative to open surgical removal. In the procedure, ultrasound imaging is used to guide a probe into the mass of breast tissue. Extremely cold temperatures are then used to destroy the abnormal cells, and over time the cells are reabsorbed into the body. The procedure can be performed in an office setting with local anesthesia only, and leaves substantially less scarring than open surgical procedures. The American Society of Breast Surgeons recommends the following criteria to establish a patient as a candidate for cryoablation of a fibroadenoma: Fibroadenoma Histology (H&E). The image demonstrates intracanalicular morphology (top right) and pericanalicular morphology (bottom left) Fibroadenoma, Fine Needle Aspiration Biopsy (Giemsa or DiffQuickTM stain). The image shows abundant bare bipolar stromal nuclei surrounding sheets of metachromatic epithelial cells. Fibroadenoma, Fine Needle Aspiration Biopsy (Papanicolou stain). The image shows a sheet of epithelial cells in the typical antler pattern. Histopathologic image of breast fibroadenoma. Core needle biopsy. Hematoxylin & eosin stain.
. M: MUS, DF+DRCT anat (h/n, u, t/d, a/p, l)/phys/devp/hist noco (m, s, c)/cong (d)/tumr, sysi/epon, injr proc, drug (M1A/3)
A lesion is any abnormality in the tissue of an organism (in layman's terms, "damage"), usually caused by disease or trauma. Lesion is derived from the Latin word laesio meaning injury. DuVerney was the first to use experimental ablation method on animals in 1679. Flourens first published the method in 1824, describing the method and behavioral effect of brain damage. Lesions done by knife cuts and suction techniques, called mechanical lesions, were tried by Veyssiere and Nothnagel in 1874. This process was done by inserting a fine wire blade through the head, rotating the curved or angled wire, and cutting neural projection. Baginski and Lehmann used this method with thin glass tube lowered through a small hole in the skull in 1886. In 1895, Golsinger was the first to make electrolytic lesions in animals. In 1898, Sellier and Verger destroyed discrete areas in the caudate and anterior segment of internal capsule by passing current through double-needle insulated electrodes. This process kills neurons surrounding the electrodes. In 1908, Horsley and Clark developed the stereotaxic method and combined it with electrolytic lesions to improve localization, precision, and reliability of brain damage in subcortical structures. In the 1940s to 1950s, Lobotomy was a popular procedure for curing various psychological conditions which relied on lesioning the frontal lobes. Because the definition of a lesion is so broad, the varieties of lesions are virtually endless. Lesions can occur anywhere in the body that consists of soft tissue or osseous matter, though most frequently found in the mouth, skin, and the brain, or anywhere where a tumour may occur.][ They are subsequently classified by their features. If a lesion is caused by a tumor it will be classified as malignant or benign. Lesions may be classified by the shape they form, as is the case with many ulcers, which can have a bullseye or 'target' appearance. Their size may be specified as gross or histologic depending on whether they are visible to the unaided eye or require a microscope to see. An additional classification that is sometimes used is based on whether or not a lesion occupies space. A space-occupying lesion, as the name suggests, has a recognizable volume and may impinge on nearby structures, whereas a non space-occupying lesion is simply a hole in the tissue, e.g. a small area of the brain that has turned to fluid following a stroke. Some lesions have specialized names, such as Ghon lesions in the lungs of tuberculosis victims. The characteristic skin lesions of a varicella zoster virus (VZV) infection are called chickenpox. Lesions of the teeth are usually called dental caries. Another type of lesion is excitotoxic lesions that can be caused by excitatory amino acid like kainic acid that kills neuron by stimulating to death. Sham lesions are the process of putting stereotaxic apparatus and insert it inside the skull to produce a lesion to see if behavior correlates with the brain lesion. Finally, lesions are often classified by their location. For example, a 'skin lesion' or a 'brain lesion'. Lesions are caused by any process that damages tissues. Lesions can also be caused by metabolic processes, like an ulcer or autoimmune activity, as in the case with many forms of arthritis. Lesions are sometimes intentionally inflicted during neurosurgery, such as the carefully placed brain lesion used to treat epilepsy and other brain disorders. (See Ablative brain surgery.) Note that lesions are not limited to animals or humans; damaged plants are said to have lesions. Lesions to the brain can result from many factors, including vascular disorders, traumatic brain injuries, and tumors. Vascular disorders of the brain, often called strokes, disrupt the flow of blood to the brain, resulting in a lesion called an infarct. Vascular disorders of the brain include thrombosis, embolisms, angiomas, aneurysms, and cerebral arteriosclerosis. Traumatic brain injuries (TBI) damage the brain by causing swelling and bleeding inside the brain, leading to inter-cranial pressure. TBIs are divided into open-head injuries, in which the brain is penetrated, and closed head injuries, typically caused by blunt force to the head. Closed head injuries typically cause damage both at the site of the blow (referred to as the coup) and at the opposite side of the skull (referred to as the contrecoup). Brain tumors increased inter-cranial pressure, causing brain damage. Lesions are used as a treatment for epilepsy and in neuropsychological research using animals. These lesions can be induced with electric shocks (electrolytic lesions) to the exposed brain or commonly by infusion of exictotoxins to specific areas. Studies show there is a correlation between brain lesion and language, speech, and category-specific disorders. However, lesions in Broca's and Wernicke's areas are not found to alter language comprehension. Lesions to the fusiform gyrus often result in prosopagnosia, the inability to distinguish faces and other complex objects from each other. Lesions to the visual cortex have different effects depending on the sub-area effected. Lesions to V1, for example, can cause blindness in different areas of the brain depending on the size of the lesion and location relative to the calcarine fissure. Lesions to V4 can cause color-blindness, and bilateral lesions to V5 can cause the loss of the ability to perceive motion. Lesion in amygdala would eliminate the enhanced activation seen in occipital and fusiform visual areas in response to fear with the area intact. Amygdala lesions change the functional pattern of activation to emotional stimuli in regions that are distant from the amygdala. Lesion size is correlated with severity, recovery, and comprehension. In the Wisconsin Card Sorting Test with unilateral frontal or nonfrontal lesions, patients with left frontal lesions did more poorly but had high perseverative error scores. In right frontal and nonfrontal lesions are impaired but due to differences in patients. As a result, medial frontal lesions are associated with poor performance. An impairment following damage to a region of the brain does not necessarily imply that the damaged area is wholly responsible for the cognitive process which is impaired, however. For example, in pure alexia, the ability to read is destroyed by a lesion damaging both the left visual field and the connection between the right visual field and the language areas (Broca’s Area and Wernicke’s area). However, this does not mean one suffering from pure alexia is incapable of comprehending speech -- merely that there is no connection between their working visual cortex and language areas -- as is demonstrated by the fact that pure alexics can still write, speak, and even transcribe letters without understanding their meeting. Lesions are useful to researchers in understanding how the components of the brain produce cognition. Research involving lesions is predicated on the formal logic that if impaired performance implies a model of damaged cognition and that the model of the damaged cognition is equal to the normal system plus the effect of the lesion, then the impaired performance implies the normal cognitive system plus the effect of the lesion. Humans with brain lesions are often the subjects of research with the goal of establishing the function of the area where their lesion occurred. A drawback to the use of human subjects is the difficulty in finding subjects who have a lesion to the area which the researcher wishes to study. Using animal subjects gives researchers the ability to lesion specific areas in the subjects, allowing them to quickly acquire a large group of subjects. An example of such a study is the lesioning of rat hippocampi to establish the role of the hippocampus in object recognition and object recency. The major disadvantage of animal subjects is the limited extendability of the results to humans, whose brains differ to varying degrees from the animals. 2. Alexander, M.P., Naeser, M.A., & Palumbo, C.L. (1987). Correlations Of Subcortical CT Lesion Sites And Aphasia Profiles. Brain, 110, 961-991. 3. Cancelliere, A.E.B, Kertesz, A. (1990). Lesion Localization In Acquired Deficits Of Emotional Expression And Comprehension. Brain and Cognition, 13(2), 133-147. 4. Carlson, N.R. (1977). Physiology of behavior. Boston: Allyn and Bacon. 5. Drewe, E.A. (1974). The Effect Of Type And Area Of Brain Lesion On Wisconsin Card Sorting Test Performance. A Journal Devoted to the Study of the Nervous System and Behavior, 10(2), 159-170. 6. Dronkers, N.F., Wilkins, D.P., Van Valin Jr., R.D., Redfern, B.B, Jaeger, J.J. (2004). Lesion Analysis Of The Brain Areas Involved In Language Comprehension. Cognition, 92(1-2), 145-177. 7. Gainotti, G. (2000). What the Locus of Brain Lesion Tells us About the Nature of the Cognitive Defect Underlying Category-Specific Disorders: A Review. Cortex, 36(4), 539-559. 8. Kent, R.D. (1982). Prosodic Disturbance And Neurologic Lesion. Brain and Language, 15(2), 259-291. 9. Kertesz, A., Harlock, W., & Coates, R. (2004). Computer Tomographic Localization, Lesion Size, And Prognosis In Aphasia And Nonverbal Impairment. Brain and Language, 8(1), 34-50. 10. Schallert, T., & Wilcox, R.E. (1986). Neurotransimitter-Selective Brain Lesions. Biomedical and Life Sciences, 1, 343-387. 11. Vuilleumier, P., Richardson, M.P., Armony, J.L., Driver, J. & Dolan, R.J. (2004). Distant Influences Of Amygdala Lesion On Visual Cortical Activation During Emotional Face Processing. Nature Neuroscience, 7, 1271-1278. 12. Kolb, Bryan, Whishaw, Ian Q. (2009). Fundamentals of Human Neuropsychology 6th Edition, 749 - 756.
A hemangioma is a benign, and usually a self-involuting tumor, (swelling or growth) of the endothelial cells that line blood vessels and is characterised by increased number of normal or abnormal vessels filled with blood. It usually appears during the first weeks of life and generally resolves by age 10. In more severe cases hemangiomas may leave residual tissue damage. In infancy, it is the most common tumor. The word "hemangioma" comes from the Greek haema- (αίμα), "blood"; angeio (αγγείο), "vessel"; -oma (-ωμα), "tumor". The terminology used to define, describe and categorize vascular anomalies, abnormal lumps made up of blood vessels, has changed. The term hemangioma was originally used to describe any vascular tumor-like structure, whether it was present at or around birth or appeared later in life. Mulliken et al. categorized these conditions into two families: a family of self-involuting tumors, growing lesions that eventually disappear, and another family of malformations, enlarged or abnormal vessels present at birth and essentially permanent. The importance of this distinction is that it makes it possible for early-in-life differentiation between lesions that will resolve versus those that are permanent. Examples of permanent malformations include port-wine stains (capillary vascular malformation) and masses of abnormal swollen veins (venous malformations). Unfortunately][ it is taking some time for other branches of medicine to adopt the new terminology which causes confusion.][ The Mulliken categorisation has received major confirmation following discovery of the Glut-1 marker][ (see below). Hemangiomas are connected to the circulatory system. The appearance depends on location. If they are on the surface of the skin, they are reminiscent of a ripe strawberry (hence, they are sometimes referred to as "strawberry hemangiomas"); however, if they are just under the skin they present as a bluish swelling. Sometimes they grow in internal organs such as the liver, larynx, or small and large intestine. In most cases, hemangiomas will disappear over time. Some are formed during gestation; the most common are not congenital, but appear during the first few weeks of life. They are often initially misdiagnosed as a scratch or bruise; but the correct diagnosis becomes obvious with further growth. Typically, at the earliest phase in a superficial lesion, one will see a bluish red area with obvious blood vessels and surrounding pallor. Sometimes they present as a flat red or pink area. Hemangiomas are the most common childhood tumor, occurring in approximately ten percent of Caucasians, and are less prevalent in other ethnicities. Females are three to five times as likely to have hemangiomas as males. Hemangiomas are also more common in twin pregnancies. Approximately 80% are located on the face and neck, or on the legs and arms; with the next most prevalent location being the liver. In infants, It may present itself soon after birth and is different than other vascular abnormalities present. They grow to around 80% of their maximum size in the first 3 months and most reach maximum size at around 5 months. Hemangioma on forehead showing signs of early regression Hemangioma on the scalp of a two year old female, in the "rest stage" Hemangioma of the liver as seen on ultrasound A liver hemangioma as seen on CT The cause of hemangioma is currently unknown; however, several studies have suggested the importance of estrogen signaling in hemangioma proliferation. In 2007, a paper from the Stanford Children's Surgical Laboratory revealed that localized soft tissue hypoxia coupled with increased circulating estrogen after birth may be the stimulus. There is also a hypothesis presented by researchers at Harvard and the University of Arkansas that maternal placenta embolizes to the fetal dermis during gestation resulting in hemangiomagenesis. However, researchers at Duke University conducted genetic analyses of single-nucleotide polymorphism in hemangioma tissue compared to the mother's DNA that contradicted this hypothesis. More research is required in order to fully understand the explosive nature of hemangioma growth, which will hopefully yield targeted therapeutics to treat its most complicated presentations. Under the microscope, hemangiomas are unencapsulated aggregates of closely packed, thin-walled capillaries, usually with endothelial lining. Blood-filled vessels are separated by scant connective tissue. Their lumens may be thrombosed and organized. Hemosiderin pigment due to vessel rupture sometimes can be noticed. Glut1 is a histochemical marker, highly specific for Haemangioma and can be used to differentiate Haemangioma from vascular malformations. The vast majority of hemangiomas are not associated with complications. Hemangiomas may break down on the surface, called ulceration. If the ulceration is deep, significant bleeding may occur in rare occasions. Ulceration on the deeper area can be painful and problematic. If a hemangioma develops in the larynx, breathing can be compromised. A hemangioma can grow and block one of the eyes, causing an occlusion amblyopia. Very rarely, extremely large hemangiomas can cause high-output heart failure due to the amount of blood that must be pumped to excess blood vessels. Lesions adjacent to bone can also cause erosion of the bone. The most frequent complaints about hemangiomas, however, stem from psychosocial complications: the condition can affect a person's appearance and can provoke attention and malicious reactions from others. Particular problems occur if the lip or nose is involved, as distortion can be difficult to treat surgically. The potential for psychological injury develops from school age onward. It is therefore important to consider treatment prior to school if adequate spontaneous improvement has not occurred. Children with large segmental hemangiomas of the head and neck can be associated with a disorder called PHACES Syndrome. Most hemangiomas disappear without treatment, leaving minimal or no visible marks. Large hemangiomas can leave visible skin changes secondary to severe stretching of the skin or damage to surface texture. When hemangiomas interfere with vision, breathing, or threaten significant cosmetic injury (facial lesions and in particular, nose and lips), they are usually treated. Until recently, the mainstay of treatment was oral corticosteroid therapy, but there are now alternative treatments. A randomized trial showed that the beta-blocker propranolol reduced severe hemangiomas in infants. The topically applied beta blocker solution/gel Timolol is also being trialled for small facial hemangiomas that do not justify systemic treatment. Other treatments that have been used include interferon or vincristine. They may be considered if first-line therapy fails. Surgical removal is sometimes indicated, particularly if there has been delay in commencing treatment and structural changes have become irreversible. Surgery may also be necessary to correct distortion of facial features, again in the case of inadequate or failed early medical intervention. Blockage of the airway will often require a tracheostomy to be performed, which involves the insertion of an external airway through the front of the neck into the trachea below the level of the obstruction. Smaller raised lesions are sometimes treated with injection of corticosteroid directly into the lesion. A pulsed dye laser can be useful for very early, flat, superficial lesions, if they appear in cosmetically significant areas or for those lesions that leave residual surface blood vessels in the case of incomplete resolution. Sometimes a pulsed dye laser can be used to accelerate healing. Unfortunately, raised lesions or lesions under the skin do not respond to laser treatment. Ulceration will usually heal with topical medication and special dressings under medical supervision. Applying pressure is not beneficial, thus not recommended. Hemangiomas go through three stages of development and decay: M: VAS anat (a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot noco/syva/cong/lyvd/tumr, sysi/epon, injr proc, drug (C2s+n/3/4/5/7/8/9)
A benign tumor is a mass of cells (tumor) that lacks the ability to invade neighboring tissue or metastasize. These characteristics are required for a tumor to be defined as cancerous and therefore benign tumors are non-cancerous. Also, benign tumors generally have a slower growth rate than malignant tumors and the tumor cells are usually more differentiated (cells have normal features). Benign tumors are typically surrounded by an outer surface (fibrous sheath of connective tissue) or remain with the epithelium. Common examples of benign tumors include moles (nevi) and uterine fibroids (leiomyomas). Although benign tumors will not metastasize or locally invade tissues, some types may still produce negative health effects. The growth of benign tumors produce a "mass effect" that can compress tissues and may cause nerve damage, reduction of blood to an area of the body (ischaemia), tissue death (necrosis) and organ damage. The mass effect of tumors are more prominent if the tumor is within an enclosed space such as the cranium, respiratory tract, sinus or inside bones. Tumors of endocrine tissues may overproduce certain hormones, especially when the cells are well differentiated. Examples include thyroid adenomas and adrenocortical adenomas. Although most benign tumors are not life-threatening, many types of benign tumors have the potential to become cancerous (malignant) through a process known as tumour progression. For this reason and other possible negative health effects, some benign tumors are removed by surgery. Benign neoplasms are typically but not always composed of cells which bear a strong resemblance to a normal cell type in their organ of origin. These tumors are named for the cell or tissue type from which they originate, followed by the suffix "-oma" (but not -carcinoma, -sarcoma, or -blastoma, which are generally cancers). For example, a lipoma is a common benign tumor of fat cells (lipocytes), and a chondroma is a benign tumor of cartilage-forming cells (chondrocytes). Adenomas are benign tumors of gland-forming cells, and are usually specified further by their cell or organ of origin, as in hepatic adenoma (a benign tumor of hepatocytes, or liver cells). Teratomas contain many cell types such as skin, nerve, brain and thyroid, among others, because they are derived from germ cells. Hamartomas are a group of benign tumors that have relatively normal cellular differentiation but the architecture of the tissue is disorganised. There are a few cancers with 'benign-sounding' names which have been retained for historical reasons, including melanoma (a cancer of pigmented skin cells, or melanocytes) and seminoma (a cancer of male reproductive cells). Skin tags, vocal chord polyps and hyperplastic polyps of the colon are often referred to as benign but they are actually overgrowths of normal tissue rather than neoplasms. Benign tumors are very diverse, and may be asymptomatic or may cause specific symptoms depending on their anatomic location and tissue type. They grow outwards, producing large rounded masses, which can cause what is known as a "mass effect". This growth can cause compression of local tissues or organs, which can cause many effects such as blockage of ducts, reduced blood flow (ischaemia), tissue death (necrosis) and nerve pain or damage. Some tumors also produce hormones that can lead to life-threatening situations. Insulinomas can produce large amounts of insulin leading to hypoglycemia. Pituitary adenomas can cause elevated levels of hormones such as growth hormone and insulin-like growth factor-1, which cause acromegaly; prolactin; ACTH and cortisol, which cause Cushings disease; TSH, which causes hyperthyroidism; and FSH and LH. Bowel intussusception can occur with various benign colonic tumors. Cosmetic effects can be caused by tumors, especially those of the skin, possibly causing psychological effects on the person with the tumor. Vascular tumors can bleed, which in some cases can be substantial, leading to anemia. Some benign tumors need no treatment; others may be removed if they cause problems such as seizures, discomfort or cosmetic concerns. Surgery is usually the most effective approach and is used to treat most benign tumors. In some case other treatments may be of use. Adenomas of the rectum may be treated with sclerotherapy, a treatment in which chemicals are used to shrink blood vessels in order to cut off the blood supply. Most benign tumors do not respond to chemotherapy or radiation therapy, although there are exceptions; benign intercranial tumors are sometimes treated with radiation therapy and chemotherapy under certain circumstances. Radiation can also be used to treat hemangiomas in the rectum. Benign skin tumors are usually surgically ressected but other treatments such as cryotherapy, curettage, electrodesiccation, laser therapy, dermabrasion, chemical peels and topical medication are used. One of the most important factors in classifying a tumor as benign or malignant is its invasive potential. If a tumor lacks the ability to invade adjacent tissues or spread to distant sites by metastasizing then it is benign, whereas invasive or metastatic tumours are malignant. For this reason, benign tumours are not classed as cancer. Benign tumours will grow in a contained area usually encapsulated in a fibrous connective tissue capsule. The growth rates of benign and malignant tumors also differ; benign tumors generally grow more slowly than malignant tumors. Although benign tumors pose a lower health risk than malignant tumors, they can both be life-threatening in certain situations. There are many general characteristics which apply to either benign or malignant tumors, but sometimes one type may show characteristics of the other. For example, benign tumors are mostly well differentiated and malignant tumors are often undifferentiated. However, undifferentiated benign tumors and differentiated malignant tumors can occur. Although benign tumors generally grow slowly, cases of fast growing benign tumors have also been documented. Some malignant tumors are mostly non-metastatic such as in the case of basal cell carcinoma. Tumours are formed by carcinogenesis, a process in which cellular alterations lead to the formation of cancer. Multistage carcinogenesis involves the sequential genetic or epigenetic changes to a cells DNA, where each step produces a more advanced tumour. It is often broken down into three stages; initiation, promotion and progression, and several mutations may occur at each stage. Initiation is where the first genetic mutation occurs in a cell. Promotion is the clonal expansion (repeated division) of this transformed cell into a visible tumour that is usually benign. Following promotion, progression may take place where more genetic mutations are acquired in a sub-population of tumor cells. Progression changes the benign tumor into a malignant tumor. A prominent and well studied example of this phenomenon is the tubular adenoma, a common type of colon polyp which is an important precursor to colon cancer. The cells in tubular adenomas, like most tumors which frequently progress to cancer, show certain abnormalities of cell maturation and appearance collectively known as dysplasia. These cellular abnormalities are not seen in benign tumors that rarely or never turn cancerous, but are seen in other pre-cancerous tissue abnormalities which do not form discrete masses, such as pre-cancerous lesions of the uterine cervix. Some authorities][ prefer to refer to dysplastic tumors as "pre-malignant", and reserve the term "benign" for tumors which rarely or never give rise to cancer.][ PTEN hamartoma syndrome comprises four distinct hamartomatous disorders characterised by genetic mutations in the PTEN gene; Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome and Proteus-like syndrome. Although they all have distinct clinical features, the formation of hamartomas is present in all four syndromes. PTEN is a tumor suppressor gene that is involved in cellular signalling. Absent or dysfunctional PTEN protein allows cells to over-proliferate, causing hamartomas. Cowden syndrome is an autosomal dominant genetic disorder characterised by multiple benign hamartomas (trichilemmomas and mucocutaneous papillomatous papules) as well as a predisposition for cancers of multiple organs including the breast and thyroid. Bannayan-Riley-Ruvalcaba syndrome is a congenital disorder characterised by hamartomatous intestinal polyposis, macrocephaly, lipomatosis, hemangiomatosis and glans penis macules. Proteus syndrome is characterised by nevi, asymmetric overgrowth of various body parts, adipose tissue dysregulation, cystadenomas, adenomas, vascular malformation. Familial adenomatous polyposis (FAP) is a familial cancer syndrome caused by mutations in the APC gene. In this disorder adenomatous polyps are present in the colon that invariably progress into colon cancer. The APC gene is a tumor suppressor and its product is involved in many cellular processes. Inactivation of the APC gene leads to a build up of a protein called β-catenin, which activates two transcription factors; T-cell factor (TCF) and lymphoid enhancer factor (LEF). These cause the upregulation of many genes involved in cell proliferation, differentiation, migration and apoptosis (programmed cell death), causing the growth of benign tumors. Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder caused by mutations in the genesTSC1 and TSC2, which produce the proteins hamartin and tuberin, respectively. This disorder presents with many benign hamartomatous tumors including angiofibromas, renal angiomyolipomas, pulmonary lymphangiomyomatosis. Tuberin and hamartin inhibit the mTOR protein in normal cellular physiology and the inactivation of the TSC tumour suppressors causes an increase in mTOR activity. This leads to the activation of genes and the production of proteins that increase cell growth. Von Hippel-Lindau disease is a dominantly inherited cancer syndrome that massively increases the risk of various tumors including benign hemangioblastomas and malignant pheochromocytomas, renal cell carcinomas, pancreatic endocrine tumors and endolymphatic sac tumors. It is caused by genetic mutations in the Von Hippel–Lindau tumor suppressor gene. The VHL protein (pVHL) is involved in cellular signalling in oxygen starved (hypoxic) cells. One role of pVHL is to cause the cellular degradation of another protein, HIF1α. Dysfunctional pVHL leads to accumulation of HIF1α, which in turn activates the production of several genes involved in cell growth and blood vessel production (VEGF, PDGFβ, TGFα and erythropoietin). M: NEO tsoc, mrkr tumr, epon, para drug (L1i/1e/V03)
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