The term leukemoid reaction describes an increased white blood cell count (> 50,000 cells/μL), which is a physiological response to stress or infection (as opposed to a primary blood malignancy, such as leukemia). It often describes the presence of immature cells such as myeloblasts or red blood cells with nuclei in the peripheral blood.
It may be lymphoid or myeloid.[1]
https://en.wikipedia.org/wiki/Leukemoid_reaction
Diffuse infiltrative lymphocytosis syndrome occurs in HIV positive patients with low CD4 counts.[1][2]
It is similar to Sjögren's syndrome,[3] with painless parotid and submandibular swelling, and sicca symptoms.
The syndrome typically improves with HAART.[citation needed]
https://en.wikipedia.org/wiki/Diffuse_infiltrative_lymphocytosis_syndrome
https://en.wikipedia.org/wiki/Subtypes_of_HIV#HIV-2
https://en.wikipedia.org/wiki/Simian_immunodeficiency_virus
| Class | Gene name | Primary protein products | Processed protein products |
|---|---|---|---|
| Viral structural proteins | gag | Gag polyprotein | MA, CA, SP1, NC, SP2, P6 |
| pol | Pol polyprotein | RT, RNase H, IN, PR | |
| env | gp160 | gp120, gp41 | |
| Essential regulatory elements | tat | Tat | |
| rev | Rev | ||
| Accessory regulatory proteins | nef | Nef | |
| vpr | Vpr | ||
| vif | Vif | ||
| vpu | Vpu |
Viral structural proteins[edit]
- gag (group-specific antigen) codes for the precursor gag polyprotein which is processed by viral protease during maturation to MA (matrix protein, p17); CA (capsid protein, p24); SP1 (spacer peptide 1, p2); NC (nucleocapsid protein, p7); SP2 (spacer peptide 2, p1) and P6 protein.[30]
- pol codes for viral enzymes reverse transcriptase (RT) and RNase H, integrase (IN), and HIV protease (PR).[28] HIV protease is required to cleave the precursor Gag polyprotein to produce structural proteins, RT is required to transcribe DNA from RNA template, and IN is necessary to integrate the double-stranded viral DNA into the host genome.[26]
- env (for "envelope") codes for gp160, which is cleaved by a host protease, furin, within the endoplasmic reticulum of the host cell. The post-translational processing produces a surface glycoprotein, gp120 or SU, which attaches to the CD4 receptors present on lymphocytes, and gp41 or TM, which embeds in the viral envelope to enable the virus to attach to and fuse with target cells.[26][30]
https://en.wikipedia.org/wiki/Structure_and_genome_of_HIV#Genome_organization
DNA dC->dU-editing enzyme APOBEC-3F is a protein that in humans is encoded by the APOBEC3F gene.[3][4][5]
This gene is a member of the cytidine deaminase gene family. It is one of seven related genes or pseudogenes found in a cluster, thought to result from gene duplication, on chromosome 22. Members of the cluster encode proteins that are structurally and functionally related to the C to U RNA-editing cytidine deaminase APOBEC1. It is thought that the proteins may be RNA editing enzymes and have roles in growth or cell cycle control. Alternatively spliced transcriptvariants encoding different isoforms have been identified.[5]
https://en.wikipedia.org/wiki/APOBEC3F
Tripartite motif-containing protein 5 also known as RING finger protein 88 is a protein that in humans is encoded by the TRIM5 gene.[4] The alpha isoform of this protein, TRIM5α, is a retrovirus restriction factor, which mediates species-specific, early block to retrovirus infection.
TRIM5α is composed of 493 amino acids that is found in the cells of most primates. TRIM5α is an intrinsic immune factor important in the innate immune defense against retroviruses, along with the APOBEC family of proteins,[5][6] tetherin and TRIM22.
https://en.wikipedia.org/wiki/TRIM5alpha
The Simian foamy virus (SFV) is a species of the genus Spumavirus, which belongs to the family of Retroviridae. It has been identified in a wide variety of primates, including pro-simians, New World and Old World monkeys as well as apes, and each species has been shown to harbor a unique (species-specific) strain of SFV, including African green monkeys, baboons, macaques and chimpanzees.[1] As it is related to the more well-known retrovirus human immunodeficiency virus (HIV), its discovery in primates has led to some speculation that HIV may have been spread to the human species in Africa through contact with blood from apes, monkeys, and other primates, most likely through bushmeat hunting practices.
https://en.wikipedia.org/wiki/Simian_foamy_virus
Woolly monkey sarcoma virus (WMSV), with synonym Simian sarcoma virus (often abbreviated by SSV, but this may also stand for some species called 'Sulfolobus spindle-shaped virus', that belong to different genera in family Fuselloviridae) is a species of gammaretrovirus that infects primates. First isolation was from a fibrosarcoma in a woolly monkey (genus Lagothrix). For its reproduction the virus needs a helper or associated virus which is called Simian sarcoma associated virus (SSAV).[1][2][3]
https://en.wikipedia.org/wiki/Woolly_monkey_sarcoma_virus
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https://en.wikipedia.org/wiki/Template:Immunoproliferative_immunoglobulin_disorders
| Lymphomatoid granulomatosis | |
|---|---|
| Specialty | Hematology and oncology |
Lymphomatoid granulomatosis (LYG or LG) is a very rare lymphoproliferative disorder first characterized in 1972.[1]Lymphomatoid means lymphoma-like and granulomatosis denotes the microscopic characteristic of the presence of granulomaswith polymorphic lymphoid infiltrates and focal necrosis within it.
LG most commonly affects middle aged people,[2] but has occasionally been observed in young people.[3] Males are found to be affected twice as often as females.[4]
https://en.wikipedia.org/wiki/Lymphomatoid_granulomatosis
Post-transplant lymphoproliferative disorder (PTLD) is the name given to a B-cell proliferation due to therapeutic immunosuppression after organ transplantation. These patients may develop infectious mononucleosis-like lesions or polyclonal polymorphic B-cell hyperplasia. Some of these B-cells may undergo mutations which will render them malignant, giving rise to a lymphoma.[citation needed]
In some patients, the malignant cell clone can become the dominant proliferating cell type, leading to frank lymphoma, a group of B cell lymphomas occurring in immunosuppressed patients following organ transplant.
https://en.wikipedia.org/wiki/Post-transplant_lymphoproliferative_disorder
Splenic marginal zone lymphoma (SMZL) is a type of cancer (specifically a lymphoma) made up of B-cells that replace the normal architecture of the white pulp of the spleen. The neoplastic cells are both small lymphocytes and larger, transformed lymphoblasts, and they invade the mantle zone of splenic follicles and erode the marginal zone, ultimately invading the red pulp of the spleen. Frequently, the bone marrow and splenic hilar lymph nodes are involved along with the peripheral blood. The neoplastic cells circulating in the peripheral blood are termed villous lymphocytes due to their characteristic appearance.[1]
https://en.wikipedia.org/wiki/Splenic_marginal_zone_lymphoma#cite_note-who1-1
Plasmacytoma is a plasma cell dyscrasia in which a plasma cell tumour grows within soft tissue or within the axial skeleton.
The International Myeloma Working Group lists three types: solitary plasmacytoma of bone (SPB); extramedullary plasmacytoma (EP), and multiple plasmacytomas that are either primary or recurrent.[1] The most common of these is SPB, accounting for 3–5% of all plasma cell malignancies.[2] SPBs occur as lytic lesions within the axial skeleton and extramedullary plasmacytomas most often occur in the upper respiratory tract (85%), but can occur in any soft tissue. Approximately half of all cases produce paraproteinemia. SPBs and extramedullary plasmacytomas are mostly treated with radiotherapy, but surgery is used in some cases of extramedullary plasmacytoma. The skeletal forms frequently progress to multiple myeloma over the course of 2–4 years.[3]
Due to their cellular similarity, plasmacytomas have to be differentiated from multiple myeloma. For SPB and extramedullary plasmacytoma the distinction is the presence of only one lesion (either in bone or soft tissue), normal bone marrow (<5% plasma cells), normal skeletal survey, absent or low paraprotein and no end organ damage.[1]
https://en.wikipedia.org/wiki/Plasmacytoma
| Plasmacytosis |
|---|
Plasmacytosis is a condition in which there is an unusually large proportion of plasma cells in tissues, exudates, or blood.[1]:743Plasmacytosis may be divided into two types—cutaneous and systemic—both of which have identical skin findings.[1]:743
Patients with plasmacytosis have been predominantly found to have lung infections (pneumonia, tuberculosis, abscess) whereas multiple myeloma is rarely found.[2]
https://en.wikipedia.org/wiki/Plasmacytosis
Terminal deoxynucleotidyl transferase (TdT), also known as DNA nucleotidylexotransferase (DNTT) or terminal transferase, is a specialized DNA polymerase expressed in immature, pre-B, pre-T lymphoid cells, and acute lymphoblastic leukemia/lymphoma cells. TdT adds N-nucleotides to the V, D, and J exons of the TCR and BCR genes during antibody gene recombination, enabling the phenomenon of junctional diversity. In humans, terminal transferase is encoded by the DNTT gene.[5][6] As a member of the X family of DNA polymerase enzymes, it works in conjunction with polymerase λ and polymerase μ, both of which belong to the same X family of polymerase enzymes. The diversity introduced by TdT has played an important role in the evolution of the vertebrate immune system, significantly increasing the variety of antigen receptors that a cell is equipped with to fight pathogens. Studies using TdT knockout mice have found drastic reductions (10-fold) in T-cell receptor (TCR) diversity compared with that of normal, or wild-type, systems. The greater diversity of TCRs that an organism is equipped with leads to greater resistance to infection.[7][8] Although TdT was one of the first DNA polymerases identified in mammals in 1960,[9] it remains one of the least understood of all DNA polymerases.[7] In 2016–18, TdT was discovered to demonstrate in trans template dependant behaviour in addition to its more broadly known template independent behaviour[10][11]
TdT is absent in fetal liver HSCs, significantly impairing junctional diversity in B-cells during the fetal period.[12]
https://en.wikipedia.org/wiki/Terminal_deoxynucleotidyl_transferase
T-lymphoblastic leukemia/lymphoma (WHO 2008),[1]:219 previously labeled precursor T-lymphoblastic leukemia/lymphoma(WHO 2001)[1]:219 is a form of lymphoid leukemia[2][3] and lymphoma[4] in which too many T-cell lymphoblasts (immature white blood cells) are found in the blood, bone marrow, and tissues, particularly mediastinal lymph nodes.[1]:635 Labeling as leukemia or lymphoma depends on which feature is more pronounced in a given situation, but has no biological or treatment implication.[1]:635
It is uncommon in adults, but represents 15% of childhood acute lymphoblastic leukemia and 90% of lymphoblastic lymphoma.[1]:635
The 2008 terminology dropped "precursor" to avoid linguistic redundancy because the lymphoblast is an immature precursor cell by definition.[1]:219
https://en.wikipedia.org/wiki/T-lymphoblastic_leukemia/lymphoma
T-cell-prolymphocytic leukemia (T-PLL) is a mature T-cell leukemia with aggressive behavior and predilection for blood, bone marrow, lymph nodes, liver, spleen, and skin involvement.[1] T-PLL is a very rare leukemia, primarily affecting adults over the age of 30. It represents 2% of all small lymphocytic leukemias in adults.[2] Other names include T-cell chronic lymphocytic leukemia, "knobby" type of T-cell leukemia, and T-prolymphocytic leukemia/T-cell lymphocytic leukemia.[1]
https://en.wikipedia.org/wiki/T-cell_prolymphocytic_leukemia
Anaplastic large cell lymphoma (ALCL) refers to a group of non-Hodgkin lymphomas in which aberrant T cells proliferate uncontrollably. Considered as a single entity, ALCL is the most common type of peripheral lymphoma[1] and represents ~10% of all peripheral lymphomas in children.[2] The incidence of ALCL is estimated to be 0.25 cases per 100,000 people in the United States of America.[3] There are four distinct types of anaplastic large cell lymphomas that on microscopic examination share certain key histopathological features and tumor marker proteins. However, the four types have very different clinical presentations, gene abnormalities, prognoses, and/or treatments.[1]
https://en.wikipedia.org/wiki/Anaplastic_large-cell_lymphoma
Lymphomatoid papulosis (LyP) is a rare skin disorder. The overall prevalence rate of lymphomatoid papulosis is estimated at 1.2 to 1.9 cases per 1,000,000 population. [This is a widespread misinterpretation of a 1992 study saying "the period prevalence rate of lymphomatoid papulosis was estimated to be 1.9 per 1,000,000 population for Massachusetts and 1.2 per 1,000,000 population for Pennsylvania". The authors of that study said clearly "Our estimate of 1.2-1.9 cases per 1,000,000 population should be considered a minimum estimate of the prevalence rate". That estimate was based on the 78 patients involved in the study, not the LvP population. The study recruited 11 patients from Massachusetts and 15 from Pennsylvania [1]]. This rare condition has only been studied in depth since 1968.[2]
https://en.wikipedia.org/wiki/Lymphomatoid_papulosis
Pagetoid reticulosis (also known as "acral mycoses fungoides",[1] "localized epidermotropic reticulosis",[1] "mycosis fungoides palmaris et plantaris",[1] "unilesional mycosis fungoides",[2] and "Woringer–Kolopp disease"[1]) is a cutaneous condition, an uncommon lymphoproliferative disorder, sometimes considered a form of mycosis fungoides.[1]:734
https://en.wikipedia.org/wiki/Pagetoid_reticulosis
Mycosis fungoides, also known as Alibert-Bazin syndrome or granuloma fungoides,[1] is the most common form of cutaneous T-cell lymphoma. It generally affects the skin, but may progress internally over time. Symptoms include rash, tumors, skin lesions, and itchy skin.
While the cause remains unclear, most cases are not hereditary. Most cases are in people over 20 years of age, and it is more common in men than women. Treatment options include sunlight exposure, ultraviolet light, topical corticosteroids, chemotherapy, and radiotherapy.
sp - fungus, fungal derivatives et priming by alkylation agents rads radk immunosups overvac genotox-viral gene transplant-activation of tumor gene-cell signal dysfunction/decay matter/fungai susecept/etc..
https://en.wikipedia.org/wiki/Mycosis_fungoides
Lymphoid leukemias are a group of leukemias affecting circulating lymphocytes, a type of white blood cells. The lymphocytic leukemias are closely related to lymphomas of the lymphocytes, to the point that some of them are unitary disease entities that can be called by either name (for example, adult T-cell leukemia/lymphoma). Such diseases are all lymphoproliferative disorders. Most lymphoid leukemias involve a particular subtype of lymphocytes, the B cells.
https://en.wikipedia.org/wiki/Lymphoid_leukemia
| Tumors of the hematopoietic and lymphoid tissues | |
|---|---|
 | |
| Micrograph of a plasmacytoma, a hematological malignancy |
Tumors of the hematopoietic and lymphoid tissues (American English) or tumours of the haematopoietic and lymphoid malignancies (British English) are tumors that affect the blood, bone marrow, lymph, and lymphatic system.[1][2]Because these tissues are all intimately connected through both the circulatory system and the immune system, a disease affecting one will often affect the others as well, making myeloproliferation and lymphoproliferation (and thus the leukemiasand the lymphomas) closely related and often overlapping problems.
While uncommon in solid tumors, chromosomal translocations are a common cause of these diseases. This commonly leads to a different approach in diagnosis and treatment of haematological malignancies.
Haematological malignancies are malignant neoplasms ("cancer"), and they are generally treated by specialists in hematology and/or oncology. In some centers "haematology/oncology" is a single subspecialty of internal medicine while in others they are considered separate divisions (there are also surgical and radiation oncologists). Not all haematological disorders are malignant ("cancerous"); these other blood conditions may also be managed by a hematologist.
Hematological malignancies may derive from either of the two major blood cell lineages: myeloid and lymphoid cell lines. The myeloid cell line normally produces granulocytes, erythrocytes, thrombocytes, macrophages and mast cells; the lymphoid cell line produces B, T, NK and plasma cells. Lymphomas, lymphocytic leukemias, and myeloma are from the lymphoid line, while acute and chronic myelogenous leukemia, myelodysplastic syndromes and myeloproliferative diseases are myeloid in origin.
A subgroup of them are more severe and are known as haematological malignancies (British English)/hematological malignancies (American English) or blood cancer. They may also be referred to as liquid tumors.[3][4]
https://en.wikipedia.org/wiki/Tumors_of_the_hematopoietic_and_lymphoid_tissues
| Lymphoproliferative disorders | |
|---|---|
| Specialty | Hematology and oncology |
Lymphoproliferative disorders (LPDs) refer to a specific class of diagnoses, comprising a group of several conditions, in which lymphocytes are produced in excessive quantities. These disorders primarily present in patients who have a compromised immune system. Due to this factor, there are instances of these conditions being equated with "immunoproliferative disorders"; although, in terms of nomenclature, lymphoproliferative disorders are a subclass of immunoproliferative disorders—along with hypergammaglobulinemia and paraproteinemias.
https://en.wikipedia.org/wiki/Lymphoproliferative_disorders
mune lymphoproliferative syndromeOther namesCanale-Smith syndrome,[1]SpecialtyImmunology
Autoimmune lymphoproliferative syndrome (ALPS), is a form of lymphoproliferative disorder (LPDs). It affects lymphocyteapoptosis.[2]
It is a rare genetic disorder of abnormal lymphocyte survival caused by defective Fas mediated apoptosis.[3] Normally, after infectious insult, the immune system down-regulates by increasing Fas expression on activated B and T lymphocytes and Fas-ligand on activated T lymphocytes. Fas and Fas-ligand interact to trigger the caspase cascade, leading to cell apoptosis. Patients with ALPS have a defect in this apoptotic pathway, leading to chronic non-malignant lymphoproliferation, autoimmune disease, and secondary cancers.[4]
https://en.wikipedia.org/wiki/Autoimmune_lymphoproliferative_syndrome
X-linked lymphoproliferative disease (also known as Duncan's disease[1]:86 or Purtilo syndrome[2]) is a lymphoproliferative disorder.[3]
https://en.wikipedia.org/wiki/X-linked_lymphoproliferative_disease
Biphenotypic acute leukaemia (BAL) is an uncommon type of leukemia which arises in multipotent progenitor cells which have the ability to differentiate into both myeloid and lymphoid lineages.[1][2][3] It is a subtype of "leukemia of ambiguous lineage".[4]
The direct reasons leading to BAL are still not clear. BAL can be de novo or secondary to previous cytotoxic therapy. Many factors, such viruses, hereditary factors, and radiation, might have a relationship with BAL.
BAL is hard to treat. Usually the chemotherapy is chosen according to the morphology of the blast (ALL or AML). A blood-forming stem-cell transplantation is highly recommended. About 5% of acute leukaemia cases are BAL. BAL can occur in all ages of people but occurs more in adults than in children.[5]
https://en.wikipedia.org/wiki/Biphenotypic_acute_leukaemia
Large granular lymphocytic (LGL) leukemia is a chronic lymphoproliferative disorder that exhibits an unexplained, chronic (> 6 months) elevation in large granular lymphocytes (LGLs) in the peripheral blood.[1]
It is divided in two main categories: T-cell LGL leukemia (T-LGLL) and natural-killer (NK)-cell LGL leukemia (NK-LGLL). As the name suggests, T-cell large granular lymphocyte leukemia is characterized by involvement of cytotoxic-T cells).[2]
In a study based in the US, the average age of diagnosis was 66.5 years[3] whereas in a French study the median age at diagnosis was 59 years (with an age range of 12-87 years old).[4] In the French study, only 26% of patients were younger than 50 years which suggests that this disorder is associated with older age at diagnosis.[4] Due to lack of presenting symptoms, the disorder is likely to be underdiagnosed in the general population.[5]
https://en.wikipedia.org/wiki/Large_granular_lymphocytic_leukemia
Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare hematologic malignancy. It was initially regarded as a form of lymphocyte-derived cutaneous lymphoma and alternatively named CD4+CD56+ hematodermic tumor, blastic NK cell lymphoma,[1] and agranular CD4+ NK cell leukemia.[2] Later, however, the disease was determined to be a malignancy of plasmacytoid dendritic cells rather than lymphocytes and therefore termed blastic plasmacytoid dendritic cell neoplasm. In 2016, the World Health Organization designated BPDCN to be in its own separate category within the myeloid class of neoplasms.[3] It is estimated that BPDCN constitutes 0.44% of all hematological malignancies.[4]
Blastic plasmacytoid dendritic cell neoplasm is an aggressive malignancy with features of cutaneous lymphoma (e.g. malignant plasmacytoid dendritic cell infiltrations into the skin to form single or multiple lesions) and/or leukemia (i.e. malignant plasmacytoid dendritic cells in blood and bone marrow).[2] While commonly presenting with these clinical features, BPDCN, particularly in its more advanced stages, may also involve malignant plasmacytoid dendritic cell infiltrations in and thereby injury to the liver, spleen, lymph nodes, central nervous system, or other tissues. The neoplasm occurs in individuals of all ages but predominates in the elderly; in children, it afflicts males and females equally but in adults is far more common (~75% of cases) in males.[5]
Blastic plasmacytoid dendritic cell neoplasm typically responds to chemotherapy regimens used to treat hematological malignancies. All too often, however, the disease rapidly recurs and does so in a more drug-resistant form.[5] Furthermore, the disease may occur in association with the myelodysplastic syndrome or transform to acute myeloid leukemia.[4] Consequently, BPDCN has a very low 5 year survival rate.[5]Current translational research studies on treating BPDCN have therefore focused on non-chemotherapeutic regimens that target the molecular pathways which may promote the disease.[6]
https://en.wikipedia.org/wiki/Blastic_plasmacytoid_dendritic_cell_neoplasm
Human T-cell lymphotropic virus type 1 or human T-lymphotropic virus (HTLV-I), also called the adult T-cell lymphoma virus type 1, is a retrovirus of the human T-lymphotropic virus (HTLV) family that has been implicated in several kinds of diseases including very aggressive adult T-cell lymphoma (ATL), HTLV-I-associated myelopathy, uveitis, Strongyloides stercoralis hyper-infection and some other diseases. It is thought that about 1–5% of infected persons develop cancer as a result of the infection with HTLV-I over their lifetimes.[1]
Adult T-cell lymphoma (ATL) was discovered in 1977 in Japan. The symptoms of ATL were different from other lymphomas known at the time. It was suggested that ATL is caused by the infection of a retrovirus called ATLV.[2] Strikingly, ATLV had the transforming activity in vitro.[3] These studies established that the retrovirus infection is the cause of ATL. The retrovirus is now generally called HTLV-I because later studies proved that ATLV is the same as the firstly identified human retrovirus called HTLV discovered by Bernard Poiesz and Francis Ruscetti and their co-workers in the laboratory of Robert C. Gallo at the National Cancer Institute.[4] Infection with HTLV-I, like infection with other retroviruses, probably occurs for life. A patient infected with HTLV can be diagnosed when antibodies against HTLV-1 are detected in the serum.[1]
https://en.wikipedia.org/wiki/Human_T-lymphotropic_virus_1
Enteropathy-associated T-cell lymphoma (EATL), previously termed enteropathy-associated T-cell lymphoma, type I and at one time termed enteropathy-type T-cell lymphoma (ETTL), is a complication of coeliac disease in which a malignant T-cell lymphoma develops in areas of the small intestine afflicted by the disease's intense inflammation.[1] While a relatively rare disease, it is the most common type of primary gastrointestinal T-cell lymphoma.[2]
https://en.wikipedia.org/wiki/Enteropathy-associated_T-cell_lymphoma
Angioimmunoblastic T-cell lymphoma (AITL, sometimes misspelled AILT, formerly known as "angioimmunoblastic lymphadenopathy with dysproteinemia"[2]:747) is a mature T-cell lymphoma of blood or lymph vessel immunoblastscharacterized by a polymorphous lymph node infiltrate showing a marked increase in follicular dendritic cells (FDCs) and high endothelial venules (HEVs) and systemic involvement.[1]
https://en.wikipedia.org/wiki/Angioimmunoblastic_T-cell_lymphoma
Hepatosplenic T-cell lymphoma is a rare form of lymphoma that is generally incurable, except in the case of an allogeneic stem cell transplant.[2][3] It is a systemic neoplasm comprising medium-sized cytotoxic T-cells that show significant sinusoidal infiltration in the liver, spleen, and bone marrow.[1]
https://en.wikipedia.org/wiki/Hepatosplenic_T-cell_lymphoma
CD30+ cutaneous T-cell lymphoma, also known as primary cutaneous anaplastic large cell lymphoma, is a cutaneous (skin) condition characterized by solitary or localized skin lesions that have a tendency to ulcerate.[1]:738
https://en.wikipedia.org/wiki/CD30%2B_cutaneous_T-cell_lymphoma
Secondary cutaneous CD30+ large-cell lymphoma is a cutaneous condition that may arise in cases of mycosis fungoides, and in patients with lymphomatoid papulosis.[1]:738
https://en.wikipedia.org/wiki/Secondary_cutaneous_CD30%2B_large-cell_lymphoma
Non-mycosis fungoides CD30− cutaneous large T-cell lymphoma is a cutaneous condition that usually presents as solitary or generalized plaques, nodules, or tumors of short duration.[1]:738
https://en.wikipedia.org/wiki/Non-mycosis_fungoides_CD30%E2%88%92_cutaneous_large_T-cell_lymphoma
CD30, also known as TNFRSF8, is a cell membrane protein of the tumor necrosis factor receptor family and tumor marker.
https://en.wikipedia.org/wiki/CD30
Adult T-cell leukemia/lymphoma (ATL or ATLL) is a rare cancer of the immune system's T-cells[1][2][3] caused by human T cell leukemia/lymphotropic virus type 1 (HTLV-1).[4] All ATL cells contain integrated HTLV-1 provirus further supporting that causal role of the virus in the cause of the neoplasm.[4] A small amount of HTLV-1 individuals progress to develop ATL with a long latency period between infection and ATL development. ATL is categorized into 4 subtypes: acute, smoldering, lymphoma-type, chronic. Acute and Lymphoma-type are known to particularity be aggressive with poorer prognosis. [5]
Globally, the retrovirus HTLV-1 is estimated to infect 20 million people with the incidence of ATL approximately 0.05 per 100,000 with endemic regions such as regions of Japan, as high as 27 per 100,000.[6] However, cases have increased in non-endemic regions with highest incidence of HTLV-1 in southern/northern islands of Japan, Caribbean, Central and South America, intertropical Africa, Romania, northern Iran. ATL normally occurs around the age of 62 years but median age at diagnosis does depend on prevalence of the HTLV-1 infection in the geographic location.[7]
Current treatment regiments for ATL are based on clinical subtype and response to initial therapy. Some therapy modalities for treatment may not available in all countries therefore strategies differ across the world. All patients are referred to clinical trials if available. Beyond clinical trials, treatments are centered on multiagent chemotherapy, zidovudine plus interferon a (AZT/IFN), and allogenic hematopoietic stem cell transplantation (alloHSCT).[6]
https://en.wikipedia.org/wiki/Adult_T-cell_leukemia/lymphoma
Granulomatous slack skin (GSS) is a rare cutaneous condition, a variant of lymphoma that typically presents in middle-aged adults.[2]:735
It is a form of cutaneous T-cell lymphoma[3] and a variant of mycosis fungoides.[4]
https://en.wikipedia.org/wiki/Granulomatous_slack_skin
In the mycotic stage, infiltrative plaques appear and biopsy shows a polymorphous inflammatory infiltrate in the dermis that contains small numbers of frankly atypical lymphoid cells. These cells may line up individually along the epidermal basal layer. The latter finding if unaccompanied by spongiosis is highly suggestive of mycosis fungoides. In the tumorous stage a dense infiltrate of medium-sized lymphocytes with cerebriform nuclei expands the dermis.
https://en.wikipedia.org/wiki/Mycosis_fungoides
Simian-T-lymphotropic viruses, also Simian T-cell leukemia viruses (STLVs), are retroviruses closely related to the human sexually and breastfeeding transmissible viruses HTLV. They have subtypes 1 through 4 as compared to HTLV 1 through 4, and each subtype has its own serovars.[1] Together they comprise PTLVs (primate T-lymphotropic viruses)[1] A study has shown that STLV-1 Tax and SBZ proteins have similar functions to their counterparts of HTLV-1. STLV-1 is oncogenic in Japanese macaques.[2]
In particular, the HTLV-I/STLV-I history might suggest a simian migration from Asia to Africa not much earlier than 19,500–60,000 years ago.[1]
https://en.wikipedia.org/wiki/Simian-T-lymphotropic_virus
The oral polio vaccine (OPV) AIDS hypothesis states that the AIDS pandemic originated from live polio vaccines prepared in chimpanzee tissue cultures, accidentally contaminated with SIV virus and then administered to up to one million Africans between 1957 and 1960 in experimental mass vaccination campaigns.
Data analyses in molecular biology and phylogenetic studies contradict the OPV AIDS hypothesis; consequently, scientific consensus regards the hypothesis as disproven.[1][2][3][4] The journal Nature has described the hypothesis as "refuted".[5]
https://en.wikipedia.org/wiki/Oral_polio_vaccine_AIDS_hypothesis
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