Clonal Evolution
Evolution, Molecular
Clone Cells
Chromosome Aberrations
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Philadelphia Chromosome
Chromosome Disorders
Leukemia, Lymphocytic, Chronic, B-Cell
Pyrimidines
Immunoglobulin Heavy Chains
Blast Crisis
Cytogenetic Analysis
Mutation
In Situ Hybridization, Fluorescence
Neoplastic Stem Cells
Gene Rearrangement, B-Lymphocyte, Heavy Chain
Cell Transformation, Neoplastic
Directed Molecular Evolution
Genes, abl
Molecular Sequence Data
Disease Progression
Anemia, Aplastic
Fusion Proteins, bcr-abl
Translocation, Genetic
Base Sequence
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma
Chromosomes, Human, Pair 8
Sequence Analysis, DNA
Comparative Genomic Hybridization
Aneuploidy
Polymerase Chain Reaction
Phenotype
Immunoglobulin Variable Region
Loss of Heterozygosity
Selection, Genetic
Leukemia, Myeloid, Acute
Models, Biological
Myelodysplastic Syndromes
Genome, Human
Drug Resistance, Neoplasm
Prognosis
Cell Lineage
Cultural Evolution
Models, Genetic
Bone Marrow
Interferon-alpha
Species Specificity
Neoplasms
Survival Analysis
Stem Cells
Amino Acid Sequence
Adaptation, Biological
Genetic evolution of pancreatic cancer: lessons learnt from the pancreatic cancer genome sequencing project. (1/77)
(+info)Clonal evolution through loss of chromosomes and subsequent polyploidization in chondrosarcoma. (2/77)
(+info)Psychological stress and aging: role of glucocorticoids (GCs). (3/77)
(+info)Silencing, positive selection and parallel evolution: busy history of primate cytochromes C. (4/77)
(+info)Somatic retrotransposition alters the genetic landscape of the human brain. (5/77)
(+info)High order chromatin architecture shapes the landscape of chromosomal alterations in cancer. (6/77)
(+info)Screening ethnically diverse human embryonic stem cells identifies a chromosome 20 minimal amplicon conferring growth advantage. (7/77)
(+info)Unilateral retinitis pigmentosa: a proposal of genetic pathogenic mechanisms. (8/77)
(+info)There are several types of chromosome aberrations, including:
1. Chromosomal deletions: Loss of a portion of a chromosome.
2. Chromosomal duplications: Extra copies of a chromosome or a portion of a chromosome.
3. Chromosomal translocations: A change in the position of a chromosome or a portion of a chromosome.
4. Chromosomal inversions: A reversal of a segment of a chromosome.
5. Chromosomal amplifications: An increase in the number of copies of a particular chromosome or gene.
Chromosome aberrations can be detected through various techniques, such as karyotyping, fluorescence in situ hybridization (FISH), or array comparative genomic hybridization (aCGH). These tests can help identify changes in the chromosomal makeup of cells and provide information about the underlying genetic causes of disease.
Chromosome aberrations are associated with a wide range of diseases, including:
1. Cancer: Chromosome abnormalities are common in cancer cells and can contribute to the development and progression of cancer.
2. Birth defects: Many birth defects are caused by chromosome abnormalities, such as Down syndrome (trisomy 21), which is caused by an extra copy of chromosome 21.
3. Neurological disorders: Chromosome aberrations have been linked to various neurological disorders, including autism and intellectual disability.
4. Immunodeficiency diseases: Some immunodeficiency diseases, such as X-linked severe combined immunodeficiency (SCID), are caused by chromosome abnormalities.
5. Infectious diseases: Chromosome aberrations can increase the risk of infection with certain viruses, such as human immunodeficiency virus (HIV).
6. Ageing: Chromosome aberrations have been linked to the ageing process and may contribute to the development of age-related diseases.
7. Radiation exposure: Exposure to radiation can cause chromosome abnormalities, which can increase the risk of cancer and other diseases.
8. Genetic disorders: Many genetic disorders are caused by chromosome aberrations, such as Turner syndrome (45,X), which is caused by a missing X chromosome.
9. Rare diseases: Chromosome aberrations can cause rare diseases, such as Klinefelter syndrome (47,XXY), which is caused by an extra copy of the X chromosome.
10. Infertility: Chromosome abnormalities can contribute to infertility in both men and women.
Understanding the causes and consequences of chromosome aberrations is important for developing effective treatments and improving human health.
The BCR-ABL gene is a fusion gene that is present in the majority of cases of CML. It is created by the translocation of two genes, called BCR and ABL, which leads to the production of a constitutively active tyrosine kinase protein that promotes the growth and proliferation of abnormal white blood cells.
There are three main phases of CML, each with distinct clinical and laboratory features:
1. Chronic phase: This is the earliest phase of CML, where patients may be asymptomatic or have mild symptoms such as fatigue, night sweats, and splenomegaly (enlargement of the spleen). The peripheral blood count typically shows a high number of blasts in the blood, but the bone marrow is still functional.
2. Accelerated phase: In this phase, the disease progresses to a higher number of blasts in the blood and bone marrow, with evidence of more aggressive disease. Patients may experience symptoms such as fever, weight loss, and pain in the joints or abdomen.
3. Blast phase: This is the most advanced phase of CML, where there is a high number of blasts in the blood and bone marrow, with significant loss of function of the bone marrow. Patients are often symptomatic and may have evidence of spread of the disease to other organs, such as the liver or spleen.
Treatment for CML typically involves targeted therapy with drugs that inhibit the activity of the BCR-ABL protein, such as imatinib (Gleevec), dasatinib (Sprycel), or nilotinib (Tasigna). These drugs can slow or stop the progression of the disease, and may also produce a complete cytogenetic response, which is defined as the absence of all Ph+ metaphases in the bone marrow. However, these drugs are not curative and may have significant side effects. Allogenic hematopoietic stem cell transplantation (HSCT) is also a potential treatment option for CML, but it carries significant risks and is usually reserved for patients who are in the blast phase of the disease or have failed other treatments.
In summary, the clinical course of CML can be divided into three phases based on the number of blasts in the blood and bone marrow, and treatment options vary depending on the phase of the disease. It is important for patients with CML to receive regular monitoring and follow-up care to assess their response to treatment and detect any signs of disease progression.
Synonyms: BCR-ABL fusion gene, t(9;22)(q34;q11), p210 protein, bcr-abl fusion transcript, breakpoint cluster region (BCR) - Abelson tyrosine kinase (ABLE) fusion gene.
Word Origin: Named after the city of Philadelphia, where it was first described in 1960.
There are many different types of chromosome disorders, including:
1. Trisomy: This is a condition in which there is an extra copy of a chromosome. For example, Down syndrome is caused by an extra copy of chromosome 21.
2. Monosomy: This is a condition in which there is a missing copy of a chromosome.
3. Turner syndrome: This is a condition in which there is only one X chromosome instead of two.
4. Klinefelter syndrome: This is a condition in which there are three X chromosomes instead of the typical two.
5. Chromosomal translocations: These are abnormalities in which a piece of one chromosome breaks off and attaches to another chromosome.
6. Inversions: These are abnormalities in which a segment of a chromosome is reversed end-to-end.
7. Deletions: These are abnormalities in which a portion of a chromosome is missing.
8. Duplications: These are abnormalities in which there is an extra copy of a segment of a chromosome.
Chromosome disorders can have a wide range of effects on the body, depending on the type and severity of the condition. Some common features of chromosome disorders include developmental delays, intellectual disability, growth problems, and physical abnormalities such as heart defects or facial anomalies.
There is no cure for chromosome disorders, but treatment and support are available to help manage the symptoms and improve the quality of life for individuals with these conditions. Treatment may include medications, therapies, and surgery, as well as support and resources for families and caregivers.
Preventive measures for chromosome disorders are not currently available, but research is ongoing to understand the causes of these conditions and to develop new treatments and interventions. Early detection and diagnosis can help identify chromosome disorders and provide appropriate support and resources for individuals and families.
In conclusion, chromosome disorders are a group of genetic conditions that affect the structure or number of chromosomes in an individual's cells. These conditions can have a wide range of effects on the body, and there is no cure, but treatment and support are available to help manage symptoms and improve quality of life. Early detection and diagnosis are important for identifying chromosome disorders and providing appropriate support and resources for individuals and families.
In LLCB, the B cells undergo a mutation that causes them to become cancerous and multiply rapidly. This can lead to an overproduction of these cells in the bone marrow, causing the bone marrow to become crowded and unable to produce healthy red blood cells, platelets, and white blood cells.
LLCB is typically a slow-growing cancer, and it can take years for symptoms to develop. However, as the cancer progresses, it can lead to a range of symptoms including fatigue, weakness, weight loss, fever, night sweats, and swollen lymph nodes.
LLCB is typically diagnosed through a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as X-rays or CT scans. Treatment options for LLCB include chemotherapy, radiation therapy, and in some cases, stem cell transplantation.
Overall, while LLCB is a serious condition, it is typically slow-growing and can be managed with appropriate treatment. With current treatments, many people with LLCB can achieve long-term remission and a good quality of life.
The term "blast crisis" was first used in the medical literature in 1998 to describe this phenomenon, which was previously known as "accelerated phase." The blast crisis is the most advanced stage of CML and is associated with a poor prognosis if left untreated.
The exact cause of blast crisis is not fully understood, but it is believed to be related to the development of resistance to TKIs, which can lead to an increase in the number of abnormal cells in the bone marrow and blood. The condition typically occurs after several years of TKI therapy, although it can sometimes occur within the first few months of treatment.
The symptoms of blast crisis are non-specific and can include fatigue, fever, night sweats, and weight loss. Laboratory tests will show an elevated white blood cell count, anemia, and thrombocytopenia. The diagnosis of blast crisis is based on the presence of blasts in the blood and bone marrow, as well as other laboratory and radiological findings.
Treatment of blast crisis typically involves the use of more intensive chemotherapy or hematopoietic stem cell transplantation (HSCT). In some cases, the TKI therapy may be discontinued and replaced with a different medication or combination of medications. The prognosis for patients with blast crisis is generally poor, with a five-year survival rate of around 50%. However, with appropriate treatment, some patients can achieve long-term remission or even a cure.
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.
Trisomy is caused by an extra copy of a chromosome, which can be due to one of three mechanisms:
1. Trisomy 21 (Down syndrome): This is the most common type of trisomy and occurs when there is an extra copy of chromosome 21. It is estimated to occur in about 1 in every 700 births.
2. Trisomy 13 (Patau syndrome): This type of trisomy occurs when there is an extra copy of chromosome 13. It is estimated to occur in about 1 in every 10,000 births.
3. Trisomy 18 (Edwards syndrome): This type of trisomy occurs when there is an extra copy of chromosome 18. It is estimated to occur in about 1 in every 2,500 births.
The symptoms of trisomy can vary depending on the type of trisomy and the severity of the condition. Some common symptoms include:
* Delayed physical growth and development
* Intellectual disability
* Distinctive facial features, such as a flat nose, small ears, and a wide, short face
* Heart defects
* Vision and hearing problems
* GI issues
* Increased risk of infection
Trisomy can be diagnosed before birth through prenatal testing, such as chorionic villus sampling (CVS) or amniocentesis. After birth, it can be diagnosed through a blood test or by analyzing the child's DNA.
There is no cure for trisomy, but treatment and support are available to help manage the symptoms and improve the quality of life for individuals with the condition. This may include physical therapy, speech therapy, occupational therapy, and medication to manage heart defects or other medical issues. In some cases, surgery may be necessary to correct physical abnormalities.
The prognosis for trisomy varies depending on the type of trisomy and the severity of the condition. Some forms of trisomy are more severe and can be life-threatening, while others may have a more mild impact on the individual's quality of life. With appropriate medical care and support, many individuals with trisomy can lead fulfilling lives.
In summary, trisomy is a genetic condition that occurs when there is an extra copy of a chromosome. It can cause a range of symptoms and can be diagnosed before or after birth. While there is no cure for trisomy, treatment and support are available to help manage the symptoms and improve the quality of life for individuals with the condition.
Symptoms of aplastic anemia may include fatigue, weakness, shortness of breath, pale skin, and increased risk of bleeding or infection. Treatment options for aplastic anemia typically involve blood transfusions and immunosuppressive drugs to stimulate the bone marrow to produce new blood cells. In severe cases, a bone marrow transplant may be necessary.
Overall, aplastic anemia is a rare and serious condition that requires careful management by a healthcare provider to prevent complications and improve quality of life.
https://www.medicinenet.com › Medical Dictionary › G
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Definition & Facts | Britannica
https://www.britannica.com › science › Genetic-tr...
Genetic translocation, also called chromosomal translocation, a type of chromosomal aberration in which a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material. Genetic translocations are often found in cancer cells and may play a role in the development and progression of cancer.
Translocation, Genetic | health Encyclopedia - UPMC
https://www.upmc.com › health-library › gene...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Genetics Home Reference - NIH
https://ghr.nlm.nih.gov › condition › ge...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
In conclusion, Genetic Translocation is an abnormality in the number or arrangement of chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome, resulting in a gain or loss of genetic material that can have significant effects on the individual.
The symptoms of PRE-B-ALL can include fever, fatigue, night sweats, weight loss, and swollen lymph nodes. The cancer can also spread to other parts of the body, such as the central nervous system, spleen, and bones.
PRE-B-ALL is most commonly seen in children, but it can also occur in adults. It is a rare cancer, accounting for only about 5% of all childhood leukemias and less than 1% of all adult leukemias.
The exact cause of PRE-B-ALL is not known, but it is believed to be linked to genetic mutations that occur during fetal development or early childhood. Some risk factors that may increase the likelihood of developing PRE-B-ALL include:
1. Genetic disorders, such as Down syndrome or Fanconi anemia.
2. Exposure to radiation or certain chemicals during pregnancy or early childhood.
3. Infections, such as HIV or Epstein-Barr virus.
4. Family history of PRE-B-ALL or other blood cancers.
To diagnose PRE-B-ALL, a bone marrow biopsy and aspiration are typically performed to collect a sample of cells for analysis. Additional tests, such as flow cytometry, immunophenotyping, and cytogenetic analysis, may also be conducted to confirm the diagnosis and identify any specific genetic abnormalities.
Treatment for PRE-B-ALL usually involves a combination of chemotherapy and/or bone marrow transplantation. The prognosis for PRE-B-ALL varies depending on the patient's age, overall health, and the specific genetic abnormalities present in the cancer cells. With current treatments, the 5-year survival rate for PRE-B-ALL is approximately 70-80%. However, the disease can sometimes relapse, and patients may require ongoing monitoring and treatment to prevent relapse and manage any long-term complications.
There are several types of aneuploidy, including:
1. Trisomy: This is the presence of an extra copy of a chromosome. For example, Down syndrome is caused by an extra copy of chromosome 21 (trisomy 21).
2. Monosomy: This is the absence of a chromosome.
3. Mosaicism: This is the presence of both normal and abnormal cells in the body.
4. Uniparental disomy: This is the presence of two copies of a chromosome from one parent, rather than one copy each from both parents.
Aneuploidy can occur due to various factors such as errors during cell division, exposure to certain chemicals or radiation, or inheritance of an abnormal number of chromosomes from one's parents. The risk of aneuploidy increases with age, especially for women over the age of 35, as their eggs are more prone to errors during meiosis (the process by which egg cells are produced).
Aneuploidy can be diagnosed through various methods such as karyotyping (examining chromosomes under a microscope), fluorescence in situ hybridization (FISH) or quantitative PCR. Treatment for aneuploidy depends on the underlying cause and the specific health problems it has caused. In some cases, treatment may involve managing symptoms, while in others, it may involve correcting the genetic abnormality itself.
In summary, aneuploidy is a condition where there is an abnormal number of chromosomes present in a cell, which can lead to various developmental and health problems. It can occur due to various factors and can be diagnosed through different methods. Treatment depends on the underlying cause and the specific health problems it has caused.
AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.
There are several subtypes of AML, including:
1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.
The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:
* Fatigue
* Weakness
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Headache
* Confusion or seizures
AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:
1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.
Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:
1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.
It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.
Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.
In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.
There are several subtypes of MDS, each with distinct clinical features and prognosis. The most common subtype is refractory anemia with excess blasts (RAEB), followed by chronic myelomonocytic leukemia (CMMoL) and acute myeloid leukemia (AML).
The exact cause of MDS is not fully understood, but it is believed to result from a combination of genetic mutations and environmental factors. Risk factors for developing MDS include exposure to certain chemicals or radiation, age over 60, and a history of previous cancer treatment.
Symptoms of MDS can vary depending on the specific subtype and severity of the disorder, but may include fatigue, weakness, shortness of breath, infection, bleeding, and easy bruising. Diagnosis is typically made through a combination of physical examination, medical history, blood tests, and bone marrow biopsy.
Treatment for MDS depends on the specific subtype and severity of the disorder, as well as the patient's overall health and preferences. Options may include supportive care, such as blood transfusions and antibiotics, or more intensive therapies like chemotherapy, bone marrow transplantation, or gene therapy.
Overall, myelodysplastic syndromes are a complex and heterogeneous group of disorders that can have a significant impact on quality of life and survival. Ongoing research is focused on improving diagnostic accuracy, developing more effective treatments, and exploring novel therapeutic approaches to improve outcomes for patients with MDS.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
Clonal hematopoiesis
Clonal interference
Evolutionary therapy
Evolution of sexual reproduction
Hugh Loxdale
Aphid
Cancer stem cell
Somatic evolution in cancer
Carcinogenesis
Tumour heterogeneity
Cancer
Clonally transmissible cancer
Christopher E. Mason
Canine transmissible venereal tumor
Genetic marker
Pemphigus spyrothecae
Crayfish as food
Marbled crayfish
Cancer genome sequencing
Ophiactis savignyi
Daniel S. Fisher
Elaine Mardis
Muller's ratchet
Large-cell lung carcinoma with rhabdoid phenotype
Alberto Bardelli
Mouse models of breast cancer metastasis
Gynogenesis
Hybridogenesis in water frogs
Fucus radicans
List of phylogenetics software
Gonozooid
Microsporum canis
Polypodium appalachianum
Hamiltosporidium
Ciliate
Automixis
Fluorescence in situ hybridization
Pest (organism)
Marco Marra
Immunosenescence
Daphnia magna
Molecular anthropology
Embryonal fyn-associated substrate
Cystic fibrosis transmembrane conductance regulator
Oak
Black sigatoka
Uveitis
Ex situ conservation
Fragaria vesca
Seagrass
Antigen
Anne-Maree Pearse
Calamites
Streptococcus
Armillaria ostoyae
Fungal genome
DNA mismatch repair
Radial glial cell
Asexual reproduction
Clonal Evolution - MeSH - NCBI
Clonal evolution of glioblastoma under therapy - PubMed
The clonal evolution of metastatic colorectal cancer.
Figure 3 - Evolution of Sequence Type 4821 Clonal Complex Hyperinvasive and Quinolone-Resistant Meningococci - Volume 27,...
Predictors of clonal evolution and myeloid neoplasia following immunosuppressive therapy in severe aplastic anemia - PubMed
Paper: Single-Cell Transcriptomics of Human <em>TET2</Em> Knockout CD4 T-Cells and Their...
Clonal evolution and genomic diversification of Bordetella hinzii in an immunocompromised host | NIH Research Festival
Invariant patterns of clonal succession determine specific clinical features of myelodysplastic syndromes | Nature...
Clonal evolution and hierarchy in myeloid malignancies. | Trends Cancer;9(9): 707-715, 2023 09. | MEDLINE
Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study | Steidl Laboratory
One thousand somatic SNVs per skin fibroblast cell set baseline of mosaic mutational load with patterns that suggest...
Search Strategy Used to Create the PubMed Cancer Filter
NIH Clinical Center Search the Studies: Study Number, Study Title
c-Kit M541L variant is related to ineffective hemopoiesis predisposing to clonal evolution in 3D in vitro biomimetic co-culture...
Malignant clonal evolution from high proportion of monocytes in patients with aplastic anemia: a case report - Fu- Stem Cell...
APS -APS March Meeting 2016
- Event - Adapting populations in space: clonal interference and genetic diversity
Xiaotu Ma, PhD - St. Jude Children's Research Hospital
58th ASH Annual Meeting | NHLBI, NIH
IJMS | Free Full-Text | Are We Ready to Implement Molecular Subtyping of Bladder Cancer in Clinical Practice? Part 1: General...
Null allele, allelic dropouts or rare sex detection in clonal organisms: simulations and application to real data sets of...
Bioinformatic Exploration Hematology Cohort Data Webinar - 2020 - NIDDK
Identification and functional dissection of key genetic events in early chronic lymphocytic leukemia | CLL INCLONEL | Project |...
Nahla Bassil : USDA ARS
Publications | Tanay Group
Biomarkers Search
PAR-18-552: Partnership for Aging and Cancer Research (U01 - Clinical Trial Not Allowed)
Wissenschaftskolleg zu Berlin: Carlo C. Maley, Ph.D.
Coupy Amanda
Hematopoiesis2
- While strong driver hits result in MDS instantly in form of a de novo disease, some of the founder mutations in MDS originate from subclinical clonal expansions, referred to as clonal hematopoiesis (CH) present in the blood of some otherwise healthy individuals 18 , 19 . (nature.com)
- Recent advancements in clonal hematopoiesis research and the use of cutting-edge single cell technologies have shed new light on the developmental process of myeloid malignancies . (bvsalud.org)
Follicular Lymphoma1
- Our work on the Histological Transformation and Progression in Follicular Lymphoma: A Clonal Evolution Study has been published in PLoS Medicine! (ubc.ca)
Myeloid malignancies2
- Clonal evolution and hierarchy in myeloid malignancies. (bvsalud.org)
- In this review , we delve into the intricacies of clonal evolution in myeloid malignancies and its implications for the development of new diagnostic and therapeutic approaches . (bvsalud.org)
Germline1
- Here we describe extensive adaptive evolution of B. hinzii in a patient with recessive germline IL-12Rβ1 deficiency who presented with chronic bloodstream and gastrointestinal tract infection. (nih.gov)
Somatic2
- Irrespective of origins, MDS pathogenesis includes initial ancestral lesion followed by the stepwise acquisition of subsequent somatic mutations resulting in a highly diverse clonal hierarchy 17 . (nature.com)
- In particular, I am interested in methods to slow somatic evolution for cancer prevention and to delay, prevent, or target the evolution of therapeutic resistance in malignant neoplasms. (wiko-berlin.de)
Hierarchy2
- All 3,971 mutations are grouped based on their rank in the deduced clonal hierarchy (dominant and secondary). (nature.com)
- The clonal hierarchy has distinct ranking and the resultant invariant combinations of dominant/secondary mutations yield novel insights into the specific clinical phenotype of MDS. (nature.com)
Mutations3
- Here, analyzing 1809 MDS patients, we infer clonal architecture by using a stringent, the single-cell sequencing validated PyClone bioanalytic pipeline, and assess the position of the mutations within the clonal architecture. (nature.com)
- Recent large-scale sequencing studies have identified putative driver genetic events of CLL, uncovered the vast inter-personal and intratumoral genetic heterogeneity in CLL and have linked the presence of aggressive subclonal mutations with clonal evolution and poorer outcome. (europa.eu)
- The evolution of drug resistance in HIV occurs by the fixation of specific, well-known, drug-resistance mutations, but the underlying population genetic processes are not well understood. (harvard.edu)
Therapeutic1
- The adaptive landscape analogy has found practical use in recent years, as many have explored how their understanding can inform therapeutic strategies that subvert the evolution of drug resistance. (harvard.edu)
Purely2
- We consider a simple model of a spatially-extended, adapting population and show that, while clonal interference severely limits the adaptation of purely asexual populations, even rare recombination is enough to allow adaptation at rates approaching those of well-mixed populations. (aps.org)
- We use the narrow relationship that links Wright's F IS to genetic diversity in purely clonal populations as assessment criterion, since this relationship disappears faster with sexual recombination than with amplification problems of certain alleles. (biomedcentral.com)
Populations1
- We have performed various simulations of clonal and partially clonal populations. (biomedcentral.com)
Adaptive evolution2
- How does this spatial structure interact with adaptive evolution? (aps.org)
- Adaptive evolution by natural selection is the primary force shaping biological diversity. (harvard.edu)
Yeast1
- The application of this method to reinterpret published data sets of pathogenic clonal microbes (yeast and trypanosomes) confirms its usefulness and allows refining previous estimates concerning important pathogenic agents. (biomedcentral.com)
Cells2
- The clonal nature of hiPSC lines allows a high-resolution analysis of the genomes of the founder fibroblast cells without being confounded by the artifacts of single-cell whole-genome amplification. (nih.gov)
- This pauses the evolution of new and diverse B cells that could potentially beat back new virus variants. (nih.gov)
Distinct1
- Finally, AF distribution of mosaic SNVs had distinct narrow peaks, which could be a characteristic of clonal cell selection, clonal expansion, or both. (nih.gov)
Relapse2
- Late relapse in acute myeloid leukemia (AML): clonal evolution or therapy-related leukemia? (nature.com)
- Clonal evolution represents a central feature of tumor progression and relapse. (europa.eu)
Clinical1
- This work was co-led by Robert Kridel and Fong Chun Chan and illuminates the contrasting modes of evolution shaping the clinical histories of transformation and progression with implications in the context of treatment-induced selective pressures. (ubc.ca)
Cell2
- Whole transcriptome sequencing and single-cell transcriptome sequencing were used to study the cell evolution after KO. (confex.com)
- 9. Clonal evolution in diffuse large B-cell lymphoma with central nervous system recurrence. (nih.gov)
Resistance1
- Spatially divergent clonal evolution in multiple myeloma: overcoming resistance to BRAF inhibition. (uni-heidelberg.de)
Cancer7
- The clonal evolution of metastatic colorectal cancer. (osu.edu)
- My plan is to write a graduate-level textbook on Evolution and Cancer. (wiko-berlin.de)
- The field of evolution and cancer currently lacks a textbook that summarizes the field and identifies the open questions and promising avenues for research. (wiko-berlin.de)
- Thus, writing the book will benefit greatly from regular discussions with other evolutionary biologists and ecologists in residence at the Wissenschaftskolleg and specifically from discussions with the Cancer Evolution focus group. (wiko-berlin.de)
- In the process of writing the textbook, I propose to develop a vision of which experiments and projects in the evolution of cancer are both feasible and likely to have a large impact on the management of prevention of cancer. (wiko-berlin.de)
- This will form the basis of a large collaborative grant proposal to help fund our Center for Evolution and Cancer at UCSF. (wiko-berlin.de)
- Clonal evolution in cancer. (wiko-berlin.de)
Study2
Population1
- This is especially critical in clonal organisms in which deviation from panmixia, as measured by Wright's F IS , can, in principle, be used to infer both the extent of clonality and structure in a given population. (biomedcentral.com)
Patients1
- To directly test these ideas, I will systematically examine the clonal dynamics of a cohort of 17 CLL patients that were recurrently sampled over years from diagnosis until the time of first treatment. (europa.eu)
Data2
- Phylogenetic tree and data of clonal complex 4821 Neisseria meningitidis sublineage L44.1 (China CC4821-R1-C/B ) isolates. (cdc.gov)
- We introduce allelic dropouts and null alleles in clonal data sets and compare the results with those that exhibit increasing rates of sexual recombination. (biomedcentral.com)
Department1
- Dr. Nahla Victor Bassil is a Molecular Plant Geneticist with the United States Department of Agriculture (USDA) - Agricultural Research Service (ARS) - National Clonal Germplasm Repository (NCGR) in Corvallis, Oregon. (usda.gov)
48213
- Phylogenetic tree and data of clonal complex 4821 Neisseria meningitidis sublineage L44.1 (China CC4821-R1-C/B ) isolates. (cdc.gov)
- Expansion of quinolone-resistant Neisseria meningitidis clone China CC4821-R1-C/B from sequence type (ST) 4821 clonal complex (CC4821) caused a serogroup shift from serogroup A to serogroup C invasive meningococcal disease (IMD) in China. (cdc.gov)
- In China, the national dissemination of hyperinvasive sequence type (ST) 4821 clonal complex (CC4821) meningococci led to a shift in IMD epidemiology from mostly MenA to predominantly MenC ( 3 , 4 ). (cdc.gov)
Isolates2
- Comparative analyses demonstrated that all isolates were clonal, but had undergone extensive genomic diversification. (nih.gov)
- genetic relationships among isolates are defined by clonal complexes (CCs) identified by multilocus sequence typing (MLST), which are surrogates for lineages ( 2 ). (cdc.gov)