Tumor Suppressor Protein p53
Tumor Suppressor Proteins
Genes, Tumor Suppressor
Proto-Oncogene Proteins c-mdm2
Von Hippel-Lindau Tumor Suppressor Protein
Cyclin-Dependent Kinase Inhibitor p21
Tumor Suppressor Protein p14ARF
Molecular Sequence Data
Tumor Cells, Cultured
Amino Acid Sequence
Promoter Regions, Genetic
Cell Cycle Proteins
Gene Expression Regulation, Neoplastic
Oncogene Proteins, Viral
Protein Structure, Tertiary
Adenovirus E1B Proteins
Gene Expression Regulation
Adenomatous Polyposis Coli Protein
Antigens, Polyomavirus Transforming
bcl-2-Associated X Protein
Recombinant Fusion Proteins
Proteasome Endopeptidase Complex
Cyclin-Dependent Kinase Inhibitor p16
Cell Transformation, Neoplastic
Proto-Oncogene Proteins c-bcl-2
E2F Transcription Factors
RNA, Small Interfering
Tumor Markers, Biological
Retinoblastoma-Like Protein p107
E2F1 Transcription Factor
Retinoblastoma-Like Protein p130
Transcription Factor DP1
Suppressor of Cytokine Signaling Proteins
Papillomavirus E7 Proteins
Retinoblastoma-Binding Protein 1
Loss of Heterozygosity
Reverse Transcriptase Polymerase Chain Reaction
Tumor Necrosis Factor-alpha
Hypoxia-Inducible Factor 1, alpha Subunit
Intracellular Signaling Peptides and Proteins
Genes, Neurofibromatosis 2
Phosphoric Monoester Hydrolases
Polymerase Chain Reaction
Apoptosis Regulatory Proteins
Adenovirus E1A Proteins
Carcinoma, Renal Cell
Cell Line, Transformed
Sequence Homology, Amino Acid
Adaptor Proteins, Signal Transducing
von Hippel-Lindau Disease
Two-Hybrid System Techniques
Cyclin-Dependent Kinase Inhibitor p27
NIH 3T3 Cells
Cyclin-Dependent Kinase 4
Proto-Oncogene Proteins c-myc
Carcinoma, Squamous Cell
Suppressor Factors, Immunologic
Adenovirus E4 Proteins
Gene Expression Profiling
Hypoxia-Inducible Factor 1
Amino Acid Motifs
Cyclin-Dependent Kinase 2
Active Transport, Cell Nucleus
C-myc overexpression and p53 loss cooperate to promote genomic instability. (1/16353)p53 monitors genomic integrity at the G1 and G2/M cell cycle checkpoints. Cells lacking p53 may show gene amplification as well as the polyploidy or aneuploidy typical of many tumors. The pathways through which this develops, however, are not well defined. We demonstrate here that the combination of p53 inactivation and c-myc overexpression in diploid cells markedly accelerates the spontaneous development of tetraploidy. This is not seen with either N-myc or L-myc. Tetraploidy is accompanied by significantly higher levels of cyclin B and its associated cdc2 kinase activity. Mitotic spindle poisons accelerate the appearance of tetraploidy in cells either lacking functional p53 or overexpressing c-myc whereas the combination is additive. Restoration of p53 function in cells overexpressing c-myc causing rapid apoptosis, indicating that cells yet to become tetraploid have nonetheless suffered irreversible genomic and/or mitotic spindle damage. In the face of normal p53 function, such damage would either be repaired or trigger apoptotis. We propose that loss of p53 and overexpression of c-myc permits the emergence and survival of cells with increasingly severe damage and the eventual development of tetraploidy. (+info)
Gadd45, a p53-responsive stress protein, modifies DNA accessibility on damaged chromatin. (2/16353)This report demonstrates that Gadd45, a p53-responsive stress protein, can facilitate topoisomerase relaxing and cleavage activity in the presence of core histones. A correlation between reduced expression of Gadd45 and increased resistance to topoisomerase I and topoisomerase II inhibitors in a variety of human cell lines was also found. Gadd45 could potentially mediate this effect by destabilizing histone-DNA interactions since it was found to interact directly with the four core histones. To evaluate this possibility, we investigated the effect of Gadd45 on preassembled mononucleosomes. Our data indicate that Gadd45 directly associates with mononucleosomes that have been altered by histone acetylation or UV radiation. This interaction resulted in increased DNase I accessibility on hyperacetylated mononucleosomes and substantial reduction of T4 endonuclease V accessibility to cyclobutane pyrimidine dimers on UV-irradiated mononucleosomes but not on naked DNA. Both histone acetylation and UV radiation are thought to destabilize the nucleosomal structure. Hence, these results imply that Gadd45 can recognize an altered chromatin state and modulate DNA accessibility to cellular proteins. (+info)
Regulation of p53 function and stability by phosphorylation. (3/16353)The p53 tumor suppressor protein can be phosphorylated at several sites within the N- and C-terminal domains, and several protein kinases have been shown to phosphorylate p53 in vitro. In this study, we examined the activity of p53 proteins with combined mutations at all of the reported N-terminal phosphorylation sites (p53N-term), all of the C-terminal phosphorylation sites (p53C-term), or all of the phosphorylation sites together (p53N/C-term). Each of these mutant proteins retained transcriptional transactivation functions, indicating that phosphorylation is not essential for this activity of p53, although a subtle contribution of the C-terminal phosphorylation sites to the activation of expression of the endogenous p21(Waf1/Cip1)-encoding gene was detected. Mutation of the phosphorylation sites to alanine did not affect the sensitivity of p53 to binding to or degradation by Mdm2, although alteration of residues 15 and 37 to aspartic acid, which could mimic phosphorylation, resulted in a slight resistance to Mdm2-mediated degradation, consistent with recent reports that phosphorylation at these sites inhibits the p53-Mdm2 interaction. However, expression of the phosphorylation site mutant proteins in both wild-type p53-expressing and p53-null lines showed that all of the mutant proteins retained the ability to be stabilized following DNA damage. This indicates that phosphorylation is not essential for DNA damage-induced stabilization of p53, although phosphorylation could clearly contribute to p53 stabilization under some conditions. (+info)
Different regulation of the p53 core domain activities 3'-to-5' exonuclease and sequence-specific DNA binding. (4/16353)In this study we further characterized the 3'-5' exonuclease activity intrinsic to wild-type p53. We showed that this activity, like sequence-specific DNA binding, is mediated by the p53 core domain. Truncation of the C-terminal 30 amino acids of the p53 molecule enhanced the p53 exonuclease activity by at least 10-fold, indicating that this activity, like sequence-specific DNA binding, is negatively regulated by the C-terminal basic regulatory domain of p53. However, treatments which activated sequence-specific DNA binding of p53, like binding of the monoclonal antibody PAb421, which recognizes a C-terminal epitope on p53, or a higher phosphorylation status, strongly inhibited the p53 exonuclease activity. This suggests that at least on full-length p53, sequence-specific DNA binding and exonuclease activities are subject to different and seemingly opposing regulatory mechanisms. Following up the recent discovery in our laboratory that p53 recognizes and binds with high affinity to three-stranded DNA substrates mimicking early recombination intermediates (C. Dudenhoeffer, G. Rohaly, K. Will, W. Deppert, and L. Wiesmueller, Mol. Cell. Biol. 18:5332-5342), we asked whether such substrates might be degraded by the p53 exonuclease. Addition of Mg2+ ions to the binding assay indeed started the p53 exonuclease and promoted rapid degradation of the bound, but not of the unbound, substrate, indicating that specifically recognized targets can be subjected to exonucleolytic degradation by p53 under defined conditions. (+info)
Analysis of genomic integrity and p53-dependent G1 checkpoint in telomerase-induced extended-life-span human fibroblasts. (5/16353)Life span determination in normal human cells may be regulated by nucleoprotein structures called telomeres, the physical ends of eukaryotic chromosomes. Telomeres have been shown to be essential for chromosome stability and function and to shorten with each cell division in normal human cells in culture and with age in vivo. Reversal of telomere shortening by the forced expression of telomerase in normal cells has been shown to elongate telomeres and extend the replicative life span (H. Vaziri and S. Benchimol, Curr. Biol. 8:279-282, 1998; A. G. Bodnar et al., Science 279:349-352, 1998). Extension of the life span as a consequence of the functional inactivation of p53 is frequently associated with loss of genomic stability. Analysis of telomerase-induced extended-life-span fibroblast (TIELF) cells by G banding and spectral karyotyping indicated that forced extension of the life span by telomerase led to the transient formation of aberrant structures, which were subsequently resolved in higher passages. However, the p53-dependent G1 checkpoint was intact as assessed by functional activation of p53 protein in response to ionizing radiation and subsequent p53-mediated induction of p21(Waf1/Cip1/Sdi1). TIELF cells were not tumorigenic and had a normal DNA strand break rejoining activity and normal radiosensitivity in response to ionizing radiation. (+info)
Immunohistochemical expression of mdm2 and p21WAF1 in invasive cervical cancer: correlation with p53 protein and high risk HPV infection. (6/16353)AIM: To investigate the immunocytochemical staining pattern of mdm2 and p21WAF1 proteins in invasive cervical cancer and to determine its relation with the expression of p53 and with the high risk HPV infection. METHODS: Immunocytochemistry for p53, mdm2, and p21WAF1 was performed in 31 paraffin embedded sections of invasive cervical cancer. The results were assessed by image analysis, evaluating for each protein the optical density of the immunostained area, scored as percentage of the total nuclear area. The presence of high risk human papillomavirus (HPV) infection was detected by using the polymerase chain reaction. RESULTS: Immunostaining for both mdm2 and p21WAF1 was correlated with p53 expression; however, the correlation between p53 and mdm2 (R = 0.49; p < 0.01) was more significant than between p53 and p21WAF1 (R = 0.31; p < 0.05); the less stringent correlation between p53 and p21WAF1 might reflect the p53 independent mechanisms of p21WAF1 induction. Similar average levels of p53, mdm2, and p21WAF1 immunostaining were found in the presence or absence of high risk HPV-DNA, without significant differences between the two groups. CONCLUSIONS: These data suggest that mdm2 and p21WAF1 proteins are expressed in invasive cervical cancer and that their immunocytochemical staining pattern is not abrogated by the presence of high risk HPV genomic sequences. (+info)
Definition of a major p53 binding site on Ad2E1B58K protein and a possible nuclear localization signal on the Ad12E1B54K protein. (7/16353)Previous studies have established that adenovirus 2/5 early region 1B (Ad E1B) 58K protein binds p53 strongly and co-localizes with it to cytoplasmic dense bodies whilst the homologous Ad12E1B54K protein binds only weakly and co-localizes primarily to the nucleus in Ad12E1 transformed cells. We have used these properties of the E1B proteins from different viral serotypes to map the p53 binding site on the Ad2/5 protein. A set of chimaeric genes was constructed containing different proportions of the Ad12 and Ad2E1B DNA. These, together with Ad12E1A and E1B19K DNA, were transfected into baby rat kidney cells and transformed lines isolated. From an examination of the properties of these Ad12/Ad2E1B fusion proteins in co-immunoprecipitation and subcellular localization experiments it has been concluded that the p53 binding site on Ad2E1B58K protein lies between amino acids 216 and 235 and that the homologous region on Ad12E1B54K protein also binds p53. In addition, a unique nuclear localization signal is located on Ad12E1B54K between residues 228 and 239. We suggest that primary structure differences in these regions of the Ad2 and Ad12E1B proteins are responsible for the different subcellular localizations in AdE1 transformants. (+info)
Correlation between the status of the p53 gene and survival in patients with stage I non-small cell lung carcinoma. (8/16353)The association of p53 abnormalities with the prognosis of patients with non-small cell lung carcinoma (NSCLC) has been extensively investigated to date, however, this association is still controversial. Therefore, we investigated the prognostic significance of p53 mutations through exons 2 to 11 and p53 protein expression in 103 cases of stage I NSCLC. p53 mutations were detected in 49 of 103 (48%) tumors. Two separate mutations were detected in four tumors giving a total of 53 unique mutations in 49 tumors. Ten (19%) of mutations occurred outside exons 5-8. Positive immunohistochemical staining of p53 protein was detected in 41 of 103 (40%) tumors. The concordance rate between mutations and protein overexpression was only 69%. p53 mutations, but not expression, were significantly associated with a shortened survival of patients (P<0.001). Furthermore, we investigated the correlation between the types of p53 mutations and prognosis. p53 missense mutations rather than null mutations were associated with poor prognosis (P < 0.001 in missense mutations and P=0.243 in null mutations). These results indicated that p53 mutations, in particular missense mutations, rather than p53 expression could be a useful molecular marker for the prognosis of patients with surgically resected stage I NSCLC. (+info)
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
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.
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
Symptoms of Kidney Neoplasms can include blood in the urine, pain in the flank or abdomen, weight loss, fever, and fatigue. Diagnosis is made through a combination of physical examination, imaging studies such as CT scans or ultrasound, and tissue biopsy. Treatment options vary depending on the type and stage of the neoplasm, but may include surgery, ablation therapy, targeted therapy, or chemotherapy.
It is important for individuals with a history of Kidney Neoplasms to follow up with their healthcare provider regularly for monitoring and check-ups to ensure early detection of any recurrences or new tumors.
There are different types of Breast Neoplasms such as:
1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.
2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.
3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.
4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.
5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.
Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.
Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.
It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.
Wilms tumor accounts for about 5% of all childhood kidney cancers and usually affects only one kidney. The cancerous cells in the kidney are called blastema cells, which are immature cells that have not yet developed into normal kidney tissue.
The symptoms of Wilms tumor can vary depending on the size and location of the tumor, but they may include:
* Abdominal pain or swelling
* Blood in the urine
* Weight loss
* Loss of appetite
Wilms tumor is diagnosed through a combination of imaging tests such as ultrasound, CT scans, and MRI scans, and a biopsy to confirm the presence of cancer cells.
Treatment for Wilms tumor typically involves a combination of surgery, chemotherapy, and radiation therapy. The specific treatment plan will depend on the stage and location of the tumor, as well as the age and overall health of the child. In some cases, the affected kidney may need to be removed if the cancer is not completely removable by surgery or if it has spread to other parts of the body.
The prognosis for Wilms tumor has improved significantly over the past few decades due to advances in treatment and early detection. According to the American Cancer Society, the 5-year survival rate for children with Wilms tumor is about 90% if the cancer is diagnosed before it has spread to other parts of the body. However, the cancer can recur in some cases, especially if it has spread to other parts of the body at the time of initial diagnosis.
Overall, while Wilms tumor is a serious and potentially life-threatening condition, with prompt and appropriate treatment, many children with this disease can achieve long-term survival and a good quality of life.
There are several types of osteosarcomas, including:
1. High-grade osteosarcoma: This is the most common type of osteosarcoma and tends to grow quickly.
2. Low-grade osteosarcoma: This type of osteosarcoma grows more slowly than high-grade osteosarcoma.
3. Chondrosarcoma: This is a type of osteosarcoma that arises in the cartilage cells of the bone.
4. Ewing's family of tumors: These are rare types of osteosarcoma that can occur in any bone of the body.
The exact cause of osteosarcoma is not known, but certain risk factors may increase the likelihood of developing the disease. These include:
1. Previous radiation exposure
2. Paget's disease of bone
3. Li-Fraumeni syndrome (a genetic disorder that increases the risk of certain types of cancer)
4. Familial retinoblastoma (a rare inherited condition)
5. Exposure to certain chemicals, such as herbicides and industrial chemicals.
Symptoms of osteosarcoma may include:
1. Pain in the affected bone, which may be worse at night or with activity
2. Swelling and redness around the affected area
3. Limited mobility or stiffness in the affected limb
4. A visible lump or mass on the affected bone
5. Fractures or breaks in the affected bone
If osteosarcoma is suspected, a doctor may perform several tests to confirm the diagnosis and determine the extent of the disease. These may include:
1. Imaging studies, such as X-rays, CT scans, or MRI scans
2. Biopsy, in which a sample of tissue is removed from the affected bone and examined under a microscope for cancer cells
3. Blood tests to check for elevated levels of certain enzymes that are produced by osteosarcoma cells
4. Bone scans to look for areas of increased activity or metabolism in the bones.
There are several subtypes of RCC, including clear cell, papillary, chromophobe, and collecting duct carcinoma. The most common subtype is clear cell RCC, which accounts for approximately 70-80% of all RCC cases.
RCC can be difficult to diagnose as it may not cause any symptoms in its early stages. However, some common symptoms of RCC include blood in the urine (hematuria), pain in the flank or abdomen, weight loss, and fatigue. RCC is typically diagnosed through a combination of imaging studies such as computed tomography (CT) scans, magnetic resonance imaging (MRI), and positron emission tomography (PET) scans, along with a biopsy to confirm the presence of cancer cells.
Treatment for RCC depends on the stage and location of the cancer. Surgery is the primary treatment for localized RCC, and may involve a partial or complete nephrectomy (removal of the affected kidney). For more advanced cases, treatment may involve a combination of surgery and systemic therapies such as targeted therapy or immunotherapy. Targeted therapy drugs, such as sunitinib and pazopanib, work by blocking specific molecules that promote the growth and spread of cancer cells. Immunotherapy drugs, such as checkpoint inhibitors, work by stimulating the body's immune system to attack cancer cells.
The prognosis for RCC is generally good if the cancer is detected early and treated promptly. However, the cancer can be aggressive and may spread to other parts of the body (metastasize) if left untreated. The 5-year survival rate for RCC is about 73% for patients with localized disease, but it drops to about 12% for those with distant metastases.
There are several risk factors for developing RCC, including:
* Age: RCC is more common in people over the age of 50.
* Gender: Men are slightly more likely to develop RCC than women.
* Family history: People with a family history of RCC or other kidney diseases may be at increased risk.
* Chronic kidney disease: Patients with chronic kidney disease are at higher risk for developing RCC.
* Hypertension: High blood pressure is a common risk factor for RCC.
* Smoking: Smoking may increase the risk of developing RCC.
* Obesity: Being overweight or obese may increase the risk of developing RCC.
There are several complications associated with RCC, including:
* Metastasis: RCC can spread to other parts of the body, such as the lymph nodes, liver, and bones.
* Hematuria: Blood in the urine is a common complication of RCC.
* Pain: RCC can cause pain in the flank or abdomen.
* Fatigue: RCC can cause fatigue and weakness.
* Weight loss: RCC can cause weight loss and loss of appetite.
There are several treatment options for RCC, including:
* Surgery: Surgery is often the first line of treatment for RCC that is localized and has not spread to other parts of the body.
* Ablation: Ablation therapies, such as cryotherapy or radiofrequency ablation, can be used to destroy the tumor.
* Targeted therapy: Targeted therapies, such as sunitinib or pazopanib, can be used to slow the growth of the tumor.
* Immunotherapy: Immunotherapies, such as checkpoint inhibitors, can be used to stimulate the immune system to attack the tumor.
* Chemotherapy: Chemotherapy may be used in combination with other treatments or as a last resort for patients with advanced RCC.
The prognosis for RCC varies depending on the stage and location of the cancer, but in general, the earlier the cancer is detected and treated, the better the outcome. According to the American Cancer Society, the 5-year survival rate for RCC is about 73% for patients with localized disease (cancer that has not spread beyond the kidney) and about 12% for patients with distant disease (cancer that has spread to other parts of the body).
The main features of NF2 include:
1. Tumor growth: NF2 patients develop meningiomas or schwannomas, which are benign tumors that can grow and compress nearby nerves.
2. Vision loss: The compression of optic nerves by tumors can lead to vision loss or blindness.
3. Hearing loss: Tumors can also affect the auditory nerve, leading to hearing loss or deafness.
4. Balance and coordination problems: Tumors can cause balance and coordination problems due to their effects on the cranial nerves.
5. Cognitive impairment: NF2 patients may experience cognitive impairment, including memory loss, confusion, and difficulty with concentration.
6. Seizures: Some patients with NF2 may experience seizures as a result of tumor growth or other factors.
7. Pain: Tumors can cause pain, either due to their size or location.
8. Headaches: NF2 patients may experience frequent headaches due to the pressure of tumors on surrounding nerves and brain tissue.
9. Endocrine dysfunction: Some patients with NF2 may experience endocrine dysfunction, including thyroid problems or growth hormone deficiency.
10. Increased risk of other cancers: NF2 patients have an increased risk of developing other types of cancer, particularly malignant melanoma.
The diagnosis of NF2 is based on a combination of clinical features, imaging studies (such as MRI), and genetic testing. Treatment options for NF2 include observation, surgery, radiation therapy, and chemotherapy, depending on the size and location of the tumors and the severity of symptoms.
Types of experimental neoplasms include:
* Xenografts: tumors that are transplanted into animals from another species, often humans.
* Transgenic tumors: tumors that are created by introducing cancer-causing genes into an animal's genome.
* Chemically-induced tumors: tumors that are caused by exposure to certain chemicals or drugs.
The use of experimental neoplasms in research has led to significant advances in our understanding of cancer biology and the development of new treatments for the disease. However, the use of animals in cancer research is a controversial topic and alternatives to animal models are being developed and implemented.
Adenocarcinoma is a term used to describe a variety of different types of cancer that arise in glandular tissue, including:
1. Colorectal adenocarcinoma (cancer of the colon or rectum)
2. Breast adenocarcinoma (cancer of the breast)
3. Prostate adenocarcinoma (cancer of the prostate gland)
4. Pancreatic adenocarcinoma (cancer of the pancreas)
5. Lung adenocarcinoma (cancer of the lung)
6. Thyroid adenocarcinoma (cancer of the thyroid gland)
7. Skin adenocarcinoma (cancer of the skin)
The symptoms of adenocarcinoma depend on the location of the cancer and can include:
1. Blood in the stool or urine
2. Abdominal pain or discomfort
3. Changes in bowel habits
4. Unusual vaginal bleeding (in the case of endometrial adenocarcinoma)
5. A lump or thickening in the breast or elsewhere
6. Weight loss
8. Coughing up blood (in the case of lung adenocarcinoma)
The diagnosis of adenocarcinoma is typically made through a combination of imaging tests, such as CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a sample of tissue from the affected area and examining it under a microscope for cancer cells.
Treatment options for adenocarcinoma depend on the location of the cancer and can include:
1. Surgery to remove the tumor
2. Chemotherapy, which involves using drugs to kill cancer cells
3. Radiation therapy, which involves using high-energy X-rays or other particles to kill cancer cells
4. Targeted therapy, which involves using drugs that target specific molecules on cancer cells to kill them
5. Immunotherapy, which involves using drugs that stimulate the immune system to fight cancer cells.
The prognosis for adenocarcinoma is generally good if the cancer is detected and treated early, but it can be more challenging to treat if the cancer has spread to other parts of the body.
The symptoms of VHL disease can vary widely depending on the location and size of the tumors that develop. They may include:
* Tumors in the retina, leading to vision loss or blindness
* Tumors in the brain, leading to seizures, headaches, and neurological problems
* Tumors in the spinal cord, leading to back pain, weakness, and paralysis
* Tumors in the kidneys, leading to high blood pressure, proteinuria, and hematuria (blood in the urine)
* Tumors in the pancreas, leading to diabetes and other endocrine problems
* Tumors in the adrenal glands, leading to hormonal imbalances and adrenal insufficiency
The diagnosis of VHL disease is based on a combination of clinical findings, laboratory tests, and genetic analysis. Imaging studies such as CT or MRI scans may be used to visualize the tumors, and genetic testing can confirm the presence of a VHL gene mutation.
There is no cure for VHL disease, but various treatments can help manage the symptoms and prevent complications. These may include:
* Surgery to remove tumors in the retina, brain, spinal cord, kidneys, pancreas, or adrenal glands
* Chemotherapy to treat malignant tumors
* Radiation therapy to shrink tumors and relieve symptoms
* Medications to control seizures, high blood pressure, diabetes, and hormonal imbalances
* Regular monitoring and follow-up to detect and manage any new or recurring tumors.
The prognosis for VHL disease varies depending on the location and type of tumors, as well as the presence of other health problems. In general, the earlier the diagnosis and treatment, the better the prognosis. With current treatments, many people with VHL disease can lead active and productive lives, but they require ongoing medical care and monitoring to manage their condition.
Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.
There are several types of liver neoplasms, including:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.
The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.
Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.
Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.
Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.
There are several different types of brain neoplasms, including:
1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.
These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.
The symptoms of retinoblastoma can vary depending on the location and size of the tumor, but may include:
* A white or colored mass in one eye
* Redness or swelling of the eye
* Sensitivity to light
* Blurred vision or vision loss
* Crossed eyes (strabismus)
* Eye pain or discomfort
Retinoblastoma is usually diagnosed with a combination of physical examination, imaging tests such as ultrasound and MRI, and genetic testing. Treatment options depend on the stage and location of the tumor, but may include:
* Chemotherapy to shrink the tumor before surgery
* Surgery to remove the tumor and/or the affected eye (enucleation)
* Radiation therapy to kill any remaining cancer cells
* Targeted therapy with drugs that specifically target cancer cells
The prognosis for retinoblastoma depends on the stage of the disease at diagnosis. If the tumor is confined to one eye and has not spread to other parts of the body, the 5-year survival rate is high (around 90%). However, if the tumor has spread to other parts of the body (known as metastatic retinoblastoma), the prognosis is much poorer.
Retinoblastoma can be inherited in an autosomal dominant pattern, meaning that a single copy of the mutated RB1 gene is enough to cause the condition. Families with a history of retinoblastoma may undergo genetic testing and counseling to determine their risk of developing the disease.
There are several types of colonic neoplasms, including:
1. Adenomas: These are benign growths that are usually precursors to colorectal cancer.
2. Carcinomas: These are malignant tumors that arise from the epithelial lining of the colon.
3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.
4. Lymphomas: These are cancers of the immune system that can affect the colon.
Colonic neoplasms can cause a variety of symptoms, including bleeding, abdominal pain, and changes in bowel habits. They are often diagnosed through a combination of medical imaging tests (such as colonoscopy or CT scan) and biopsy. Treatment for colonic neoplasms depends on the type and stage of the tumor, and may include surgery, chemotherapy, and/or radiation therapy.
Overall, colonic neoplasms are a common condition that can have serious consequences if left untreated. It is important for individuals to be aware of their risk factors and to undergo regular screening for colon cancer to help detect and treat any abnormal growths or tumors in the colon.
There are several risk factors for developing HCC, including:
* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:
* Yellowing of the skin and eyes (jaundice)
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss
If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:
* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope
Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:
* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer
Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.
SCC typically appears as a firm, flat, or raised bump on the skin, and may be pink, red, or scaly. The cancer cells are usually well-differentiated, meaning they resemble normal squamous cells, but they can grow rapidly and invade surrounding tissues if left untreated.
SCC is more common in fair-skinned individuals and those who spend a lot of time in the sun, as UV radiation can damage the skin cells and increase the risk of cancer. The cancer can also spread to other parts of the body, such as lymph nodes or organs, and can be life-threatening if not treated promptly and effectively.
Treatment for SCC usually involves surgery to remove the cancerous tissue, and may also include radiation therapy or chemotherapy to kill any remaining cancer cells. Early detection and treatment are important to improve outcomes for patients with SCC.
There are several types of skin neoplasms, including:
1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.
While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.
There are several types of lung neoplasms, including:
1. Adenocarcinoma: This is the most common type of lung cancer, accounting for approximately 40% of all lung cancers. It is a malignant tumor that originates in the glands of the respiratory tract and can be found in any part of the lung.
2. Squamous cell carcinoma: This type of lung cancer accounts for approximately 25% of all lung cancers and is more common in men than women. It is a malignant tumor that originates in the squamous cells lining the airways of the lungs.
3. Small cell lung cancer (SCLC): This is a highly aggressive form of lung cancer that accounts for approximately 15% of all lung cancers. It is often found in the central parts of the lungs and can spread quickly to other parts of the body.
4. Large cell carcinoma: This is a rare type of lung cancer that accounts for only about 5% of all lung cancers. It is a malignant tumor that originates in the large cells of the respiratory tract and can be found in any part of the lung.
5. Bronchioalveolar carcinoma (BAC): This is a rare type of lung cancer that originates in the cells lining the airways and alveoli of the lungs. It is more common in women than men and tends to affect older individuals.
6. Lymphangioleiomyomatosis (LAM): This is a rare, progressive, and often fatal lung disease that primarily affects women of childbearing age. It is characterized by the growth of smooth muscle-like cells in the lungs and can lead to cysts, lung collapse, and respiratory failure.
7. Hamartoma: This is a benign tumor that originates in the tissue of the lungs and is usually found in children. It is characterized by an overgrowth of normal lung tissue and can be treated with surgery.
8. Secondary lung cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
9. Metastatic cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
10. Mesothelioma: This is a rare and aggressive form of cancer that originates in the lining of the lungs or abdomen. It is caused by asbestos exposure and can be treated with surgery, chemotherapy, and radiation therapy.
Lung diseases can also be classified based on their cause, such as:
1. Infectious diseases: These are caused by bacteria, viruses, or other microorganisms and can include pneumonia, tuberculosis, and bronchitis.
2. Autoimmune diseases: These are caused by an overactive immune system and can include conditions such as sarcoidosis and idiopathic pulmonary fibrosis.
3. Genetic diseases: These are caused by inherited mutations in genes that affect the lungs and can include cystic fibrosis and primary ciliary dyskinesia.
4. Environmental diseases: These are caused by exposure to harmful substances such as tobacco smoke, air pollution, and asbestos.
5. Radiological diseases: These are caused by exposure to ionizing radiation and can include conditions such as radiographic breast cancer and lung cancer.
6. Vascular diseases: These are caused by problems with the blood vessels in the lungs and can include conditions such as pulmonary embolism and pulmonary hypertension.
7. Tumors: These can be benign or malignant and can include conditions such as lung metastases and lung cancer.
8. Trauma: This can include injuries to the chest or lungs caused by accidents or other forms of trauma.
9. Congenital diseases: These are present at birth and can include conditions such as bronchopulmonary foregut malformations and congenital cystic adenomatoid malformation.
Each type of lung disease has its own set of symptoms, diagnosis, and treatment options. It is important to seek medical attention if you experience any persistent or severe respiratory symptoms, as early diagnosis and treatment can improve outcomes and quality of life.
Neoplastic metastasis can occur in any type of cancer but are more common in solid tumors such as carcinomas (breast, lung, colon). It is important for cancer diagnosis and prognosis because metastasis indicates that the cancer has spread beyond its original site and may be more difficult to treat.
Metastases can appear at any distant location but commonly found sites include the liver, lungs, bones, brain, and lymph nodes. The presence of metastases indicates a higher stage of cancer which is associated with lower survival rates compared to localized cancer.
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.
Carcinoid tumors are usually found in the appendix, small intestine, rectum, or other parts of the gastrointestinal tract. They can also occur in the lungs, pancreas, or other organs. These tumors tend to grow slowly and often do not cause any symptoms until they have grown quite large.
Carcinoid tumors are diagnosed through a combination of imaging tests such as CT scans, MRI scans, and endoscopies, along with a biopsy to confirm the presence of cancer cells. Treatment for carcinoid tumors depends on the location, size, and stage of the tumor, as well as the patient's overall health. Treatment options may include surgery, chemotherapy, radiation therapy, or a combination of these.
Some of the symptoms that may be associated with carcinoid tumors include:
* Flushing (redness and warmth of the skin)
* Shortness of breath
* Abdominal pain
* Weight loss
Carcinoid tumors are relatively rare, accounting for only about 1% to 5% of all cancer cases. However, they tend to be more common in certain parts of the world, such as North America and Europe. The exact cause of carcinoid tumors is not known, but they are thought to be linked to genetic mutations that occur during fetal development.
Overall, while carcinoid tumors are rare and can be challenging to diagnose and treat, advances in medical technology and cancer research have improved the outlook for patients with these types of tumors. With early detection and appropriate treatment, many people with carcinoid tumors can achieve long-term survival and a good quality of life.
Glioblastomas are highly malignant tumors that can grow rapidly and infiltrate surrounding brain tissue, making them difficult to remove surgically. They often recur after treatment and are usually fatal within a few years of diagnosis.
The symptoms of glioblastoma can vary depending on the location and size of the tumor but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory or cognitive function.
Glioblastomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and a biopsy to confirm the presence of cancerous cells. Treatment typically involves surgery to remove as much of the tumor as possible, followed by radiation therapy and chemotherapy to slow the growth of any remaining cancerous cells.
Prognosis for glioblastoma is generally poor, with a five-year survival rate of around 5% for newly diagnosed patients. However, the prognosis can vary depending on factors such as the location and size of the tumor, the patient's age and overall health, and the effectiveness of treatment.
Examples of 'Mammary Neoplasms, Experimental' in a sentence:
1. The researchers studied the effects of hormone therapy on mammary neoplasms in experimental animals to better understand its potential role in human breast cancer.
2. The lab used mice with genetic mutations that predispose them to developing mammary neoplasms to test the efficacy of new cancer drugs.
3. In order to investigate the link between obesity and breast cancer, the researchers conducted experiments on mammary neoplasms in rats with diet-induced obesity.
NETs can be benign (non-cancerous) or malignant (cancerous). Malignant NETs can spread to other parts of the body through a process called metastasis, which can lead to serious health complications.
The symptoms of NETs vary depending on their location and size, but may include:
* Abdominal pain or discomfort
* Diarrhea or constipation
* Shortness of breath
* Skin changes such as flushing or sweating
The diagnosis of NETs is based on a combination of imaging tests such as CT scans, MRI scans, and PET scans, as well as biopsy samples. Treatment options for NETs depend on the type, size, location, and stage of the tumor, but may include:
* Medications to slow or stop hormone production
* Chemotherapy to shrink the tumor
* Radiation therapy to kill cancer cells
* Surgery to remove the tumor
Overall, NETs are rare and can be challenging to diagnose and treat. However, with advances in medical technology and ongoing research, there are more effective treatment options available for patients with NETs.
Benign ovarian neoplasms include:
1. Serous cystadenoma: A fluid-filled sac that develops on the surface of the ovary.
2. Mucinous cystadenoma: A tumor that is filled with mucin, a type of protein.
3. Endometrioid tumors: Tumors that are similar to endometrial tissue (the lining of the uterus).
4. Theca cell tumors: Tumors that develop in the supportive tissue of the ovary called theca cells.
Malignant ovarian neoplasms include:
1. Epithelial ovarian cancer (EOC): The most common type of ovarian cancer, which arises from the surface epithelium of the ovary.
2. Germ cell tumors: Tumors that develop from germ cells, which are the cells that give rise to eggs.
3. Stromal sarcomas: Tumors that develop in the supportive tissue of the ovary.
Ovarian neoplasms can cause symptoms such as pelvic pain, abnormal bleeding, and abdominal swelling. They can also be detected through pelvic examination, imaging tests such as ultrasound and CT scan, and biopsy. Treatment options for ovarian neoplasms depend on the type, stage, and location of the tumor, and may include surgery, chemotherapy, and radiation therapy.
Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.
There are several different types of pathologic neovascularization, including:
* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.
The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.
In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.
1. Activation of oncogenes: Some viruses contain genes that code for proteins that can activate existing oncogenes in the host cell, leading to uncontrolled cell growth.
2. Inactivation of tumor suppressor genes: Other viruses may contain genes that inhibit the expression of tumor suppressor genes, allowing cells to grow and divide uncontrollably.
3. Insertional mutagenesis: Some viruses can insert their own DNA into the host cell's genome, leading to disruptions in normal cellular function and potentially causing cancer.
4. Epigenetic changes: Viral infection can also cause epigenetic changes, such as DNA methylation or histone modification, that can lead to the silencing of tumor suppressor genes and the activation of oncogenes.
Viral cell transformation is a key factor in the development of many types of cancer, including cervical cancer caused by human papillomavirus (HPV), and liver cancer caused by hepatitis B virus (HBV). In addition, some viruses are specifically known to cause cancer, such as Kaposi's sarcoma-associated herpesvirus (KSHV) and Merkel cell polyomavirus (MCV).
Early detection and treatment of viral infections can help prevent the development of cancer. Vaccines are also available for some viruses that are known to cause cancer, such as HPV and hepatitis B. Additionally, antiviral therapy can be used to treat existing infections and may help reduce the risk of cancer development.
There are several types of gliomas, including:
1. Astrocytoma: This is the most common type of glioma, accounting for about 50% of all cases. It arises from the star-shaped cells called astrocytes that provide support and nutrients to the brain's nerve cells.
2. Oligodendroglioma: This type of glioma originates from the oligodendrocytes, which are responsible for producing the fatty substance called myelin that insulates the nerve fibers.
3. Glioblastoma (GBM): This is the most aggressive and malignant type of glioma, accounting for about 70% of all cases. It is fast-growing and often spreads to other parts of the brain.
4. Brain stem glioma: This type of glioma arises in the brain stem, which is responsible for controlling many of the body's vital functions such as breathing, heart rate, and blood pressure.
The symptoms of glioma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory, or speech.
Gliomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and tissue biopsy to confirm the presence of cancer cells. Treatment options for glioma depend on the type and location of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment to remove as much of the tumor as possible, followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells.
The prognosis for glioma patients varies depending on the type and location of the tumor, as well as the patient's overall health. In general, the prognosis is better for patients with slow-growing, low-grade tumors, while those with fast-growing, high-grade tumors have a poorer prognosis. Overall, the 5-year survival rate for glioma patients is around 30-40%.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.
There are several different types of neuroblastoma, including:
1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.
Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:
* Abdominal pain
* Loss of appetite
* Weight loss
* Bone pain
* Swelling in the abdomen or neck
* Increased heart rate
Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.
Some common effects of chromosomal deletions include:
1. Genetic disorders: Chromosomal deletions can lead to a variety of genetic disorders, such as Down syndrome, which is caused by a deletion of a portion of chromosome 21. Other examples include Prader-Willi syndrome (deletion of chromosome 15), and Williams syndrome (deletion of chromosome 7).
2. Birth defects: Chromosomal deletions can increase the risk of birth defects, such as heart defects, cleft palate, and limb abnormalities.
3. Developmental delays: Children with chromosomal deletions may experience developmental delays, learning disabilities, and intellectual disability.
4. Increased cancer risk: Some chromosomal deletions can increase the risk of developing certain types of cancer, such as chronic myelogenous leukemia (CML) and breast cancer.
5. Reproductive problems: Chromosomal deletions can lead to reproductive problems, such as infertility or recurrent miscarriage.
Chromosomal deletions can be diagnosed through a variety of techniques, including karyotyping (examination of the chromosomes), fluorescence in situ hybridization (FISH), and microarray analysis. Treatment options for chromosomal deletions depend on the specific effects of the deletion and may include medication, surgery, or other forms of therapy.
Pancreatic adenocarcinoma is the most common type of malignant pancreatic neoplasm and accounts for approximately 85% of all pancreatic cancers. It originates in the glandular tissue of the pancreas and has a poor prognosis, with a five-year survival rate of less than 10%.
Pancreatic neuroendocrine tumors (PNETs) are less common but more treatable than pancreatic adenocarcinoma. These tumors originate in the hormone-producing cells of the pancreas and can produce excess hormones that cause a variety of symptoms, such as diabetes or high blood sugar. PNETs are classified into two main types: functional and non-functional. Functional PNETs produce excess hormones and are more aggressive than non-functional tumors.
Other rare types of pancreatic neoplasms include acinar cell carcinoma, ampullary cancer, and oncocytic pancreatic neuroendocrine tumors. These tumors are less common than pancreatic adenocarcinoma and PNETs but can be equally aggressive and difficult to treat.
The symptoms of pancreatic neoplasms vary depending on the type and location of the tumor, but they often include abdominal pain, weight loss, jaundice, and fatigue. Diagnosis is typically made through a combination of imaging tests such as CT scans, endoscopic ultrasound, and biopsy. Treatment options for pancreatic neoplasms depend on the type and stage of the tumor but may include surgery, chemotherapy, radiation therapy, or a combination of these.
Prognosis for patients with pancreatic neoplasms is generally poor, especially for those with advanced stages of disease. However, early detection and treatment can improve survival rates. Research into the causes and mechanisms of pancreatic neoplasms is ongoing, with a focus on developing new and more effective treatments for these devastating diseases.
The main features of PJS include:
* Multiple hamartomas in the gastrointestinal tract, which can lead to abdominal pain, nausea, vomiting, and rectal bleeding.
* Hamartomas in the lungs, which can cause coughing, wheezing, and shortness of breath.
* Hamartomas in the sex organs, which can lead to infertility, irregular menstrual cycles, and breast tumors.
* An increased risk of developing various types of cancer, including colon, lung, pancreatic, and breast cancer.
* A characteristic "speckled" appearance of the skin, caused by the accumulation of pigmented cells.
PJS is usually diagnosed in children or young adults, and it affects approximately 1 in 250,000 to 1 in 500,000 individuals worldwide. There is no cure for PJS, but regular monitoring and surveillance can help detect and treat hamartomas and cancerous lesions early on. Treatment options may include surgery, chemotherapy, and radiation therapy, depending on the location and severity of the tumors.
Precancerous changes in the uterine cervix are called dysplasias, and they can be detected by a Pap smear, which is a routine screening test for women. If dysplasia is found, it can be treated with cryotherapy (freezing), laser therapy, or cone biopsy, which removes the affected cells.
Cervical cancer is rare in developed countries where Pap screening is widely available, but it remains a common cancer in developing countries where access to healthcare and screening is limited. The human papillomavirus (HPV) vaccine has been shown to be effective in preventing cervical precancerous changes and cancer.
Cervical cancer can be treated with surgery, radiation therapy, or chemotherapy, depending on the stage and location of the cancer. The prognosis for early-stage cervical cancer is good, but advanced-stage cancer can be difficult to treat and may have a poor prognosis.
The following are some types of uterine cervical neoplasms:
1. Adenocarcinoma in situ (AIS): This is a precancerous condition that occurs when glandular cells on the surface of the cervix become abnormal and grow out of control.
2. Cervical intraepithelial neoplasia (CIN): This is a precancerous condition that occurs when abnormal cells are found on the surface of the cervix. There are several types of CIN, ranging from mild to severe.
3. Squamous cell carcinoma: This is the most common type of cervical cancer and arises from the squamous cells that line the cervix.
4. Adnexal carcinoma: This is a rare type of cervical cancer that arises from the glands or ducts near the cervix.
5. Small cell carcinoma: This is a rare and aggressive type of cervical cancer that grows rapidly and can spread quickly to other parts of the body.
6. Micropapillary uterine carcinoma: This is a rare type of cervical cancer that grows in a finger-like shape and can be difficult to diagnose.
7. Clear cell carcinoma: This is a rare type of cervical cancer that arises from clear cells and can be more aggressive than other types of cervical cancer.
8. Adenocarcinoma: This is a type of cervical cancer that arises from glandular cells and can be less aggressive than squamous cell carcinoma.
9. Sarcoma: This is a rare type of cervical cancer that arises from the connective tissue of the cervix.
The treatment options for uterine cervical neoplasms depend on the stage and location of the cancer, as well as the patient's overall health and preferences. The following are some common treatments for uterine cervical neoplasms:
1. Hysterectomy: This is a surgical procedure to remove the uterus and may be recommended for early-stage cancers or precancerous changes.
2. Cryotherapy: This is a minimally invasive procedure that uses liquid nitrogen to freeze and destroy abnormal cells in the cervix.
3. Laser therapy: This is a minimally invasive procedure that uses a laser to remove or destroy abnormal cells in the cervix.
4. Cone biopsy: This is a surgical procedure to remove a small cone-shaped sample of tissue from the cervix to diagnose and treat early-stage cancers or precancerous changes.
5. Radiation therapy: This is a non-surgical treatment that uses high-energy rays to kill cancer cells and may be recommended for more advanced cancers or when the cancer has spread to other parts of the body.
6. Chemotherapy: This is a non-surgical treatment that uses drugs to kill cancer cells and may be recommended for more advanced cancers or when the cancer has spread to other parts of the body.
7. Immunotherapy: This is a non-surgical treatment that uses drugs to stimulate the immune system to fight cancer cells and may be recommended for more advanced cancers or when other treatments have failed.
8. Targeted therapy: This is a non-surgical treatment that uses drugs to target specific genes or proteins that contribute to cancer growth and development and may be recommended for more advanced cancers or when other treatments have failed.
It is important to note that the choice of treatment will depend on the stage and location of the cancer, as well as the patient's overall health and preferences. Patients should discuss their treatment options with their doctor and develop a personalized plan that is right for them.
Examples of mammary neoplasms in animals include:
* Mammary adenocarcinoma: A type of tumor that develops in the mammary gland of animals and is characterized by the growth of abnormal cells that produce milk.
* Mammary fibroadenoma: A benign tumor that develops in the mammary gland of animals and is characterized by the growth of fibrous and glandular tissue.
* Inflammatory mammary carcinoma: A type of tumor that develops in the mammary gland of animals and is characterized by the presence of inflammatory cells and abnormal cells.
These tumors can be caused by a variety of factors, including genetic mutations, hormonal imbalances, and exposure to certain environmental agents. They can also be induced experimentally using chemical carcinogens or viruses.
The study of mammary neoplasms in animals is important for understanding the molecular mechanisms underlying breast cancer development and progression, as well as for identifying potential therapeutic targets and developing new treatments.
Symptoms of rhabdoid tumor may include abdominal pain, fever, weight loss, and difficulty with movement or coordination. The exact cause of rhabdoid tumors is not well understood, but genetic mutations are thought to play a role in their development. Treatment typically involves a combination of surgery, chemotherapy, and radiation therapy. The prognosis for rhabdoid tumors is generally poor, with a survival rate of approximately 30-40%.
Rhabdoid tumor is also known as "rhabdoid sarcoma" or "infantile fibrosarcoma." It is important to note that while this condition is rare, it can be difficult to diagnose and treat due to its aggressive nature and the limited understanding of its causes.
1. Tumor size and location: Larger tumors that have spread to nearby tissues or organs are generally considered more invasive than smaller tumors that are confined to the original site.
2. Cellular growth patterns: The way in which cancer cells grow and divide can also contribute to the overall invasiveness of a neoplasm. For example, cells that grow in a disorganized or chaotic manner may be more likely to invade surrounding tissues.
3. Mitotic index: The mitotic index is a measure of how quickly the cancer cells are dividing. A higher mitotic index is generally associated with more aggressive and invasive cancers.
4. Necrosis: Necrosis, or the death of cells, can be an indication of the level of invasiveness of a neoplasm. The presence of significant necrosis in a tumor is often a sign that the cancer has invaded surrounding tissues and organs.
5. Lymphovascular invasion: Cancer cells that have invaded lymphatic vessels or blood vessels are considered more invasive than those that have not.
6. Perineural invasion: Cancer cells that have invaded nerve fibers are also considered more invasive.
7. Histological grade: The histological grade of a neoplasm is a measure of how abnormal the cancer cells look under a microscope. Higher-grade cancers are generally considered more aggressive and invasive than lower-grade cancers.
8. Immunohistochemical markers: Certain immunohistochemical markers, such as Ki-67, can be used to evaluate the proliferative activity of cancer cells. Higher levels of these markers are generally associated with more aggressive and invasive cancers.
Overall, the degree of neoplasm invasiveness is an important factor in determining the likelihood of the cancer spreading to other parts of the body (metastasizing) and in determining the appropriate treatment strategy for the patient.
Malignant prostatic neoplasms are cancerous tumors that can be aggressive and spread to other parts of the body (metastasize). The most common type of malignant prostatic neoplasm is adenocarcinoma of the prostate, which accounts for approximately 95% of all prostate cancers. Other types of malignant prostatic neoplasms include sarcomas and small cell carcinomas.
Prostatic neoplasms can be diagnosed through a variety of tests such as digital rectal examination (DRE), prostate-specific antigen (PSA) test, imaging studies (ultrasound, CT scan or MRI), and biopsy. Treatment options for prostatic neoplasms depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health. Treatment options can include active surveillance, surgery (robotic-assisted laparoscopic prostatectomy or open prostatectomy), radiation therapy (external beam radiation therapy or brachytherapy), and hormone therapy.
In summary, Prostatic Neoplasms are tumors that occur in the prostate gland, which can be benign or malignant. The most common types of malignant prostatic neoplasms are adenocarcinoma of the prostate, and other types include sarcomas and small cell carcinomas. Diagnosis is done through a variety of tests, and treatment options depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health.
The exact cause of fibrosarcoma is not known, but it is believed to be linked to genetic mutations that occur during a person's lifetime. Some risk factors for developing fibrosarcoma include previous radiation exposure, chronic inflammation, and certain inherited conditions such as neurofibromatosis type 1 (NF1).
The symptoms of fibrosarcoma can vary depending on the location and size of the tumor. In some cases, there may be no symptoms until the tumor has grown to a significant size. Common symptoms include pain, swelling, and limited mobility in the affected limb. If the tumor is near a nerve, it can also cause numbness or tingling sensations in the affected area.
Diagnosis of fibrosarcoma typically involves a combination of imaging tests such as X-rays, CT scans, and MRI scans, as well as a biopsy to confirm the presence of cancer cells. Treatment options for fibrosarcoma may include surgery, radiation therapy, and chemotherapy, depending on the size and location of the tumor, as well as the patient's overall health.
Prognosis for fibrosarcoma is generally good if the tumor is caught early and treated aggressively. However, if the cancer has spread to other parts of the body (metastasized), the prognosis is generally poorer. In some cases, the cancer can recur after treatment, so it is important for patients to follow their doctor's recommendations for regular check-ups and follow-up testing.
Overall, fibrosarcoma is a rare and aggressive form of cancer that can be challenging to diagnose and treat. However, with early detection and appropriate treatment, many people with this condition can achieve long-term survival and a good quality of life.
There are several subtypes of astrocytoma, including:
1. Low-grade astrocytoma: These tumors grow slowly and are less aggressive. They can be treated with surgery, radiation therapy, or chemotherapy.
2. High-grade astrocytoma: These tumors grow more quickly and are more aggressive. They are often resistant to treatment and may recur after initial treatment.
3. Anaplastic astrocytoma: These are the most aggressive type of astrocytoma, growing rapidly and spreading to other parts of the brain.
4. Glioblastoma (GBM): This is the most common and deadliest type of primary brain cancer, accounting for 55% of all astrocytomas. It is highly aggressive and resistant to treatment, often recurring after initial surgery, radiation, and chemotherapy.
The symptoms of astrocytoma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality or behavior.
Astrocytomas are diagnosed through a combination of imaging tests such as MRI or CT scans, and tissue biopsy. Treatment options vary depending on the type and location of the tumor, but may include surgery, radiation therapy, chemotherapy, or a combination of these.
The prognosis for astrocytoma varies based on the subtype and location of the tumor, as well as the patient's age and overall health. In general, low-grade astrocytomas have a better prognosis than high-grade tumors. However, even with treatment, the survival rate for astrocytoma is generally lower compared to other types of cancer.
Adenomas are caused by genetic mutations that occur in the DNA of the affected cells. These mutations can be inherited or acquired through exposure to environmental factors such as tobacco smoke, radiation, or certain chemicals.
The symptoms of an adenoma can vary depending on its location and size. In general, they may include abdominal pain, bleeding, or changes in bowel movements. If the adenoma becomes large enough, it can obstruct the normal functioning of the affected organ or cause a blockage that can lead to severe health complications.
Adenomas are usually diagnosed through endoscopy, which involves inserting a flexible tube with a camera into the affected organ to visualize the inside. Biopsies may also be taken to confirm the presence of cancerous cells.
Treatment for adenomas depends on their size, location, and severity. Small, non-pedunculated adenomas can often be removed during endoscopy through a procedure called endoscopic mucosal resection (EMR). Larger adenomas may require surgical resection, and in some cases, chemotherapy or radiation therapy may also be necessary.
In summary, adenoma is a type of benign tumor that can occur in glandular tissue throughout the body. While they are not cancerous, they have the potential to become malignant over time if left untreated. Therefore, it is important to seek medical attention if symptoms persist or worsen over time. Early detection and treatment can help prevent complications and improve outcomes for patients with adenomas.
There are several types of GISTs, including:
1. Gastrointestinal stromal tumor (GIST): This is the most common type of GIST, accounting for about 90% of all cases. It typically occurs in the stomach or small intestine and can range in size from a few millimeters to several centimeters.
2. Leiomyoma: This type of GIST is made up of smooth muscle cells and is more common in women than men.
3. Leioyobbroma: This type of GIST is a rare variant of leiomyoma that contains both smooth muscle cells and glands.
4. Mucormyxoid fibroma: This type of GIST is rare and typically occurs in the small intestine. It is made up of mucin-producing cells and has a better prognosis than other types of GISTs.
5. Secondary gastrointestinal stromal tumors (SGISTs): These are GISTs that occur in other parts of the body, such as the liver or peritoneum, as a result of the spread of cancer cells from the primary tumor in the digestive system.
The symptoms of GISTs can vary depending on the location and size of the tumor, but may include:
* Abdominal pain or discomfort
* Nausea and vomiting
* Diarrhea or constipation
* Weight loss
* Feeling full after eating only a small amount of food (early satiety)
GISTs are usually diagnosed using a combination of imaging tests such as CT scans, MRI scans, and PET scans, and a biopsy to confirm the presence of cancer cells. Treatment for GISTs may include:
* Surgery to remove the tumor
* Chemotherapy to kill any remaining cancer cells
* Targeted therapy with drugs that specifically target the KIT or PDGFRA genes, which are mutated in many GISTs.
The prognosis for GISTs is generally good if the tumor is completely removed by surgery, but if the tumor cannot be removed or has spread to other parts of the body, the prognosis is poorer. The specific treatment and prognosis will depend on the type of GIST, its location, and the severity of the symptoms.
These tumors can be benign or malignant, and their growth and behavior vary depending on the type of cancer. Malignant tumors can invade the surrounding tissues and spread to other parts of the body through the bloodstream or lymphatic system, causing serious complications and potentially life-threatening consequences.
The risk factors for developing urinary bladder neoplasms include smoking, exposure to certain chemicals, recurrent bladder infections, and a family history of bladder cancer. The symptoms of these tumors can include blood in the urine, pain during urination, frequent urination, and abdominal pain.
Diagnosis of urinary bladder neoplasms is typically made through a combination of imaging tests such as ultrasound, computed tomography (CT) scan or magnetic resonance imaging (MRI), and cystoscopy, which involves inserting a flexible tube with a camera into the bladder to visualize the tumor.
Treatment options for urinary bladder neoplasms depend on the type of cancer, stage, and location of the tumor. Treatment may include surgery to remove the tumor, chemotherapy, radiation therapy, or a combination of these modalities. Early detection and treatment can improve the prognosis for patients with urinary bladder neoplasms.
The APC gene is a tumor suppressor gene that helps regulate cell growth and prevent the formation of tumors. Mutations in the APC gene can cause the development of adenomas, which are precancerous growths that can eventually become colon cancer if left untreated.
APC mutations can be inherited from one's parents or can occur spontaneously. The risk of developing colorectal cancer is increased in people with an APC mutation, and regular screening and monitoring is recommended to detect and remove any precancerous growths before they become cancerous.
Symptoms of APC may include abdominal pain, diarrhea, rectal bleeding, and weight loss. Treatment for APC typically involves removal of the affected portion of the colon and rectum, followed by ongoing monitoring and screening to detect any recurrences.
In summary, adenomatous polyposis coli (APC) is a genetic condition that increases the risk of developing colorectal cancer and other cancers. It is caused by mutations in the APC gene and can be inherited or acquired spontaneously. Symptoms may include abdominal pain, diarrhea, rectal bleeding, and weight loss, and treatment typically involves removal of the affected portion of the colon and rectum, followed by ongoing monitoring and screening.
There are several types of lymphoma, including:
1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.
The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:
* Swollen lymph nodes
* Weight loss
* Night sweats
Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.
Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.
There are several types of stomach neoplasms, including:
1. Adenocarcinoma: This is the most common type of stomach cancer, accounting for approximately 90% of all cases. It begins in the glandular cells that line the stomach and can spread to other parts of the body.
2. Squamous cell carcinoma: This type of cancer begins in the squamous cells that cover the outer layer of the stomach. It is less common than adenocarcinoma but more likely to be found in the upper part of the stomach.
3. Gastric mixed adenocarcinomasquamous cell carcinoma: This type of cancer is a combination of adenocarcinoma and squamous cell carcinoma.
4. Lymphoma: This is a cancer of the immune system that can occur in the stomach. It is less common than other types of stomach cancer but can be more aggressive.
5. Carcinomas of the stomach: These are malignant tumors that arise from the epithelial cells lining the stomach. They can be subdivided into adenocarcinoma, squamous cell carcinoma, and others.
6. Gastric brunner's gland adenoma: This is a rare type of benign tumor that arises from the Brunner's glands in the stomach.
7. Gastric polyps: These are growths that occur on the lining of the stomach and can be either benign or malignant.
The symptoms of stomach neoplasms vary depending on the location, size, and type of tumor. Common symptoms include abdominal pain, nausea, vomiting, weight loss, and difficulty swallowing. Diagnosis is usually made through a combination of endoscopy, imaging studies (such as CT or PET scans), and biopsy. Treatment depends on the type and stage of the tumor and may include surgery, chemotherapy, radiation therapy, or a combination of these. The prognosis for stomach neoplasms varies depending on the type and stage of the tumor, but early detection and treatment can improve outcomes.
2. Our research focuses on identifying the genetic mutations that contribute to experimental melanoma and developing targeted therapies.
3. The patient's experimental melanoma had spread to her lungs and liver, so we recommended chemotherapy and immunotherapy treatments.
Some common types of bone neoplasms include:
* Osteochondromas: These are benign tumors that grow on the surface of a bone.
* Giant cell tumors: These are benign tumors that can occur in any bone of the body.
* Chondromyxoid fibromas: These are rare, benign tumors that develop in the cartilage of a bone.
* Ewing's sarcoma: This is a malignant tumor that usually occurs in the long bones of the arms and legs.
* Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow.
Symptoms of bone neoplasms can include pain, swelling, or deformity of the affected bone, as well as weakness or fatigue. Treatment options depend on the type and location of the tumor, as well as the severity of the symptoms. Treatment may involve surgery, radiation therapy, chemotherapy, or a combination of these.
Example sentence: The patient was diagnosed with experimental sarcoma and underwent a novel chemotherapy regimen that included a targeted therapy drug.
There are different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
Cell cycle withdrawal
Frederick Pei Li
Cyclin-dependent kinase 5
SV40 large T antigen
Small nucleolar rna host gene 1
5.8S ribosomal RNA
Bcl-2 homologous antagonist killer
NAD(P)H dehydrogenase (quinone 1)
Monomorphic epitheliotropic intestinal T cell lymphoma
P53 upregulated modulator of apoptosis
Aurora kinase A
Cyclin-dependent kinase 1
G2-M DNA damage checkpoint
Tumor Suppressor Protein p53 - MeSH - NCBI
Bacterial redox protein azurin, tumor suppressor protein p53, and regression of cancer - PubMed
Novel proteasome inhibitor delanzomib sensitizes cervical cancer cells to doxorubicin-induced apoptosis via stabilizing tumor...
NIH VideoCast - The Human Tumor Suppressor p53 Links Chromosomal Stress and Immune Responses
p53 Protein News, Research - Page 13
Category D - Chemicals and Drugs
The Tanapoxvirus 142R Protein is a Serine-Threonine Kinase that Phosphorylates the Tumor Suppressor p53
TP53 mutations in myelodysplastic syndromes and secondary AML confer an immunosuppressive phenotype
AbMiner - Antibody Detail | Genomics and Pharmacology Facility
Genome Study Yields Insights Into Bladder Cancer | National Institutes of Health (NIH)
DeCS 2006 - Changed terms
Pharmacological action - T | GreenMedInfo | Natural Medicine
p53 in health and disease | Nature Reviews Molecular Cell Biology
Nilay Singh Sethi, M.D., Ph.D. | Harvard Catalyst Profiles | Harvard Catalyst
A Cancerous Conversation Fuels Oral Tumors | National Institute of Dental and Craniofacial Research
Frontiers | Identification of AIDS-Associated Kaposi Sarcoma: A Functional Genomics Approach
CDKN2A gene: MedlinePlus Genetics
The lncRNA APOLO interacts with the transcription factor WRKY42 to trigger root hair cell expansion in response to cold |...
Sarcomatoid and Rhabdoid Renal Cell Carcinoma Pathology: Definition, Epidemiology, Etiology
Camptothecin | Cell Signaling Technology
People - The University of Nottingham
talks.cam : Babraham Distinguished Lecture - 'Regulating p53 and beyond: from cell death to sudden death'
Victor B. Zhurkin, Ph.D. | Center for Cancer Research
IJMS | Free Full-Text | Linking Endoplasmic Reticular Stress and Alternative Splicing
British Library EThOS: Study of the molecular details of p53 redox-regulation using Fourier transform ion cyclotron resonance...
MDM2 (phospho S186/S188), Rabbit anti-Human, Mouse, Rat, Polyclonal Antibody, | Fisher Scientific
Journal of Veterinary Medical Science
- Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. (nih.gov)
- Novel proteasome inhibitor delanzomib sensitizes cervical cancer cells to doxorubicin-induced apoptosis via stabilizing tumor suppressor proteins in the p53. (oncotarget.com)
- Several proteins that inhibit host immmunomodulatory cytokines and apoptosis of infected cells have been characterized in vaccinia virus (VV). (openvirologyjournal.com)
- We demonstrate that like B1R, TPV142R encodes a serine threonine kinase that can phosphorylate the tumor suppressor p53 and therefore has the potential for inhibiting apoptosis of infected cells. (openvirologyjournal.com)
- p53 activates various responses, including cell-cycle arrest and apoptosis. (nature.com)
- TIGAR, a p53-inducible regulator of glycolysis and apoptosis. (nature.com)
- DRAM, a p53-induced modulator of autophagy, is critical for apoptosis. (nature.com)
- The p53 protein is an important tumor suppressor that is essential for regulating cell division, senescence, and self-destruction (apoptosis). (medlineplus.gov)
- Among them are well-known p53 sites in the genes BAX, CASP6, Cyclin G, 14-3-3 Sigma and Killer/DR5, genes known to be critical for induction of apoptosis and cell cycle arrest. (cancer.gov)
- The p53 tetramer exhibits high binding affinity to its response elements associated with cell cycle arrest (CCA-sites), but low affinity to those associated with apoptosis (Apo-sites). (cancer.gov)
- The tumour-suppressor protein p53 is involved in the regulation of a diverse range of cellular processes including apoptosis, differentiation, senescence, DNArepair, cell-cycle arrest, autophagy, glycolysis and oxidative stress. (bl.uk)
- This protein also affects the cell cycle, apoptosis, and tumorigenesis through interactions with other proteins, including retinoblastoma 1 and ribosomal protein L5. (fishersci.com)
- The p53 tumor suppressor protein is important in cell-cycle control, apoptosis, and DNA repair. (nih.gov)
- We also examined the functionality of the p53 variants in apoptosis and DNA repair. (nih.gov)
- Subsequently, flow cytometry and western blotting indicated that involucrasin A induced apoptosis and upregulated the expression levels of apoptosis‑related proteins, such as cleaved‑caspase 6 and cleaved‑caspase 9, in a dose‑dependent manner. (spandidos-publications.com)
- Similarly, either knocking out p53 or knocking down Bax abrogated involucrasin A‑induced proliferation inhibition and apoptosis. (spandidos-publications.com)
- Depending on the type of cell and the nature of the stress, p53 controls cell fate by inducing apoptosis, arresting progression of the cell cycle, promoting differentiation, or inducing a state of senescence. (nih.gov)
- This prevents ATR-mediated signaling, which results in the inhibition of DNA damage checkpoint activation, the disruption of DNA damage repair, and the induction of tumor cell apoptosis. (nih.gov)
- Furthermore, proteasome inhibition revealed stabilization of p53 and p53 transcriptional targets and induction of p38/JNK phosphorylation. (oncotarget.com)
- Additionally, delanzomib worked synergistically with Dox to further upregulate p53 and its downstream targets and enhanced Dox-induced p38 phosphorylation. (oncotarget.com)
- Mechanistically, involucrasin A significantly inhibited the phosphorylation of Akt and murine double minute 2 homologue (MDM2), which resulted in increased intracellular levels of p53. (spandidos-publications.com)
- We have found that although each subdomain of the N-terminal transactivation domain of p53 separately binds to the Taz2 domain of its co-activator p300, structural details differ and the affinities are differentially affected by phosphorylation. (nih.gov)
- Upon oral administration,gartisertib selectively inhibits ATR activity and blocks the downstream phosphorylation of the serine/threonine protein kinase CHK1. (nih.gov)
- If p53 is inactivated, as it is in over half of all human cancers, checks and balances on cell growth fail to operate, and body cells start to accumulate mutations, which ultimately may lead to cancer. (news-medical.net)
- We further correlated the low expression levels of autophagic genes (atg12, becn1, sesn1, and dram1) with a reduced relapse free survival (RFS) and distant metastasis free survival (DMFS) of breast cancer patients carrying TP53 gene mutations conferring a prognostic value to this mutant p53-and autophagy-related signature. (nih.gov)
- They identified mutations in the TP53 gene in nearly half the tumor samples. (nih.gov)
- 16. Gain-of-function mutations in the tumor suppressor gene p53. (nih.gov)
- Most of these mutations lead to production of little or no functional p16(INK4A) protein. (medlineplus.gov)
- The CDKN2A gene mutations found in melanoma result in a nonfunctional p16(INK4A) protein. (medlineplus.gov)
- Together, the germline and somatic mutations impair the function of proteins that regulate division and senescence, leading to uncontrolled cell growth and the formation of a melanoma. (medlineplus.gov)
- CDKN2A gene mutations involved in cancer impair production of functional p16(INK4A) or, less commonly, p14(ARF), which can result in uncontrolled cell growth and tumor formation. (medlineplus.gov)
- Somatic CDKN2A gene mutations have been found in some people with brain tumors and in children with a blood cancer called acute lymphoblastic leukemia. (medlineplus.gov)
- Several reports have shown some overexpression of p53 in genital warts and squamous cell carcinomas (SCCs), but it appears that p53 mutations were not present. (medscape.com)
- Mutations in p53 have been associated with inherited cancer susceptibility. (nih.gov)
- To investigate the patterns of p53 modifications on an organismal level, we are examining tissues from mice bearing mutations at sites of post-translational modification. (nih.gov)
- The p16(INK4A) protein attaches (binds) to two other proteins called CDK4 and CDK6. (medlineplus.gov)
- The encoded protein is a nuclear phosphoprotein that binds and inhibits transactivation by tumor protein p53, as part of an autoregulatory negative feedback loop. (fishersci.com)
- The E6 protein of HPV-6 and HPV-11 binds p53 tumor suppressor protein less efficiently than that of HPV-16 and HPV-18 but, theoretically, could lead to accelerated degradation of the p53 protein. (medscape.com)
- Upon administration, ALK inhibitor RO5424802 binds to and inhibits ALK kinase, which leads to a disruption of ALK-mediated signaling and eventually inhibits tumor cell growth in ALK-overexpressing tumor cells. (nih.gov)
- SDX7539 binds to and inhibits MetAP2, which prevents MetAP2-mediated signal transduction pathways and results in tumor cell death. (nih.gov)
- Arp2-3 complex binds WASP PROTEIN and existing ACTIN FILAMENTS, and it nucleates the formation of new branch point filaments. (nih.gov)
- HN - 2006 BX - Arp2-3 Complex MH - Actin-Related Protein 3 UI - D051378 MN - D5.750.78.730.246.750 MN - D12.776.220.525.246.750 MS - A component of the Arp2-3 complex that is related in sequence and structure to ACTIN and that binds ATP. (nih.gov)
- The protein p53 is selected because it is an important tumor suppressor antigen. (frontiersin.org)
Genes up-regulated by p532
- This protein has E3 ubiquitin ligase activity, which targets tumor protein p53 for proteasomal degradation. (fishersci.com)
- Here, we report that gain-of-function mutant p53 proteins inhibit the autophagic pathway favoring antiapoptotic effects as well as proliferation of pancreas and breast cancer cells. (nih.gov)
- The RTK/RAS pathway, which is involved in regulating cell growth and development-and is affected in many cancers-was altered in 44% of the tumors analyzed. (nih.gov)
- 2. The p53 pathway in hematopoiesis: lessons from mouse models, implications for humans. (nih.gov)
- The mechanism of H2O2 oxidation was investigated, and revealed that oxidation via an alternative pathway results in indiscriminate over-oxidation of p53. (bl.uk)
- Together, the present study indicated that involucrasin A exerts antitumorigenic activities via modulating the Akt/MDM2/p53 pathway in HCT‑116 CRC cells, and it is worthy of further exploration in preclinical and clinical trials. (spandidos-publications.com)
- a vital transcription factor and tumor suppressor. (news-medical.net)
- A global map of p53 transcription-factor binding sites in the human genome. (nature.com)
- These programs are carried out through chemical modifications of DNA and proteins such as histones and transcription factors. (nih.gov)
- The focus of my research is on transcription factors and the roles that these proteins play in tumourigenesis. (nottingham.ac.uk)
- Our current focus is the Proline Rich Homeodomain protein (PRH/Hhex), an oligomeric transcription factor that regulates cell proliferation and cell migration in multiple contexts. (nottingham.ac.uk)
- Study of these proteins has provided several insights into how transcription factors find their binding sites and regulate gene expression. (nottingham.ac.uk)
- Since 1989, he has been at the National Cancer Institute, where he has studied structural aspects of the protein-DNA interactions in large nucleoprotein assemblages such as nucleosomes, the Gal-repressosome, recombination filaments, transcription elongation complexes, and a tetrameric p53-DNA complex. (cancer.gov)
- The tumor suppressor protein p53 mediates the transcription of ~2000 human genes, serving either as activator or repressor. (cancer.gov)
- This gene is a target gene of the transcription factor tumor protein p53. (fishersci.com)
- The E6 protein also inhibits p53 transcription. (medscape.com)
Loss of p533
- In addition to tumour suppression, p53 can also have a role in normal development, during which loss of p53 can be detrimental. (nature.com)
- This paper provides evidence that loss of p53 might contribute to the Warburg effect. (nature.com)
- The results suggested that loss of p53 in oral cancer enhances nerve growth and density in the tumor microenvironment. (nih.gov)
Functions of p532
- Aberrant ubiquitination and proteasome activity, both human papillomavirus and tumor derived, have been shown to contribute to tumor angiogenesis, proliferation, and invasion in many cancers, including cervical cancer. (oncotarget.com)
- The phase I clinical study will enroll 20 patients with advanced solid cancers (including most common tumor types), and is the culmination of more than a decade of work by a team of researchers led by Professor Esther H. Chang, Ph.D. at the Lombardi Comprehensive Cancer Center. (news-medical.net)
- Researchers at UT Southwestern Medical Center have determined that stem cells in a certain region of the brain may be the source of a particular type of incurable brain tumor and may be implicated in other types of brain cancers as well. (news-medical.net)
- p53 is an important tumour-suppressor protein that is altered in most cancers. (nature.com)
- 4. p53 and human cancers. (nih.gov)
- All these results reveal a novel mechanism through which mutant p53 proteins promote cancer cell proliferation with the concomitant inhibition of autophagy. (nih.gov)
- Without p16(INK4A) to regulate cell growth and division (proliferation), cells can continue to grow and divide without control, which can lead to tumor formation. (medlineplus.gov)
- Alternatively, a mutation may occur in the p53 protein, leading to clonal proliferation. (medscape.com)
- MetAP2, a member of the dimetallohydrolase family upregulated in certain tumor cell types, plays a key role in angiogenesis, proliferation and survival. (nih.gov)
- Professor John Mayer and Dr Simon Dawson, in collaboration with colleagues at Japan's Kyoto University, have discovered the function of a new liver oncoprotein - or cancer causing protein - which could be the first step to finding effective new treatments for the deadly illness. (news-medical.net)
- Camptothecin is a cytotoxic plant alkaloid originally isolated from C. acuminate that inhibits DNA and RNA synthesis in mammalian cells and is an effective anti-tumor agent (1). (cellsignal.com)
- Elevating DLX3 in keratinocytes produces a G1-S blockade associated with p53 signature transcriptional profiles. (nih.gov)
- Just as p53 impacts epigenetic change, the enzyme activities that carry out epigenetic protein modifications act on the p53 protein and its splice variants in stem and progenitor cells to silence or activate its transcriptional activities. (nih.gov)
- We found that mutant p53 significantly counteracts the formation of autophagic vesicles and their fusion with lysosomes throughout the repression of some key autophagy-related proteins and enzymes as BECN1 (and P-BECN1), DRAM1, ATG12, SESN1/2 and P-AMPK with the concomitant stimulation of mTOR signaling. (nih.gov)
- As a paradigm of this mechanism, we show that atg12 gene repression was mediated by the recruitment of the p50 NF-κB/mutant p53 protein complex onto the atg12 promoter. (nih.gov)
- Either mutant p53 or p50 NF-κB depletion downregulates atg12 gene expression. (nih.gov)
- Interestingly, the mutant p53-driven mTOR stimulation sensitized cancer cells to the treatment with the mTOR inhibitor everolimus. (nih.gov)
- These observations have implications for the re-activation of mutant p53 with Cys-targeting compounds which result in the death of cancer-cells. (bl.uk)
- One of them (HCT-116) showed a significant sensitivity to oplopantriol A. Cells from this line are p53 wild-type while those from the other (SW-480) line are mutant in the p53 suppressor gene. (nih.gov)
- Since Wip1 has been shown to be amplified in tumors, we are developing specific inhibitors of its activity that would provide selective targeting either when given alone or in combination with standard cancer chemo- or radio-therapy. (nih.gov)
- A stereochemical model for the tetrameric p53-DNA complex will be presented, accounting for such a difference between the p53-induced transactivation and repression. (cancer.gov)
- These observations may relate to the regulation of p53 activity during development by expression of a p53 isoform that lacks the first transactivation sub-domain. (nih.gov)
- If the damage is irreparable, the protein sets off programmed cell death and protects the cells from degeneration. (news-medical.net)
- The cellular cascade of molecular signals that instructs cells with fatally damaged DNA to self-destruct pivots on the p53 tumor suppressor gene. (news-medical.net)
- 1. Structure and function of p53 in normal cells and their aberrations in cancer cells: projection on the hematologic cell lineages. (nih.gov)
- The interplay between epigenetic changes and the p53 protein in stem cells. (nih.gov)
- The p53 protein not only enforces the stability of the genome by the prevention of genetic alterations in cells but also plays a role in regulating the epigenetic changes that can occur in cells. (nih.gov)
- The full-length p53 protein is largely inactive in stem cells but, when activated, helps to commit these cells to developmental lineages through a series of epigenetic changes. (nih.gov)
- MD Anderson scientists found a new role for nerves in oral cancer progression, whereby tumor cells send genetic messages that transform nerves into cancer-promoting agents. (nih.gov)
- That's because existing therapies treat only the tumor itself, and not its microenvironment, the network of connective tissue, blood vessels, cells, and molecules that surround it. (nih.gov)
- In cell culture experiments, sensory neurons developed projections called neurites when exposed to p53-deficient oral cancer cells. (nih.gov)
- Both function as tumor suppressors, which means they keep cells from growing and dividing too rapidly or in an uncontrolled way. (medlineplus.gov)
- Both proteins are also involved in stopping cell division in older cells (senescence). (medlineplus.gov)
- The p14(ARF) and p53 proteins are often made in cells that are unable to undergo cell division. (medlineplus.gov)
- Without one of these tumor suppressors, cells can grow and divide unchecked, leading to the development of cancer. (medlineplus.gov)
- Western blot analysis of extracts from MCF7 cells, untreated (-) or treated with Camptothecin (6 hr) at the indicated concentrations, using Phospho-p53 (Ser15) Antibody #9284 (upper), p53 (1C12) Mouse mAb #2524 (middle), and β-Actin (D6A8) Rabbit mAb #8457 (lower). (cellsignal.com)
- 1) During Epithelial-Mesenchymal transition (EMT) epithelial cells begin to express different cell adhesion proteins and they start to become more migratory. (nottingham.ac.uk)
- 2) Our recent work has shown that the PRH protein is important in bile duct cells and in bile duct cancer. (nottingham.ac.uk)
- The ultimate goal is to make iPS cells a valid therapeutic option by replacing the potentially dangerous retroviruses with a safer cocktail of proteins and chemicals, including vitamin C. (scientificamerican.com)
- One possible mechanism to explain this improved survival is that the cells exposed to ascorbic acid had lower levels of a tumor suppressor protein called p53 , which can elicit cell death. (scientificamerican.com)
- Kim has developed a system to improve the safety of iPS cells by delivering the four proteins that induce pluripotency directly into cells. (scientificamerican.com)
- Fortunately, doctors can now identify targets on patients' tumors that can help distinguish cancer cells from their normal cells. (cancerresearch.org)
- Sometimes these targets are normal proteins that are produced at abnormally high levels by cancer cells, such as prostatic acid phosphatase (PAP), which is often overexpressed by prostate cancer cells. (cancerresearch.org)
- His focus is on new therapies in cancer, and the systemic management of patients with solid malignancies including a number of new biomarker-based approaches, with an emphasis on circulating tumor cells and cell free DNA. (angio.org)
- These studies help us to better understand the widespread roles of p53 in cells, including its effects on various signaling pathways, and how specific modifications of p53 modulate its functions. (nih.gov)
- Upon administration of SDX-7320, the active moiety SDX7539 is released inside the tumor cells. (nih.gov)
- We wanted to understand the reciprocal tumor-nerve signals that drive cancer progression," says first author Moran Amit, MD, PhD. "This information could help scientists develop the means to target this crosstalk. (nih.gov)
- The human p53 tumor suppressor protein is centrally involved in multiple processes that reduce both the initiation of tumors and their progression. (nih.gov)
- Specific areas of expertise include RNA sequencing and ChIP sequencing and related bioinformatics, protein-DNA interactions, cell migration and cell invasion assays, and the analysis of signal transduction pathways. (nottingham.ac.uk)
- have been shown to serve as messengers in biological signal transduction, and many prokaryotic and eukaryotic proteins are now known to have their function controlled via ROS-mediated oxidation reactions occurring on critical cysteine residues. (bl.uk)
- Each of these appears to contribute to tumour suppression. (nature.com)
- Kortleverm, R. M., Higgins, P. J. & Bernards, R. Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescence. (nature.com)
- Because there is a difference in the risk of lung cancer among different ethnic groups, we examined associations between ethnicity and three polymorphisms in p53 (one exonic and two intronic) and haplotypes for the three loci and risk of lung cancer. (nih.gov)
- p53 polymorphisms may be associated with increased lung cancer risk and may affect p53 function. (nih.gov)
- Since then, Wip1 has been shown to negatively regulate p53 functions by dephosphorylating the p38 MAPK, Chk2 and ATM kinases, which are major effectors of p53 stabilization and activation. (nih.gov)
- We have also examined how mono- or di-methylation of a specific lysine residue in the C-terminal regulatory domain of p53 respectively represses or activates p53 activity through modulation of the interaction of p53 with specific proteins. (nih.gov)
- Figure 3: p53 and metabolism. (nature.com)
- P53 is known as the "guardian of the genome" as it helps in regulating the cell cycle and acts as a tumor suppressor. (news-medical.net)
- Here, we describe the identification of a protein encoded by the tanapox virus genome (142R open reading frame) that is orthologous to the B1R protein from VV. (openvirologyjournal.com)
- How are the p53 sites distributed in various genome regions (e.g., promoters, introns, intergenic regions)? (cancer.gov)
- We searched for homologues of ORF-73 and attempted to predict protein-protein interactions (PPI) based on GeneCards and UniProtKB, utilizing Position-Specific Iterated BLAST (PSI-BLAST). (frontiersin.org)
- The E2 proteins are an excellent model system in which to study DNA-protein interactions. (nottingham.ac.uk)
- We are using biophysical, biochemical, and structural methods to explore the modulation of p53 protein-protein interactions by post-translational modifications. (nih.gov)
- Collectively, similar variants of ORF-73 markers involved in the immune response may interact with targeted host proteins as predicted by our computational analysis. (frontiersin.org)
- More than 40 different alternatively spliced transcript variants have been isolated from both tumor and normal tissues. (fishersci.com)
- However, little is understood about the specific molecular mechanisms that allow p53 to discriminate between these various different functions. (bl.uk)
- The molecular mechanisms that govern p53-dependent cell fate decisions are incompletely understood but are believed to be largely mediated by multiple post-translational modifications to p53 itself as well as to other proteins with which p53 interacts. (nih.gov)
- Although the function of p53 as a tumour suppressor ensures that we can't live without it, an integrated view of p53 suggests that not all of its functions are conducive to a long and healthy life. (nature.com)
- This suggests that some activity of the p53 tumor suppressor protein (which has a role in preventing cancer formation) may be linked to the compound to achieve the antitumor effects. (nih.gov)
- The discovery of how the activities of the protein p53 initiate signals that trigger cell suicide offers critical insights for developing new anti-cancer drugs, according to investigators from St. Jude Children's Research Hospital. (news-medical.net)
- Prostate cancer, the second leading cause of cancer death for men in the United States, is caused by changes in several tummor suppressor genes including PTEN and p53. (news-medical.net)
- Up to 70 percent of men with prostate cancer have lost one copy of the PTEN gene at the time of diagnosis, and p53 is absent in a high number of patients with advanced prostate cancer. (news-medical.net)
- As a component of the response to acute stress, p53 has a well established role in protecting against cancer development. (nature.com)
- Donehower, L. A. The p53-deficient mouse: a model for basic and applied cancer studies. (nature.com)
- Genes that regulate chromatin-the DNA/protein structure that determines how genes are expressed-were more frequently mutated in bladder cancer than in any other common cancer studied to date. (nih.gov)
- DNA from viruses-notably, from HPV16, a form of the virus responsible for cervical cancer-was found in a small number of bladder tumors. (nih.gov)
- 9. On the expression of the p53 protein in human cancer. (nih.gov)
- 14. p53--a natural cancer killer: structural insights and therapeutic concepts. (nih.gov)
- 11 Division of Preventive Oncology, German Cancer Research Center (DKFZ) and National Center for Tumor Diseases (NCT), Heidelberg, Germany. (nih.gov)
- So far though, progress has been stymied by scientists' lack of understanding of how cancer-associated nerves arise and promote tumor growth. (nih.gov)
- Its protein product, p53, is a tumor suppressor that acts as a brake on cancer growth. (nih.gov)
- The researchers found that in mouse models of oral cancer, animals lacking p53 had denser nerve networks around their tumors compared to control mice with p53. (nih.gov)
- p53 Genotypes and Haplotypes Associated With Lung Cancer Susceptibility and Ethnicity. (nih.gov)
- Justin's team published in Nature Medicine the discovery of a new cancer-causing gene which has now been implicated in breast, gastrointestinal, lung, and other solid tumors, and a drug development programme around this is underway. (angio.org)
- The study first evaluated in vivo (within the cell) whether the compound―called oplopantriol A―inhibited tumor growth in mice with colon cancer. (nih.gov)
- Protein kinase CK2 inhibition suppresses neointima formation via a proline-rich homeodomain-dependent mechanism. (nottingham.ac.uk)
- Mice treated with oplopantriol A showed a significant decrease in tumor size compared with the control group, and tumor growth inhibition occurred in a dose-related manner. (nih.gov)
- It took 3 weeks for tumor growth inhibition to appear, and a more than 40-percent reduction in tumor size was evident by the end of the fifth week. (nih.gov)
- The Wip1 phosphatase (PPM1D) is a member of the PP2C family of evolutionarily conserved protein phosphatases. (nih.gov)
- 6. Prognostic and predictive significance of p53 mutation in aggressive B-cell lymphoma. (nih.gov)
- Gatz, S. A. & Wiesmuller, L. p53 in recombination and repair. (nature.com)
- Moreover, Cys176, 238 or 242 was shown to act as a nucleophile, and the intracellular antioxidant glutathione (GSH) did not prevent oxidation of the Zn2+-binding Cys residues, providing further evidence for a role in p53 redox-regulation. (bl.uk)
- Figure 4: Regulation of life and death by p53. (nature.com)
- Figure 5: Temporal regulation of p53 activity in response to DNA damage. (nature.com)
- Our work investigated the DNA binding specificity of the HPV E2 proteins and their effects on gene regulation and cell survival. (nottingham.ac.uk)
- Up- and down-regulation seems to be dependent on the length of the DNA spacer, S, separating two consensus decamers, RRRCWWGYYY in the p53 sites. (cancer.gov)
- The primary goal of the work described in this thesis was to employ FT-ICR mass spectrometry to investigate the molecular details of p53 redox-regulation. (bl.uk)
- Interestingly, Cys182 and Cys277 have previously been implicated in p53 redox-regulation. (bl.uk)
- Transforming Growth Factor-beta (TGFbeta) is up-regulated in many tumours and this protein can induce EMT and increase cell migration. (nottingham.ac.uk)
- p53 responds to both acute stress, such as genotoxic stress and the activation of oncogenes, and constitutive stress induced by factors such as hypoxia or starvation stress. (nature.com)
- We have developed antibodies that recognize specific post-translational modifications of p53 and have used these to characterize the cellular response of p53 to DNA damage and other stress signals. (nih.gov)
- DLX3 and p53 physically interact on the p21 promoter to enhance p21 expression. (nih.gov)
- This study has revealed hitherto unknown details regarding the chemistry of cysteine residues within the important tumour-suppressor protein p53. (bl.uk)
- This function is lost when tumor suppressor genes are mutated, enabling tumors to grow unrestrained. (nih.gov)