Cyclin-Dependent Kinases
Cyclin-Dependent Kinase 2
Cyclin D1
Cyclin A
Cyclin E
Cyclins
Cyclin-Dependent Kinase 4
Cyclin-Dependent Kinase Inhibitor p27
CDC2-CDC28 Kinases
Cell Cycle
Cyclin-Dependent Kinase Inhibitor p21
Cyclin-Dependent Kinase 5
Cell Cycle Proteins
Cyclin B
Cyclin C
Protein-Serine-Threonine Kinases
CDC2 Protein Kinase
Cyclin D
G1 Phase
Cyclin-Dependent Kinase Inhibitor p16
Cyclin-Dependent Kinase Inhibitor Proteins
Cyclin D3
Cyclin B1
Retinoblastoma Protein
Phosphorylation
Cyclin-Dependent Kinase 6
Cyclin-Dependent Kinase Inhibitor p57
Tumor Suppressor Proteins
S Phase
Cyclin D2
Cyclin A1
Microtubule-Associated Proteins
Protein Kinases
Purines
Cell Division
Apoptosis
Proto-Oncogene Proteins
E2F1 Transcription Factor
Cyclin A2
Phosphatidylinositol 3-Kinases
Cyclin G
Tumor Cells, Cultured
Tumor Suppressor Protein p53
Mitosis
Cyclin G1
MAP Kinase Signaling System
Transcription Factor DP1
Signal Transduction
Cells, Cultured
Blotting, Western
Enzyme Inhibitors
G2 Phase
E2F Transcription Factors
Transfection
Calcium-Calmodulin-Dependent Protein Kinases
Mutation
Proliferating Cell Nuclear Antigen
Molecular Sequence Data
DNA-Binding Proteins
Carrier Proteins
Nuclear Proteins
Base Sequence
RNA, Messenger
Protein Kinase C
Transcription Factors
src-Family Kinases
Immunohistochemistry
Reverse Transcriptase Polymerase Chain Reaction
DNA Damage
Amino Acid Sequence
p38 Mitogen-Activated Protein Kinases
Cyclic AMP-Dependent Protein Kinases
Cyclin B2
Mitogen-Activated Protein Kinase 1
Protein Binding
Enzyme Activation
Gene Expression Regulation
Transcription, Genetic
Cyclin T
Mitogen-Activated Protein Kinase Kinases
p21-Activated Kinases
Mitogen-Activated Protein Kinase 3
JNK Mitogen-Activated Protein Kinases
Protein-Tyrosine Kinases
Cyclin H
Cyclin G2
Calcium-Calmodulin-Dependent Protein Kinase Type 2
MAP Kinase Kinase Kinases
Recombinant Fusion Proteins
3T3 Cells
Creatine Kinase
Models, Biological
Calcium
Casein Kinase II
eIF-2 Kinase
Intracellular Signaling Peptides and Proteins
Binding Sites
Cell Nucleus
Ribosomal Protein S6 Kinases
Mitogen-Activated Protein Kinases
MAP Kinase Kinase 1
Down-Regulation
Extracellular Signal-Regulated MAP Kinases
Casein Kinases
Serine
Pyruvate Kinase
Glycogen Synthase Kinase 3
RNA, Small Interfering
Promoter Regions, Genetic
Receptor Protein-Tyrosine Kinases
Mice, Knockout
Thymidine Kinase
MAP Kinase Kinase 4
Saccharomyces cerevisiae Proteins
Isoenzymes
Phosphotransferases (Alcohol Group Acceptor)
I-kappa B Kinase
Proto-Oncogene Proteins c-akt
E2F4 Transcription Factor
Protein Structure, Tertiary
DNA Primers
1-Phosphatidylinositol 4-Kinase
Aurora Kinases
rho-Associated Kinases
Protein Kinase C-alpha
HeLa Cells
S Phase Cell Cycle Checkpoints
Protein Kinase C-delta
Saccharomyces cerevisiae
Rats, Sprague-Dawley
Substrate Specificity
Gene Expression Regulation, Neoplastic
Proteins
Oncogene Proteins
Transcriptional Activation
AMP-Activated Protein Kinases
Immunoblotting
Cyclin I
Flow Cytometry
Tyrosine
Dose-Response Relationship, Drug
Sequence Homology, Amino Acid
Diacylglycerol Kinase
Precipitin Tests
Retinoblastoma-Binding Protein 1
Focal Adhesion Kinase 1
Neoplasm Proteins
Fibroblasts
Janus Kinase 2
Tetradecanoylphorbol Acetate
Myosin-Light-Chain Kinase
Focal Adhesion Protein-Tyrosine Kinases
Ribosomal Protein S6 Kinases, 90-kDa
TOR Serine-Threonine Kinases
Neurons
Threonine
Gene Expression
Cloning, Molecular
Protein Kinase C-epsilon
Cyclic AMP
MAP Kinase Kinase 2
Androstadienes
MAP Kinase Kinase Kinase 1
Cell Survival
Up-Regulation
Genes, bcl-1
Protein Kinase C beta
Gene Expression Regulation, Enzymologic
Cell Differentiation
Cyclic GMP-Dependent Protein Kinases
RNA Interference
Protein Transport
Membrane Proteins
DNA
Adenosine Triphosphate
Adaptor Proteins, Signal Transducing
Phosphoprotein Phosphatases
Trans-Activators
Cell Membrane
Genes, p16
Mitogen-Activated Protein Kinase 8
Mutagenesis, Site-Directed
Phosphoglycerate Kinase
Casein Kinase I
NF-kappa B
MAP Kinase Kinase 6
A premature-termination mutation in the Mus musculus cyclin-dependent kinase 3 gene. (1/18)
Our understanding of the mammalian cell cycle is due in large part to the analysis of cyclin-dependent kinase (CDK) 2 and CDK4/6. These kinases are regulated by E and D type cyclins, respectively, and coordinate the G(1)/S-phase transition. In contrast, little is known about CDK3, a homolog of CDK2 and cell division cycle kinase 2 (CDC2). Previous studies using ectopic expression of human CDK3 suggest a role for this kinase in the G(1)/S-phase transition, but analysis of the endogenous kinase has been stymied by the low levels of protein present in cells and by the absence of an identifiable cyclin partner. Herein we report the presence of a single point mutation in the CDK3 gene from several Mus musculus strains commonly used in the laboratory. This mutation results in the replacement of a conserved tryptophan (Trp-187) within kinase consensus domain IX with a stop codon. The protein predicted to be encoded by this allele is truncated near the T loop, which is involved in activation by CDK-activating kinase. This mutation also deletes motif XI known to be required for kinase function and is, therefore, expected to generate a null allele. In stark contrast, CDK3 from two wild-mice species (Mus spretus and Mus mus castaneus) lack this mutation. These data indicate that CDK3 is not required for M. musculus development and suggest that any functional role played by CDK3 in the G(1)/S-phase transition is likely to be redundant with another CDK. (+info)ik3-1/Cables is a substrate for cyclin-dependent kinase 3 (cdk 3). (2/18)
p70ik3-1 (a 70-kDa protein) contains a cyclin box, and binds to p35cdk3 in vivo and in vitro [Matsuoka, M., Matsuura, Y., Semba, K. & Nishimoto, I. (2000) Biochem. Biophys. Res. Commun. 273, 442-447]. In spite of its structural similarity to cyclins, p70ik3-1 does not activate cyclin-dependent kinase 3 (cdk3)-mediated phosphorylation of pRb, histone H1, or the C-terminal domain of RNA polymerase II. Here, we report that Ser274 of p70ik3-1 is phosphorylated by cdk2 or cdk3 bound to cyclin A and to cyclin E in vitro. We also found that in COS7 cells in which cyclin E and cdk3 were ectopically overexpressed, the phosphorylation level of Ser274 in coexpressed p70ik3-1 is upregulated. We therefore conclude that p70ik3-1 is a substrate for cdk3-mediated phosphorylation. (+info)ik3-2, a relative to ik3-1/cables, is associated with cdk3, cdk5, and c-abl. (3/18)
A cDNA coding for ik3-2 (designated as ik3-2 from an interactor-2 with cdk3) was cloned by cross-hybridization with ik3-1 and RT-PCR. Analysis of amino acid sequence indicated that ik3-2 has the C-terminal cyclin-box-like region highly homologous to that of ik3-1 (identity in amino acids: 78%). On the other hand, the remainder of ik3-2 gene is not so similar to that of ik3-1. There are several regions other than the C-terminal cyclin-box-like region that are conserved between ik3-1 and ik3-2. In vivo binding assay indicated that like ik3-1, ik3-2 binds to cdk3, cdk5, and c-abl, although ik3-2 binds to cdk3 weakly as compared with ik3-1. The C-terminal cyclin-box-like region of ik3-2 (123 amino acids) is able to be associated with cdk5. Accordingly, ik3-2 is very similar to ik3-1 concerning its molecular interaction with other molecules, suggesting that ik3-2 function in the same biological field as ik3-1. Northern blot analysis indicated that ik3-2 is expressed ubiquitously all over tissues. (+info)Cyclin C/cdk3 promotes Rb-dependent G0 exit. (4/18)
G0 is a physiological state occupied by resting or terminally differentiated cells that have exited the cell cycle. In contrast to the well-characterized cyclin/cdk-mediated inactivation of pRb that controls the G1/S transition, little is known about regulation of the G0/G1 transition. However, pRb is likely to participate in this process because its acute somatic inactivation is sufficient for G0-arrested cells to re-enter the cell cycle. One physiological regulator of this event may be cyclin C because its highest mRNA levels occur during G0 exit. Here we show that a non-cdk8-associated cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during the G0/G1 transition, and that this phosphorylation is required for cells to exit G0 efficiently. Thus, G1 entry is regulated in an analogous fashion to S phase entry, but involves a distinct cyclin/cdk combination. (+info)Cyclin C makes an entry into the cell cycle. (5/18)
From yeast to humans, cell cycle progression is orchestrated by the oscillation of kinase activities associated with cyclins. In an article published recently in Cell, Ren and Rollins investigate mechanisms controlling the G0/G1 transition in quiescent cells and identify new cyclin C/Cdk3 complexes as key regulators of cell cycle reentry in human cells. (+info)Absolute quantification of multisite phosphorylation by selective reaction monitoring mass spectrometry: determination of inhibitory phosphorylation status of cyclin-dependent kinases. (6/18)
Multisite phosphorylation is an important mechanism for achieving intricate regulation of protein function. Here we extended the absolute quantification of abundance (AQUA) methodology and validated its applicability to quantitatively study multisite phosphorylation. As a test case, we chose the conserved inhibitory site of the cyclin-dependent kinases (CDKs), Cdk1, Cdk2, and Cdk3, which are important regulators of cell cycle transitions and apoptosis. Inhibitory phosphorylation at Thr(14) and Tyr(15) of the CDKs is modulated by complex regulatory mechanisms involving multiple kinases and phosphatases. Yet the resulting quantitative dynamics among the four possible phosphorylated and non-phosphorylated versions of CDKs (T14p-Y15p, T14p-Y15, T14-Y15p, and T14-Y15) has not been investigated to date. Hence we used the heavy isotope-labeled tryptic peptides spanning the inhibitory site as internal standards and quantified all four versions by LC-selected reaction monitoring. Quantification of the phosphorylation status of the inhibitory site in the cell extracts provided novel quantitative insights. 1) The transition to mitotic phase was dominated by the conversion of "T14p-Y15p" to the "T14-Y15" form, whereas the two monophosphorylated forms were considerably lower in abundance. 2) The amount of all four forms decreased during the progression of apoptosis but with differing kinetics. Analysis of immunoprecipitated Cdk1 and Cdk2 revealed that the inhibitory site phosphorylation state of both kinases at different stages of the cell cycle followed the same trend. Quantitative immunoblotting using antibodies to Cdk1 and Cdk2 and to the T14-Y15p form suggested that quantification by AQUA was reliable and accurate. These results highlight the utility of internal standard peptides to achieve accurate quantification of multisite phosphorylation status. (+info)Cyclin-dependent kinase 3-mediated activating transcription factor 1 phosphorylation enhances cell transformation. (7/18)
(+info)Cyclin C and cyclin dependent kinases 1, 2 and 3 in thrombin-induced neuronal cell cycle progression and apoptosis. (8/18)
(+info)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.
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
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.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
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.
The prognosis for mantle-cell lymphoma is generally poor, with a five-year survival rate of approximately 40%. Treatment options include chemotherapy, immunotherapy, and autologous stem-cell transplantation. The disease often recurs after initial therapy, and subsequent treatments may be less effective.
Mantle-cell lymphoma can be difficult to distinguish from other types of non-Hodgkin lymphoma, such as follicular lymphoma or diffuse large B-cell lymphoma, and a correct diagnosis is important for determining appropriate treatment.
Slide: Mantle Cell Lymphoma (Image courtesy of Nephron/Wikimedia Commons)
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.
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.
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.
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.
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
7. Fatigue
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.
Cyclin-dependent kinase 3
Cyclin-dependent kinase 6
E2F3
E2F2
CDKN3
Cyclin-dependent kinase 2
Cyclin-dependent kinase 4
Cyclin-dependent kinase
CABLES1
KIR3DL1
Cyclin-dependent kinase 1
Cyclin-dependent kinase 10
Cyclin-dependent kinase 5
Cyclin-dependent kinase 9
Cyclin-dependent kinase 8
Cyclin-dependent kinase inhibitor 1C
Cyclin-dependent kinase inhibitor protein
Cyclin-dependent kinase complex
Sandra Quackenbush
CDC2L2
EIF3F
Mediator (coactivator)
Chem-seq
Fanconi anemia, complementation group C
Anindya Dutta
Beta-secretase 2
Alvocidib
Schumanniophyton problematicum
Cyclin-dependent kinase regulatory subunit family
DNA end resection
HSPA1B
MiR-137
Cell cycle
Anthony Mahowald
Cyclopentenone prostaglandins
P16
7SK RNA
HSPA8
AP-1 transcription factor
Index of biochemistry articles
CUTL1
Pre-replication complex
Mitogen
IFI27
Cyclin T2
Transcription factor II B
Cdc14
CDK5R2
MECOM
Anticancer gene
Ubiquitin
Visceral leishmaniasis
PRPF4B
SCF complex
G2-M DNA damage checkpoint
PTPRK
Tat (HIV)
Structural basis for the synthesis of indirubins as potent and selective inhibitors of glycogen synthase kinase-3 and cyclin...
Human CDKN3(Cyclin Dependent Kinase Inhibitor 3) ELISA Kit - Sugar Glider University
Cyclin-Dependent Kinase 3 | Profiles RNS
CircTP53 promotes colorectal cancer by acting as a miR-876-3p sponge to increase cyclin-dependent kinase-like 3 expression. |...
AbMiner - Antibody Detail | Genomics and Pharmacology Facility
Biomarkers Search
Diffuse Large B-Cell Lymphoma (DLBCL) Clinical Presentation: History, Physical Examination
Cyclin-Dependent Kinase 2 | Harvard Catalyst Profiles | Harvard Catalyst
Iron Chaperone Poly rC Binding Protein 1 Protects Mouse Liver From Lipid Peroxidation and Steatosis - PubMed
MeSH Browser
CDKN2A (p16)
CIMB | Free Full-Text | Regenerative Potential of Blood-Derived Products in 3D Osteoarthritic Chondrocyte Culture System
Biomarkers Search
Sp1 and NF-Y synergistically mediate the effect of vitamin D(3) in the p27(Kip1) gene promoter that lacks vitamin D response...
PDB Full entry for 1W0X
Publication Detail
RCSB PDB - 1OIR: Imidazopyridines: a potent and selective class of Cyclin-dependent Kinase inhibitors identified through...
Ashok Kulkarni, Ph.D. | National Institute of Dental and Craniofacial Research
Browsing by Title
MH DELETED MN ADDED MN
Purvalanol B | â„99%(HPLC) | CDK inhibitor | AdooQÂź
ugt1a10 gene|ugt1a10 gene|C1421323|udp glucuronosyltransferase 1 family, polypeptide a10|gngm
MeSH Browser
JCI -
Volume 104, Issue 3
The canonical α-SNAP is essential for gametophytic... | proLĂ©kaĆe.cz
Reining in Runaway Enzyme Halts Neuronal Destruction | NIH Intramural Research Program
Inhibitory phosphorylation of a mitotic cyclin-dependent kinase regulates the morphogenesis, cell size and virulence of the...
Pharos : Target Details - CDK3
DeCS
Inhibitor11
- Description: A sandwich ELISA for quantitative measurement of Human Cyclin dependent kinase inhibitor 3(CDKN3) in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (glideruniversity.org)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Cyclin Dependent Kinase Inhibitor 3 (CDKN3) in Tissue homogenates and other biological fluids. (glideruniversity.org)
- It has been reported that overexpression of the cdk inhibitor p27(Kip1) results in the differentiation of the myelomonocytic U937 cell line and that this gene is the target of vitamin D(3). (nih.gov)
- Indigoids, a class of bis-indoles, represent a promising protein kinase inhibitor scaffold. (nih.gov)
- Purvalanol B is a cyclin-dependent kinase inhibitor. (adooq.com)
- CGP60474 is a potent inhibitor of cyclin-dependent kinase (CDK). (adooq.com)
- TG003 is a potent, specific, reversible, and ATP competitive inhibitor of Cdc2 like kinase(Clk). (adooq.com)
- 2008) Targeted degradation of the cyclin-dependent kinase inhibitor ICK4/KRP6 by RING-type E3 ligases is essential for mitotic cell cycle progression during Arabidopsis gametogenesis. (prolekare.cz)
- It is an endogenous inhibitor of RAF KINASES and may play a role in regulating SIGNAL TRANSDUCTION. (lookformedical.com)
- A cyclin-dependent kinase inhibitor that coordinates the activation of CYCLIN and CYCLIN-DEPENDENT KINASES during the CELL CYCLE. (lookformedical.com)
- A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. (lookformedical.com)
Phosphorylation9
- Indirubins inhibit glycogen synthase kinase-3 beta and CDK5/p25, two protein kinases involved in abnormal tau phosphorylation in Alzheimer's disease. (nih.gov)
- 3. Smad3 phosphorylation by cyclin-dependent kinases. (nih.gov)
- 18. Vascular endothelial growth factor induces protein kinase C (PKC)-dependent Akt/PKB activation and phosphatidylinositol 3'-kinase-mediates PKC delta phosphorylation: role of PKC in angiogenesis. (nih.gov)
- Cyclin-dependent kinase 5 modulates nociceptive signaling through direct phosphorylation of transient receptor potential vanilloid 1. (nih.gov)
- CDK3/cyclin-C mediated RB1 phosphorylation is required for G0-G1 transition. (nih.gov)
- Cyclin-dependent kinases are regulated by phosphorylation and dephosphorylation events. (lookformedical.com)
- Cyclin-dependent kinases (Cdks) coordinate hundreds of molecular events during the cell cycle via Ser/Thr phosphorylation. (eu.org)
- Docking motifs control the timing of cell cycle events by enabling preferential interaction and phosphorylation of substrates by a specific cyclin/Cdk complex. (eu.org)
- This study showed that silica exposure induced phosphorylation of p70S6 kinase (p70S6K) and Akt in human embryo lung fibroblasts (HELFs). (cdc.gov)
CDK43
- At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. (nih.gov)
- High-throughput screening identified the imidazo[1,2-a]pyridine and bisanilinopyrimidine series as inhibitors of the cyclin-dependent kinase CDK4. (rcsb.org)
- Our results indicated that inactivation of PI-3K, Akt, or p70S6K could inhibit silica -induced overexpression of cyclin DI and cyclin-dependent kinase 4 (CDK4) and decreased expression of E2F-4. (cdc.gov)
PROTEIN KINASE INH1
- Generation of new protein kinase inhibitors utilizing cytochrome p450 mutant enzymes for indigoid synthesis. (nih.gov)
Proteins4
- A large family of regulatory proteins that function as accessory subunits to a variety of CYCLIN-DEPENDENT KINASES. (lookformedical.com)
- This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS. (lookformedical.com)
- A group of cell cycle proteins that negatively regulate the activity of CYCLIN/CYCLIN-DEPENDENT KINASE complexes. (lookformedical.com)
- Cyclins use the conserved hydrophobic pocket (hp) to bind docking motifs on partner proteins. (eu.org)
Mediates4
- 1. p38 MAPK mediates gamma-irradiation-induced endothelial cell apoptosis, and vascular endothelial growth factor protects endothelial cells through the phosphoinositide 3-kinase-Akt-Bcl-2 pathway. (nih.gov)
- 4. Bcl-xL mediates a survival mechanism independent of the phosphoinositide 3-kinase/Akt pathway in prostate cancer cells. (nih.gov)
- 17. Migration inhibitory factor mediates angiogenesis via mitogen-activated protein kinase and phosphatidylinositol kinase. (nih.gov)
- Activation of cyclin-dependent 5 mediates orofacial mechanical hyperalgesia. (nih.gov)
Calmodulin-dependent protein1
- calcium/calmodulin dependent protein k. (gsea-msigdb.org)
Specificity3
- The c-raf Kinases are MAP kinase kinase kinases that have specificity for MAP KINASE KINASE 1 and MAP KINASE KINASE 2. (lookformedical.com)
- With cell cycle progression, different cyclins bind to Cdks to control their function by providing docking sites for substrates and also by modulating Cdk active site specificity. (eu.org)
- Cyclins show cross-specificity, for instance Cyclins E and D also bind RxL motifs ( Guiley,2019 ). (eu.org)
CDK51
- Using the cocrystal structures of various indirubins with GSK-3beta, CDK2 and CDK5/p25, we have modeled the binding of indirubins within the ATP-binding pocket of these kinases. (nih.gov)
Inhibit1
- Keywords: Indole-3-carbinol (I3C), Canine inflammatory mammary cancer (IMC), Inflammatory breast cancer (IBC), Steroid hormones, Mice model, Xenograft Background substances block tumor growth and inhibit metastasis in The relationship between cancer and nutrition has been animal models [6, 7]. (deepdyve.com)
Transcription factors1
- Consistent with the roles of these transcription factors, treatment with vitamin D(3) stimulated the DNA binding activities of these factors to each element and induced the change of one NF-Y subunit. (nih.gov)
Interacts3
- It partners with CYCLIN E to regulate entry into S PHASE and also interacts with CYCLIN A to phosphorylate RETINOBLASTOMA PROTEIN. (harvard.edu)
- Interacts with CCNC/cyclin-C during interphase. (nih.gov)
- It interacts with active CYCLIN D complexed to CYCLIN-DEPENDENT KINASE 4 in proliferating cells, while in arrested cells it binds and inhibits CYCLIN E complexed to CYCLIN-DEPENDENT KINASE 2. (lookformedical.com)
Regulates2
- 14. Insulin-like growth factor-1 regulates endogenous RUNX2 activity in endothelial cells through a phosphatidylinositol 3-kinase/ERK-dependent and Akt-independent signaling pathway. (nih.gov)
- Tumor necrosis factor-alpha regulates cyclin-dependent kinase 5 activity during pain signaling through transcriptional activation of p35. (nih.gov)
Tumor6
- 6. Differential activation of the phosphatidylinositol 3'-kinase/Akt survival pathway by ionizing radiation in tumor and primary endothelial cells. (nih.gov)
- 16. Tumor necrosis factor-alpha induces insulin resistance in endothelial cells via a p38 mitogen-activated protein kinase-dependent pathway. (nih.gov)
- Effects of indole-3-carbinol on steroid hormone profile and tumor progression in a mice model of. (deepdyve.com)
- Results: Indole-3-carbinol treatment decreased tumor proliferation and increased apoptosis, although tumor embolization and liver metastasis were observed in some animals. (deepdyve.com)
- Conclusions: Our data reveal for the first time that the ingestion of indole-3-carbinol, as administered, diminishes proliferation and increases apoptosis of tumor cells in an experimental model of inflammatory breast cancer, although this effect could not be enough to avoid the appearance of tumor embolization and metastasis. (deepdyve.com)
- BMC Cancer (2018) 18:626 Page 2 of 9 as colorectal cancer, prostate cancer, ovarian cancer, carcinoma, following a protocol previously established cervix carcinoma and hepatocarcinoma indicated that [37] as follows: Fragments (3 mm Ă 2 mm of diameter) I3C suppresses cell proliferation and induces apop- from canine primary mammary tumor obtained at tosis [17, 21-25]. (deepdyve.com)
Pharmacological3
- Pharmacological inhibitors of glycogen synthase kinase-3 (GSK-3) and cyclin-dependent kinases have a promising potential for applications against several neurodegenerative diseases such as Alzheimer's disease. (nih.gov)
- 9. The lethal effects of pharmacological cyclin-dependent kinase inhibitors in human leukemia cells proceed through a phosphatidylinositol 3-kinase/Akt-dependent process. (nih.gov)
- Search for new bioactive compounds, the main aim of the present work is preparation of fluorinated 3-substituted amino-1,2,4-triazino[3,4-b][1,3,4]thiadiazo- lones in view of their pharmacological properties. (scirp.org)
Glycogen1
- Extracts of the cultures were screened for inhibition of human cyclin-dependent kinases (CDK)-1 and -5 and glycogen synthase kinase-3 (GSK3). (nih.gov)
Apoptosis4
- Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2-mediated activation of forkhead box O1. (harvard.edu)
- 2. Opposite effects of Ha-Ras and Ki-Ras on radiation-induced apoptosis via differential activation of PI3K/Akt and Rac/p38 mitogen-activated protein kinase signaling pathways. (nih.gov)
- 7. Inhibition of phosphatidylinositol 3-kinase-Akt signaling blocks growth, promotes apoptosis, and enhances sensitivity of small cell lung cancer cells to chemotherapy. (nih.gov)
- Hypoxia-acidosis-mediated cell death was independent of p53: equivalent apoptosis occurred in cardiac myocytes isolated from wild-type and p53 knockout mice, and hypoxia caused no detectable change in p53 abundance or p53-dependent transcription. (jci.org)
Mitotic2
- 7. Takatsuka H, Umeda-Hara C, Umeda M (2015) Cyclin-dependent kinase-activating kinases CDKD;1 and CDKD;3 are essential for preserving mitotic activity in Arabidopsis thaliana. (prolekare.cz)
- Cyclins Cln1-3 are triggers for G1 and G1/S, while among B-type cyclins Clb5 and Clb6 drive S phase, Clb3 and Clb4 are specific for early mitotic events, and Clb1 and Clb2 complete the progression to mitosis. (eu.org)
Potent1
- Indirubins, a family of bis-indoles isolated from various natural sources, are potent inhibitors of several kinases, including GSK-3. (nih.gov)
20171
- Molecular Microbiology (2017) 104 (3): 487. (biologists.com)
Overexpression2
- Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms. (lookformedical.com)
- These changes were blocked by overexpression of dominant-negative mutants of phosphatidylinositol-3 kinase (Delta p85) or Akt (DN-Akt), respectively. (cdc.gov)
Progression2
- Protein kinases that control cell cycle progression in all eukaryotes and require physical association with CYCLINS to achieve full enzymatic activity. (lookformedical.com)
- The sequential attachment of different cyclins to Cdks represents the periodic driving force that ensures a controlled progression through the cell cycle. (eu.org)
20212
Synthesis2
- Synthesis and Structure-Activity relationships of cyclin-dependent kinase 11 inhibitors based on a diaminothiazole scaffold. (harvard.edu)
- Kopel P, TrĂĄvnĂÄek Z , KvĂtek L, ÄernoĆĄek Z, Wrzeszcz G, Marek J: Synthesis and characterization of Cu(II), Co(II) and Ni(II) complexes of trithiocyanuric acid: The structure of { N,N' -bis(3-aminopropyl)-1,3-propanediamine}- (trithiocyanurato) nickel(II). (upol.cz)
Transcriptional2
- The transcriptional activity of this construct was activated by vitamin D(3). (nih.gov)
- A subset of cyclins may also function as transcriptional regulators. (lookformedical.com)
Palbociclib1
- Fulvestrant plus palbociclib versus fulvestrant plus placebo for treatment of hormone-receptor-positive, HER2-negative metastatic breast cancer that progressed on previous endocrine therapy (PALOMA-3): final analysis of the multicentre, double-blind, phase 3 randomised controlled trial. (cdc.gov)
Gene5
- To identify the sequences required for the positive regulation of p27(Kip1) transcription by vitamin D(3), a 3.6-kilobase 5'-flanking region of the human p27(Kip1) gene was examined by transiently transfecting luciferase reporter constructs into U937 cells. (nih.gov)
- We conclude that vitamin D(3) stimulates transcription of the p27(Kip1) gene by a novel mechanism involving Sp1 and NF-Y, but not the vitamin D receptor, during the early stages of U937 cell differentiation. (nih.gov)
- This gene encodes a member of the cyclin-dependent protein kinase family. (nih.gov)
- IL1B), early growth response gene 3 (EGR3), and prostaglandin-endoperoxide synthase 2 (PTGS2) resolved within four months of insulin therapy and were also observed in T2D suggesting that they resulted from hyperglycemia. (gsea-msigdb.org)
- Genetic Association of rs2237572 Cyclin-Dependent Kinase 6 Gene with Breast Cancer in Iraq. (cdc.gov)
CDK11
- Here a single Cdk, Cdk1, associates with different cyclins to mediate all major cell cycle transitions. (eu.org)
Complexes1
- Although there can be functional overlap, the various cyclin/Cdk complexes are specialized for optimum performance of discrete tasks. (eu.org)
Induces1
- 8. VEGF induces Tie2 shedding via a phosphoinositide 3-kinase/Akt dependent pathway to modulate Tie2 signaling. (nih.gov)
Peptides1
- The classical cyclin docking motif pattern is mainly derived from peptides bound to Cyclin A as there are several complex structures available. (eu.org)
Pathway3
- 19. Sonic hedgehog signaling promotes motility and invasiveness of gastric cancer cells through TGF-beta-mediated activation of the ALK5-Smad 3 pathway. (nih.gov)
- 15. Cardiotrophin-1 phosphorylates akt and BAD, and prolongs cell survival via a PI3K-dependent pathway in cardiac myocytes. (nih.gov)
- This suggested that phosphatidylinositol-3 kinase (PI-3K)/AP-1 pathway was likely responsible for cell cycle changes. (cdc.gov)
Activation1
- 13. Phosphatidylinositol 3-kinase/AKT-mediated activation of estrogen receptor alpha: a new model for anti-estrogen resistance. (nih.gov)
Substrates1
- Cyclins may use additional surfaces to dock substrates, as with the mammalian Cyclin D-specific ( DOC_CYCLIN_D_Helix_1 ) and the budding yeast Cln2-specific leucine- and proline-rich LP ( DOC_CYCLIN_yCln2_LP_2 ) motifs. (eu.org)
REGULATION2
Phosphorylates1
- The protein also associates with cyclin C and phosphorylates the retinoblastoma 1 protein to promote exit from G0. (nih.gov)
Estrogen2
- Illera, Juan 2018-06-04 00:00:00 Background: Indole-3-carbinol, derived from Cruciferous vegetables is an estrogen receptor antagonist considered a preventive agent that is naturally present in diet. (deepdyve.com)
- Thus, some authors showed that pany, BioPath Stores, Cambridge) before they were sub- I3C might be useful as supplement of tamoxifen prevent- cutaneously implanted into the ventral side of 3 female ing or treating estrogen-dependent tumors [27, 28]. (deepdyve.com)
Breast cancer2
- Oral Care-BC was a phase 3 multicenter randomized clinical trial that assessed the effectiveness of professional oral care (POC) in preventing oral mucositis in patients treated with EVE and EXE for hormone-receptor-positive HER2-negative metastatic breast cancer. (biomedcentral.com)
- Breast cancer research : BCR 2008 10 (3): R47. (cdc.gov)
PHASE1
- A cyclin-dependent kinase that forms a complex with CYCLIN C and is active during the G1 PHASE of the CELL CYCLE. (musc.edu)
Promotes3
- CircTP53 promotes colorectal cancer by acting as a miR-876-3p sponge to increase cyclin-dependent kinase-like 3 expression. (bvsalud.org)
- 17. PINCH-1 promotes tubular epithelial-to-mesenchymal transition by interacting with integrin-linked kinase. (nih.gov)
- Vitamin D(3) promotes myeloid leukemic cell lines to differentiate terminally into monocytes/macrophages. (nih.gov)
Descriptor1
- Cyclin-Dependent Kinase 3" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (musc.edu)
Cell2
- Cyclin-dependent kinases (Cdks) are central regulatory enzymes of the eukaryotic cell cycle. (eu.org)
- studies suggest that certain endocrine cells may be particularly dependent on the p27 protein to control cell division. (medlineplus.gov)
Potency1
- In solution, store at -20ÂșC and use within 3 months to prevent loss of potency. (adooq.com)
Molecular2
- This modeling approach provided some insight into the molecular basis of indirubins' action and selectivity and allowed us to forecast some improvements of this family of bis-indoles as kinase inhibitors. (nih.gov)
- Future clinical trials will be needed to clarify the usefulness of indole-3-carbinol in this cancer and to understand the molecular mechanisms involved. (deepdyve.com)
Cytochrome1
- cytochrome c oxidase assembly factor 3. (gsea-msigdb.org)
Human2
- 3 Section on Human Iron MetabolismNICHD, NIHBethesdaMD. (nih.gov)
- Methods: The aim of this study was to analyze the effect of indole-3-carbinol on a SCID mice xenograft model of canine inflammatory mammary cancer, using equivalent human oral dose as a preventive therapy in humans for 3 weeks. (deepdyve.com)
Signal1
- A ubiquitously expressed raf kinase subclass that plays an important role in SIGNAL TRANSDUCTION. (lookformedical.com)
Control2
- Control, kinase-inactive indirubins were obtained by introduction of a methyl substitution on N1. (nih.gov)
- 3. McCormick S (2004) Control of male gametophyte development. (prolekare.cz)
20201
- Epub 2020 Nov 3. (nih.gov)
Function1
- 2012) Genetic framework of cyclin-dependent kinase function in Arabidopsis. (prolekare.cz)