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
Cyclin D-CDK subunit arrangement is dependent on the availability of competing INK4 and p21 class inhibitors. (1/363)
The D-type cyclins and their major kinase partners CDK4 and CDK6 regulate G0-G1-S progression by contributing to the phosphorylation and inactivation of the retinoblastoma gene product, pRB. Assembly of active cyclin D-CDK complexes in response to mitogenic signals is negatively regulated by INK4 family members. Here we show that although all four INK4 proteins associate with CDK4 and CDK6 in vitro, only p16(INK4a) can form stable, binary complexes with both CDK4 and CDK6 in proliferating cells. The other INK4 family members form stable complexes with CDK6 but associate only transiently with CDK4. Conversely, CDK4 stably associates with both p21(CIP1) and p27(KIP1) in cyclin-containing complexes, suggesting that CDK4 is in equilibrium between INK4 and p21(CIP1)- or p27(KIP1)-bound states. In agreement with this hypothesis, overexpression of p21(CIP1) in 293 cells, where CDK4 is bound to p16(INK4a), stimulates the formation of ternary cyclin D-CDK4-p21(CIP1) complexes. These data suggest that members of the p21 family of proteins promote the association of D-type cyclins with CDKs by counteracting the effects of INK4 molecules. (+info)Differential roles for cyclin-dependent kinase inhibitors p21 and p16 in the mechanisms of senescence and differentiation in human fibroblasts. (2/363)
The irreversible G1 arrest in senescent human diploid fibroblasts is probably caused by inactivation of the G1 cyclin-cyclin-dependent kinase (Cdk) complexes responsible for phosphorylation of the retinoblastoma protein (pRb). We show that the Cdk inhibitor p21(Sdi1,Cip1,Waf1), which accumulates progressively in aging cells, binds to and inactivates all cyclin E-Cdk2 complexes in senescent cells, whereas in young cells only p21-free Cdk2 complexes are active. Furthermore, the senescent-cell-cycle arrest occurs prior to the accumulation of the Cdk4-Cdk6 inhibitor p16(Ink4a), suggesting that p21 may be sufficient for this event. Accordingly, cyclin D1-associated phosphorylation of pRb at Ser-780 is lacking even in newly senescent fibroblasts that have a low amount of p16. Instead, the cyclin D1-Cdk4 and cyclin D1-Cdk6 complexes in these cells are associated with an increased amount of p21, suggesting that p21 may be responsible for inactivation of both cyclin E- and cyclin D1-associated kinase activity at the early stage of senescence. Moreover, even in the late stage of senescence when p16 is high, cyclin D1-Cdk4 complexes are persistent, albeit reduced by +info)Progesterone inhibits estrogen-induced cyclin D1 and cdk4 nuclear translocation, cyclin E- and cyclin A-cdk2 kinase activation, and cell proliferation in uterine epithelial cells in mice. (3/363)
The response of the uterine epithelium to female sex steroid hormones provides an excellent model to study cell proliferation in vivo since both stimulation and inhibition of cell proliferation can be studied. Thus, when administered to ovariectomized adult mice 17beta-estradiol (E2) stimulates a synchronized wave of DNA synthesis and cell division in the epithelial cells, while pretreatment with progesterone (P4) completely inhibits this E2-induced cell proliferation. Using a simple method to isolate the uterine epithelium with high purity, we have shown that E2 treatment induces a relocalization of cyclin D1 and, to a lesser extent, cdk4 from the cytoplasm into the nucleus and results in the orderly activation of cyclin E- and cyclin A-cdk2 kinases and hyperphosphorylation of pRb and p107. P4 pretreatment did not alter overall levels of cyclin D1, cdk4, or cdk6 nor their associated kinase activities but instead inhibited the E2-induced nuclear localization of cyclin D1 to below the control level and, to a lesser extent, nuclear cdk4 levels, with a consequent inhibition of pRb and p107 phosphorylation. In addition, it abrogated E2-induced cyclin E-cdk2 activation by dephosphorylation of cdk2, followed by inhibition of cyclin A expression and consequently of cyclin A-cdk2 kinase activity and further inhibition of phosphorylation of pRb and p107. P4 is used therapeutically to oppose the effect of E2 during hormone replacement therapy and in the treatment of uterine adenocarcinoma. This study showing a novel mechanism of cell cycle inhibition by P4 may provide the basis for the development of new antiestrogens. (+info)Re-expression of endogenous p16ink4a in oral squamous cell carcinoma lines by 5-aza-2'-deoxycytidine treatment induces a senescence-like state. (4/363)
We have previously reported that a set of oral squamous cell carcinoma lines express specifically elevated cdk6 activity. One of the cell lines, SCC4, contains a cdk6 amplification and expresses functional p16ink4a, the other cell lines express undetectable levels of p16ink4a, despite a lack of coding-region mutations. Two of the cell lines, SCC15 and SCC40 have a hypermethylated p16ink4A promoter and a third cell line, SCC9, has a mutation in the p16ink4a promoter. Using the demethylation agent 5-aza-2'-deoxycytidine, we showed that the p16ink4a protein was re-expressed after a 5-day treatment with this chemical. One cell line, SCC15 expressed high levels of p16ink4a. In this line, cdk6 activity was decreased after 5-aza-2'deoxycytidine treatment, and the hypophosphorylated, growth suppressive form of the retinoblastoma tumor suppressor protein pRB was detected. Expression of p16ink4a persisted, even after the drug was removed and the cells expressed senescence-associated beta-galactosidase activity. Ectopic expression of p16ink4a with a recombinant retrovirus in this cell line also induced a similar senescence-like phenotype. Hence, it was possible to restore a functional pRB pathway in an oral squamous cell carcinoma line by inducing re-expression of endogenous p16ink4a in response to treatment with a demethylating agent. (+info)NF-kappaB function in growth control: regulation of cyclin D1 expression and G0/G1-to-S-phase transition. (5/363)
Nuclear factor kappa B (NF-kappaB) has been implicated in the regulation of cell proliferation, transformation, and tumor development. We provide evidence for a direct link between NF-kappaB activity and cell cycle regulation. NF-kappaB was found to stimulate transcription of cyclin D1, a key regulator of G1 checkpoint control. Two NF-kappaB binding sites in the human cyclin D1 promoter conferred activation by NF-kappaB as well as by growth factors. Both levels and kinetics of cyclin D1 expression during G1 phase were controlled by NF-kappaB. Moreover, inhibition of NF-kappaB caused a pronounced reduction of serum-induced cyclin D1-associated kinase activity and resulted in delayed phosphorylation of the retinoblastoma protein. Furthermore, NF-kappaB promotes G1-to-S-phase transition in mouse embryonal fibroblasts and in T47D mammary carcinoma cells. Impaired cell cycle progression of T47D cells expressing an NF-kappaB superrepressor (IkappaBalphaDeltaN) could be rescued by ectopic expression of cyclin D1. Thus, NF-kappaB contributes to cell cycle progression, and one of its targets might be cyclin D1. (+info)Activation of cyclin A gene expression by the cyclin encoded by human herpesvirus-8. (6/363)
Human herpesvirus-8 (HHV-8), also known as Kaposi's sarcoma-associated herpesvirus, encodes a protein, referred to as HHV8-Vcyc, with sequence similarity to human G1 cyclins, in particular of the D type. HHV8-Vcyc is expressed in Kaposi's sarcoma and functional analysis suggests that it can activate cyclin-dependent kinases (cdk) and thereby trigger inactivation of the retinoblastoma protein (pRb), indicating that HHV8-Vcyc may contribute to the oncogenic potential of HHV-8. We show here that HHV8-Vcyc can activate transcription of the human cyclin A gene in quiescent cells, a property shared with known transforming oncogenes. Transcriptional activation by HHV8-Vcyc depends on an E2F-binding site in the cyclin A promoter, and cdk6 kinase activity is required. The ability of HHV8-Vcyc to activate cyclin A gene expression is shared by D-type cyclins and cyclin E. Unlike D-type cyclins, HHV8-Vcyc is unable to trigger phosphorylation of the pRb-related protein p107 and fails to induce dissociation of p107 from E2F. Unlike cyclin E, HHV8-Vcyc fails to interact physically with E2F complexes on the cyclin A promoter. These results provide additional evidence for the notion that the HHV-8-encoded cyclin differs in several properties from cellular G1 cyclins. (+info)Anchorage dependence of mitogen-induced G1 to S transition in primary T lymphocytes. (7/363)
Anchorage dependence defines the cellular requirement for integrin-mediated adhesion to substrate to initiate DNA replication in response to growth factors. In this study we investigated whether normal T cells, which spend extended periods in a nonadherent state, show similar requirements for cell cycle progression in response to TCR stimulation. Resting primary T lymphocytes were induced to enter the cell cycle by TCR triggering, and leukocyte integrins were either engaged using purified ICAM-1 or inhibited with function-blocking mAbs. Our data indicate that leukocyte integrins complement TCR-driven mitogenic signals not as a result of their direct clustering but, rather, via integrin-dependent organization of the actin cytoskeleton. Leukocyte integrin-dependent reorganization of the actin cytoskeleton cooperates with the TCR to effect mitogen-activated protein kinase activation, but also represents a required late (4-8 h poststimulation) component in the mitogenic response of normal T cells. Prolonged leukocyte integrin-dependent spreading, in the context of intercellular contact, is a requisite for the production of the mitogenic cytokine IL-2, which, in turn, is involved in the induction of D3 cyclin and is primarily responsible for the decrease in the cyclin-dependent kinase inhibitor p27kip, resulting in retinoblastoma protein inactivation and S phase entry. Thus, T lymphocytes represent a peculiar case of anchorage dependence, in which signals conveyed by integrins act sequentially with the activating stimulus to effect a sustained production of the essential mitogenic cytokine. (+info)CTLA-4-Mediated inhibition of early events of T cell proliferation. (8/363)
CTLA-4 engagement by mAbs inhibits, while CD28 enhances, IL-2 production and proliferation upon T cell activation. Here, we have analyzed the mechanisms involved in CTLA-4-mediated inhibition of T cell activation of naive CD4+ T cells using Ab cross-linking. CTLA-4 ligation inhibited CD3/CD28-induced IL-2 mRNA accumulation by inhibiting IL-2 transcription, which appears to be mediated in part through decreasing NF-AT accumulation in the nuclei. However, CTLA-4 ligation did not appear to affect the CD28-mediated stabilization of IL-2 mRNA. Further, CTLA-4 engagement inhibited progression through the cell cycle by inhibiting the production of cyclin D3, cyclin-dependent kinase (cdk)4, and cdk6 when the T cells were stimulated with anti-CD3/CD28 and with anti-CD3 alone. These results indicate that CTLA-4 signaling inhibits events early in T cell activation both at IL-2 transcription and at the level of IL-2-independent events of the cell cycle, and does not simply oppose CD28-mediated costimulation. (+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
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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 6
Cyclin-dependent kinase 2
Clb 5,6 (Cdk1)
MicroRNA 495
Cyclin-dependent kinase 1
Cyclin-dependent kinase 10
Cyclin-dependent kinase 7
Cyclin-dependent kinase 5
Cyclin-dependent kinase 3
Cyclin-dependent kinase 8
Cyclin-dependent kinase inhibitor 1C
Cyclin-dependent kinase
Splenic marginal zone lymphoma
CDKN2C
Endocrine therapy resistance in breast cancer
Mariano Barbacid
Cyclin-dependent kinase regulatory subunit family
Mir-129 microRNA precursor family
Chemotherapy
MCM4
Cellular senescence
Protein crystallization
Abemaciclib
SAAL1
Trilaciclib
PFKFB3
Cyclin D3
MiR-137
Ribociclib
P21
G1 phase
HSPA1B
Cell cycle
Cyclopentenone prostaglandins
P16
7SK RNA
HSPA8
AP-1 transcription factor
CUTL1
Pre-replication complex
IFI27
Transcription factor II B
Mediator (coactivator)
Anaphase
Cdc14
CDK5R2
MECOM
Anticancer gene
Ubiquitin
Visceral leishmaniasis
Alvocidib
PRPF4B
SCF complex
G2-M DNA damage checkpoint
PTPRK
Tat (HIV)
Period (gene)
DNA repair
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CDK451
- The aim of this article is to give a short overview of the existing efficacy data, to summarize the recommended clinical monitoring procedures for patients under CDK4/6 inhibitors, and to shed light on the clinical management of the most common treatment-emergent adverse events. (nih.gov)
- This live virtual TeleECHO educational series targets healthcare gaps related to the familiarity and understanding of CDK4/6 inhibitor clinical trial designs and results on efficacy, safety, and real-world studies, impacting outcomes through current practice patterns and treatment strategies in the management of HR+/HER2- metastatic breast cancer (mBC). (medlearninggroup.com)
- You will also be immersed in interactive, animated simulation case studies to memorably highlight key points related to the mechanism of action of CDK4/6 inhibitors and their related safety profiles. (medlearninggroup.com)
- Multiplexed relative and absolute quantitative immunopeptidomics reveals MHC I repertoire alterations induced by CDK4/6 inhibition. (nih.gov)
- Applying this platform in melanoma cell lines to profile the immunopeptidome response to CDK4/6 inhibition and interferon-γ - known modulators of antigen presentation - uncovers treatment-specific alterations, connecting the intracellular response to extracellular immune presentation. (nih.gov)
- 1. Approaching Use of CDK4/6 Inhibitors in Metastatic HR+, HER2- Breast Cancer. (nih.gov)
- 2. Comparative Efficacy of CDK4/6 Inhibitors Plus Aromatase Inhibitors Versus Fulvestrant for the First-Line Treatment of Hormone Receptor-Positive Advanced Breast Cancer: A Network Meta-Analysis. (nih.gov)
- 3. CDK4/6 and PI3K inhibitors: A new promise for patients with HER2-positive breast cancer. (nih.gov)
- 4. Abemaciclib: a CDK4/6 inhibitor for the treatment of HR+/HER2- advanced breast cancer. (nih.gov)
- 7. CDK4/6 inhibitor treatment for patients with hormone receptor-positive, HER2-negative, advanced or metastatic breast cancer: a US Food and Drug Administration pooled analysis. (nih.gov)
- 10. The impact of cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6i) on the incidence of alopecia in patients with metastatic breast cancer (BC). (nih.gov)
- 11. Targeting CDK4/6 pathways and beyond in breast cancer. (nih.gov)
- 18. Selecting the optimal position of CDK4/6 inhibitors in hormone receptor-positive advanced breast cancer - the SONIA study: study protocol for a randomized controlled trial. (nih.gov)
- Concurrent inhibition of CDK2 adds to the anti-tumour activity of CDK4/6 inhibition in GIST. (harvard.edu)
- Regulation of PRMT5-MDM4 axis is critical in the response to CDK4/6 inhibitors in melanoma. (harvard.edu)
- This protein has been shown to interact with CDK4 or CDK6, and prevent the activation of the CDK kinases, thus function as a cell growth regulator that controls cell cycle G1 progression. (nih.gov)
- One example is the closely related cyclin-dependent kinases 4 and 6 (CDK4/6). (sflorg.com)
- Many kinases, particularly cell cycle proteins such as CDK4/6, are drivers of cancer cell proliferation and drug resistance. (sflorg.com)
- The researchers took these new insights to dissect the prototypical convergent kinase pair, CDK4/6, which are closely related family members that phosphorylate the retinoblastoma protein (RB) and share overlapping phosphorylation sites. (sflorg.com)
- In most contexts, the presence of either CDK4 or CDK6 is sufficient to phosphorylate RB to levels that prohibit analysis of the activity of the other kinase. (sflorg.com)
- Also, there are CDK4/6 inhibitors, but not any specific to CDK6 or CDK4 alone, which makes it technically difficult to study them individually. (sflorg.com)
- The addition of a CDK4/6 inhibitor that has previously been shown to drive CDK6-mediated inhibitor resistance in breast cancer cells was employed. (sflorg.com)
- High-throughput screening identified the imidazo[1,2-a]pyridine and bisanilinopyrimidine series as inhibitors of the cyclin-dependent kinase CDK4. (rcsb.org)
- CDK4/6 inhibitors are a class of drugs that target particular enzymes, called CDK4 and CDK6. (drugs.com)
- CDK4/6 inhibitors interrupt signals that stimulate the proliferation of malignant (cancerous) cells. (drugs.com)
- Certain cancers, for example, hormone receptor-positive breast cancer , are more likely to have disturbances in CDK4/6, and CDK 4/6 inhibitors may form part of the treatment protocol. (drugs.com)
- Most often, CDK4/6 inhibitors are given synergistically with hormonal therapy (such as an aromatase inhibitor or fulvestrant), although the CDK4/6 inhibitor abemaciclib may be used alone to treat hormone receptor-positive, HER2-negative metastatic breast cancer in pre-treated patients. (drugs.com)
- Research shows CDK4/6 inhibitors increase the time people have before cancer spreads (progression-free survival). (drugs.com)
- In general, the side effects associated with CDK4/6 inhibitor therapy are less severe than those experienced with chemotherapy. (drugs.com)
- Kevin Kalinsky, MD, MS, spoke about future studies following results from the phase 2 MAINTAIN trial of ribociclib with or without endocrine therapy and after progression on a CDK4/6 inhibitor for patients with unresectable or metastatic hormone receptor-positive, HER2-negative breast cancer. (cancernetwork.com)
- Kalinsky also discussed the limitations for single-agent treatment in the post-CDK4/6 setting, and the benefit of the MAINTAIN regimen in this setting. (cancernetwork.com)
- If we look at patients after they've had a CDK4/6 inhibitor, giving a single agent hormonal therapy, the median progression-free survival in this study was about 2.76 months [in the placebo arm]. (cancernetwork.com)
- The other thing I want to mention just in terms of CDK4/6 inhibitors after a CDK4/6 inhibitor is that it's promising to see that all the observational data and preclinical data, that we've seen is in a randomized trial. (cancernetwork.com)
- This is the first proof of principle study demonstrating that there is benefit of CDK4/6 inhibition after CDK4/6 inhibition, and also understanding that we're waiting for other randomized trials. (cancernetwork.com)
- When combined with endocrine therapy, which blocks hormone receptors on cancer cells so that they don't grow and multiply uncontrollably, CDK4/6 inhibitors significantly increase progression-free survival, or the time it takes before the cancer spreads further, in women with advanced metastatic breast cancer who are hormone-receptor positive, like Hassen. (everydayhealth.com)
- The study is intended to show superiority of AZD9833 in combination with CDK4/6 inhibitor (palbociclib or abemaciclib) versus aromatase inhibitors (anastrozole or letrozole) in combination with CDK4/6 inhibitor in patients with hormone receptor-positive (HR-positive), human epidermal growth factor receptor 2-negative (HER2-negative) metastatic breast cancer with detectable ESR1 mutation. (mayo.edu)
- SHR6390 (Jiangsu HengRui Medicine) is Cyclin-dependent kinases 4 and 6 (CDK4/6) of cell cycle progression and are dysregulated in cancers. (delveinsight.com)
- Inhibition of CDK4/6 induces G1 phase cell cycle arrest, therefore retards tumour growth. (delveinsight.com)
- CDK4 and 6 are serine/threonine kinases that are up-regulated in many tumour cell types and play a vital role in the regulation of cell cycle progression. (delveinsight.com)
- Cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors have more recently become an important component of the management of this breast cancer subtype, significantly delaying time to the disease progres- sion and improving survival when combined with endocrine therapy. (her2support.org)
- As more women receive CDK4/6 inhibitors as part of their treatment, the management of de novo and acquired resistance to combined CDK4/CDK6 inhibitor plus endocrine therapy regimens has emerged as an important clinical chal- lenge. (her2support.org)
- Several resistance mechanisms have been described, including alterations in the CDK4/6/cyclin D complex or its major effector retinoblastoma protein(pRb), bypass signaling through other cyclin/CDK complexes and activation of upstream signaling pathways, in particular the PI3K/mTOR pathway, but robust biomarkers to predict resistance remain elusive, and the role for continuing CDK4/6 inhibitors after progression remains under investigation. (her2support.org)
- Novel strategies being evaluated in clinical trials include the continuation of CDK4/6 inhibitors through progression, as well as triplet therapy combinations with PI3K inhibitors or immune checkpoint inhibitors. (her2support.org)
- Beyond CDK4/6 Inhibitors: What Subsequent Treatment Is Best? (her2support.org)
- It has been 14 years since a collaboration between the University of California, Los Angeles (UCLA) and Pfizer identified a unique role for cyclin-dependent kinase 4/6 (CDK4/6) inhibitors in estrogen receptor (ER)-positive human cell line models and demonstrated that these agents act synergistically with agents targeting the ER pathway. (ascopost.com)
- 1 This work led to the proof-of-concept PALOMA-1 study, which for the first time demonstrated a significant improvement in progression-free survival in postmenopausal women with advanced ER-positive/HER2-negative breast cancer treated with the combination of a CDK4/6 inhibitor-palbociclib-and letrozole vs letrozole alone. (ascopost.com)
- They have since been validated in eight phase III randomized, placebo-controlled studies in advanced ER-positive/HER2-negative breast cancer with three different CDK4/6 inhibitors-palbociclib, ribociclib, and abemaciclib-in various lines of therapy and in different patient populations. (ascopost.com)
- Although the progression-free survival of the control arms differed slightly from study to study, based on differences in the inclusion/exclusion criteria and study populations, all of them showed remarkably similar magnitudes of benefit, with hazard ratios in the 0.5 range for the combination of endocrine therapy with a CDK4/6 inhibitor vs endocrine therapy alone. (ascopost.com)
- All three CDK4/6 inhibitors cause the "on-target" effect of neutropenia, to some degree, but each differs somewhat in its adverse-event profile. (ascopost.com)
- This improvement occurred despite a significant number of patients on the control arm receiving a CDK4/6 inhibitor after disease progression on front-line therapy-34.4% in the control arm vs 21.7% in the ribociclib group. (ascopost.com)
- MONALEESA-2 is the first of three trials combining CDK4/6 inhibitors with nonsteroidal aromatase inhibitors in the first-line postmenopausal population to report overall survival data. (ascopost.com)
Inhibition3
- 9. Cyclin-dependent kinase inhibition: an opportunity to target protein-protein interactions. (nih.gov)
- 8. Inhibition of cyclin-dependent kinases 4 and 6 in breast cancer. (nih.gov)
- A randomized, phase II trial of fulvestrant or exemestane with or without ribociclib after progression on anti-estrogen therapy plus cyclin-dependent kinase 4/6 inhibition (CDK 4/6i) in patients (pts) with unresectable or hormone receptor-positive (HR+), HER2-negative metastatic breast cancer (MBC): MAINTAIN trial. (cancernetwork.com)
Palbociclib4
- 5. Cyclin-dependent protein kinase inhibitors including palbociclib as anticancer drugs. (nih.gov)
- Since palbociclib was approved, CDK 4/6 inhibitors have become the recommended first-line treatment for most people with advanced or metastatic hormone receptor-positive, HER2-negative breast cancer. (lbbc.org)
- Medicines like palbociclib are called CDK 4/6 inhibitors because they block these proteins from signaling cancer cells to multiply, which helps slow the growth or spread of the cancer. (lbbc.org)
- Palbociclib is in a class of medications called kinase inhibitors. (medlineplus.gov)
Ribociclib2
- KISQALI FEMARA CO-PACK, a co-packaged product containing ribociclib, a kinase inhibitor, and letrozole, an aromatase inhibitor, is indicated as initial endocrine-based therapy for the treatment of adult patients with hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced or metastatic breast cancer. (nih.gov)
- 6. Ribociclib for the treatment of advanced hormone receptor-positive, HER2-negative breast cancer. (nih.gov)
Protein5
- Cyclin-dependent kinase 6 associates with CYCLIN D and phosphorylates RETINOBLASTOMA PROTEIN during G1 PHASE of the CELL CYCLE. (nih.gov)
- 3. Dual action of the inhibitors of cyclin-dependent kinases: targeting of the cell-cycle progression and activation of wild-type p53 protein. (nih.gov)
- It partners with CYCLIN E to regulate entry into S PHASE and also interacts with CYCLIN A to phosphorylate RETINOBLASTOMA PROTEIN. (harvard.edu)
- From NCBI Gene: The protein encoded by this gene is a member of the INK4 family of cyclin-dependent kinase inhibitors. (nih.gov)
- The assay can be used for a range of purposes such as understanding the effect of protein modulators on CDK6 function, testing engineered versions of the kinase, or studying the effects of mutations that may be involved in driving disease. (sflorg.com)
Metastatic hormone receptor-positive brea1
- 14. Cyclin-dependent kinase 4/6 inhibitors as first-line treatment for post-menopausal metastatic hormone receptor-positive breast cancer patients: a systematic review and meta-analysis of phase III randomized clinical trials. (nih.gov)
Inhibitors are a class1
- CDK 4/6 inhibitors are a class of prescription medicines that are used in combination with hormone therapies to treat adults with hormone receptor (HR)-positive, human epidermal growth factor 2 (HER2)-negative advanced or metastatic breast cancer that has spread to other parts of the body. (medlineplus.gov)
Proteins5
- Kinases are a specific family of proteins that add phosphates to other molecules - a process called phosphorylation, which can change the function of their substrates (target proteins). (sflorg.com)
- In humans, more than 500 kinases phosphorylate approximately 15% of all proteins. (sflorg.com)
- Understanding the complex kinase network is important, as dysregulation of these proteins can drive disease, such as the survival and spread of cancer cells or their resistance to therapeutics. (sflorg.com)
- It is a cyclin-dependent kinase 4/6 (CDK 4/6) inhibitor, which means it targets two specific kinases, or proteins, that help tumor cells reproduce. (lbbc.org)
- Cyclin-dependent kinases 4 and 6 are two proteins that help some breast cancers to grow. (lbbc.org)
Enzymes1
- Clearer understanding about the markers and drivers of cancer cell proliferation has emerged from research that identifies new opportunities to overcome convergence with complex enzymes, known as kinases. (sflorg.com)
Serine1
- For instance, convergent serine/threonine kinases are co-expressed in more than 70% of the study's analyzed human cell lines. (sflorg.com)
Inhibitor treatment2
- CDK6 over-expression combined with inhibitor treatment resulted in detection of CDK6-dependent RB phosphorylation. (sflorg.com)
- Interrupt CDK 4/6 inhibitor treatment in patients who have new or worsening respiratory symptoms, and permanently discontinue treatment in patients with severe ILD and/or pneumonitis. (medlineplus.gov)
Modulators1
- 6. Cyclin-dependent kinase modulators and cancer therapy. (nih.gov)
Endocrine Therapy1
- Progression-Free Survival and Overall Survival of CDK 4/6 Inhibitors Plus Endocrine Therapy in Metastatic Breast Cancer: A Systematic Review and Meta-Analysis. (drugs.com)
Induces2
- 6]-Gingerol induces cell cycle arrest and cell death of mutant p53-expressing pancreatic cancer cells. (greenmedinfo.com)
- Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2-mediated activation of forkhead box O1. (harvard.edu)
Pathways2
- The research also identified signaling pathways where reciprocal phosphorylation loops occur, when the substrate of a kinase can phosphorylate that kinase. (sflorg.com)
- Phosphoproteomic Analysis of FLCN Inactivation Highlights Differential Kinase Pathways and Regulatory TFEB Phosphoserines. (cellsignal.com)
MeSH1
- Cyclin-Dependent Kinase 2" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
20161
- 2. Investigational drugs targeting cyclin-dependent kinases for the treatment of cancer: an update on recent findings (2013-2016). (nih.gov)
Cancers3
- 4. Targeting Cyclin-Dependent Kinases and Cell Cycle Progression in Human Cancers. (nih.gov)
- 8. An insight into the emerging role of cyclin-dependent kinase inhibitors as potential therapeutic agents for the treatment of advanced cancers. (nih.gov)
- The requirement for cyclin E in c-Myc overexpressing breast cancers. (harvard.edu)
Patients2
- Interstitial Lung Disease (ILD)/Pneumonitis: Patients treated with CDK 4/6 inhibitors should be monitored for pulmonary symptoms indicative of ILD/pneumonitis. (nih.gov)
- the epidemiology and outcome of patients with LM from ER + HER2-ABC thus remain unclear because of the notably poor outcome compared with BM [ 6 - 9 ].Therefore, in the present study, we retrospectively investigated the actual situation of ER + HER2-ABC patients with LM in a single institute. (researchsquare.com)
Hormone receptor positi1
- 16. CDK 4/6 inhibitors and stereotactic radiation in the management of hormone receptor positive breast cancer brain metastases. (nih.gov)
Gene2
- Lehmann et al 9 described 6 discrete subtypes of TNBC based on gene expression profiling: basal-like 1 (BL1), basal-like 2 (BL2), immunomodulatory (IM), mesenchymal (M), mesenchymal stem-like (MSL), and luminal androgen receptor (LAR). (jnccn.org)
- Genetic Association of rs2237572 Cyclin-Dependent Kinase 6 Gene with Breast Cancer in Iraq. (cdc.gov)
Potent2
PHASE2
- It helps regulate the transition to S PHASE and its kinase activity is inhibited by CYCLIN-DEPENDENT KINASE INHIBITOR P18. (nih.gov)
- We found that [6]-gingerol inhibited the cell growth through cell cycle arrest at G1 phase in both cell lines. (greenmedinfo.com)
Progression-Free Sur2
- CDK 4/6 inhibitors have been shown to improve the amount of time after the start of treatment the cancer does not grow substantially and the patient is alive, called progression-free survival (See List of FDA-Approved CDK 4/6 Inhibitors below). (medlineplus.gov)
- As previously mentioned, the study met its primary endpoint of improving progression-free survival (hazard ratio [HR] = 0.56, 95% confidence interval [CI] = 0.43-0.72, P = 3.29 × 10 −6 for superiority). (ascopost.com)
Phosphorylate1
- However, more than one kinase can phosphorylate the same substrate, and this can occur at the same or different sites. (sflorg.com)
HER21
- HR+/HER2- Metastatic Breast Cancer: What Can You Do to Optimize Patient Access to Cyclin-dependent Kinase 4 and 6 Inhibitors? (medlearninggroup.com)
Drugs1
- 11. The use of cyclin-dependent kinase inhibitors alone or in combination with established cytotoxic drugs in cancer chemotherapy. (nih.gov)
Clinical1
- 13. Cyclin-dependent kinase 4 and 6 inhibitors in hormone receptor-positive, human epidermal growth factor receptor-2 negative advanced breast cancer: a meta-analysis of randomized clinical trials. (nih.gov)
Treatment3
- Cyclin-dependent kinase (CDK) 4/6 inhibitors have become standard of care in the treatment of hormone receptor-positive, human epidermal growth factor receptor 2-negative metastatic breast cancer. (nih.gov)
- 19. Cyclin-dependent kinase inhibitors for the treatment of chronic lymphocytic leukemia. (nih.gov)
- p53 expression was decreased by [6]-gingerol treatment in both cell lines suggesting that the induction of Cyclin-dependent kinase inhibitor, p21cip1, was p53-independent. (greenmedinfo.com)
Therapy3
- 1. Targeting cyclin-dependent kinases in anti-neoplastic therapy. (nih.gov)
- 15. Cyclin-dependent kinase inhibitors for cancer therapy: a patent review (2009 - 2014). (nih.gov)
- 17. Use of cyclin-dependent kinase (CDK) 4/6 inhibitors for hormone receptor-positive, human epidermal growth factor receptor 2-negative, metastatic breast cancer: a roundtable discussion by The Breast Cancer Therapy Expert Group (BCTEG). (nih.gov)
Resistance2
- 15. Resistance to cyclin-dependent kinase (CDK) 4/6 inhibitors confers cross-resistance to other CDK inhibitors but not to chemotherapeutic agents in breast cancer cells. (nih.gov)
- These results suggest that [6]-gingerol can circumvent the resistance of mutant p53- expressing cells towards chemotherapy by inducing apoptotic cell death while it exerts cytostatic effect on wild type p53- expressing cells by inducing temporal growth arrest. (greenmedinfo.com)
Pneumonitis1
- And two drug classes on the list, cyclin-dependent kinase 4 and 6 (CDK 4 and CDK 6) inhibitors, showed potential links with interstitial lung disease/pneumonitis. (medscape.com)
Phosphorylation2
- 6]-Gingerol induced mostly apoptotic death in the mutant p53-expressing cells, while no signs of early apoptosis were detected in wild type p53-expressing cells and this was related to the increased phosphorylation of AKT. (greenmedinfo.com)
- While most kinase research has tended to focus on characterizing phosphorylation networks between kinases and their substrates, researchers in the Janovjak Lab at Flinders University's College of Medicine and Public Health have taken a different tack by analyzing how common convergence is across all human kinases, and using these insights to dissect it experimentally. (sflorg.com)
Cell5
- Controlling cell proliferation by targeting cyclin-dependent kinase 6 using drug repurposing approach. (bvsalud.org)
- Cyclin-dependent kinase 6 (CDK6) is an essential kinase in cell cycle progression, which is a viable target for inhibitors in various malignancies , including breast cancer . (bvsalud.org)
- 13. The Roles of Cyclin-Dependent Kinases in Cell-Cycle Progression and Therapeutic Strategies in Human Breast Cancer. (nih.gov)
- The purpose of this study was to investigate the action of [6]-gingerol on two human pancreatic cancer cell lines, HPAC expressing wild- type (wt) p53 and BxPC-3 expressing mutated p53. (greenmedinfo.com)
- CDK stands for cyclin-dependent kinase, and it is an enzyme that is important for cell division. (drugs.com)
Mechanisms1
- While several molecular mechanisms have been described to underlie its effects on cells in vitro and in vivo, the underlying mechanisms by which [6]-gingerol exerts anti-tumorigenic effects are largely unknown. (greenmedinfo.com)
Study2
- This is known as convergence, and can often make it difficult to study a specific kinase or substrate, as the activity of multiple kinases can hamper analysis. (sflorg.com)
- Our aim was to find new avenues to study them more effectively, as well as analyze and dissect convergence across all human kinases," says Christina Gangemi, a research associate at the Flinders Health and Medical Research Institute. (sflorg.com)