An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene.
Sarcoma 180 is an undifferentiated, transplantable mouse tumor model originally induced by methylcholanthrene, widely used in preclinical cancer research for evaluating efficacy of potential therapeutic agents.
Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.
Anaerobic degradation of GLUCOSE or other organic nutrients to gain energy in the form of ATP. End products vary depending on organisms, substrates, and enzymatic pathways. Common fermentation products include ETHANOL and LACTIC ACID.
A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.
Leukemia associated with HYPERPLASIA of the lymphoid tissues and increased numbers of circulating malignant LYMPHOCYTES and lymphoblasts.
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.
Species of GAMMARETROVIRUS, containing many well-defined strains, producing leukemia in mice. Disease is commonly induced by injecting filtrates of propagable tumors into newborn mice.
A neoplasm characterized by abnormalities of the lymphoid cell precursors leading to excessive lymphoblasts in the marrow and other organs. It is the most common cancer in children and accounts for the vast majority of all childhood leukemias.
A malignant disease of the T-LYMPHOCYTES in the bone marrow, thymus, and/or blood.
An acute myeloid leukemia in which 80% or more of the leukemic cells are of monocytic lineage including monoblasts, promonocytes, and MONOCYTES.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) arising during the propagation of S37 mouse sarcoma, and causing lymphoid leukemia in mice. It also infects rats and newborn hamsters. It is apparently transmitted to embryos in utero and to newborns through mother's milk.

BE-31405, a new antifungal antibiotic produced by Penicillium minioluteum. I. Description of producing organism, fermentation, isolation, physico-chemical and biological properties. (1/498)

A new antifungal antibiotic, BE-31405, was isolated from the culture broth of a fungal strain, Penicillium minioluteum F31405. BE-31405 was isolated by adsorption on high porous polymer resin (Diaion HP-20), followed by solvent extraction, precipitation and crystallization. BE-31405 showed potent growth inhibitory activity against pathogenic fungal strains such as Candida albicans, Candida glabrata and Cryptococcus neoformans, but did not show cytotoxic activity against mammalian cells such as P388 mouse leukemia. The mechanism studies indicated that BE-31405 inhibited the protein synthesis of C. albicans but not of mammalian cells.  (+info)

Relationship between circadian rhythm of vinorelbine toxicity and efficacy in P388-bearing mice. (2/498)

The relevance of chronopharmacology for improving tolerability and antitumor efficacy of the antimitotic drug vinorelbine was investigated in female B6D2F1 mice standardized with 12 h of light and 12 h of darkness. A single i.v. vinorelbine dose (26 mg/kg) was given to 279 mice at 7, 11, 19, or 23 hours after light onset (HALO). Bone marrow necrosis and leukopenia were nearly twice as large in the mice injected at 7 HALO as compared with those treated at 19 HALO (ANOVA: p <.001 and p = 0.004, respectively). The relevance of vinorelbine dosing time for antitumor efficacy was assessed in 672 P388 leukemia-bearing mice. Vinorelbine was injected as a single dose (20, 24, 26, or 30 mg/kg) or weekly (20, 24, 26, or 28 mg/kg/injection x 3) at one of six circadian times, 4 h apart. A significant correlation between single dose and median survival time was limited to vinorelbine administration at 19 or 23 HALO. An increase in the vinorelbine weekly dose shortened median survival time in the mice treated at 7 HALO (20 mg/kg: 29 days; 24 mg/kg: 17 days; and 26 mg/kg: 6 days) but significantly improved it in those treated at 19 HALO (20 mg/kg: 28.5 days; 24 mg/kg: 32 days; and 26 mg/kg: 36 days). The study demonstrates the circadian rhythm dependence of maximum tolerated dose and the need to deliver maximum tolerated dose at the least toxic time to achieve survival improvement through chronotherapy. This may be obtained with an evening administration of vinorelbine in cancer patients.  (+info)

New semisynthetic vinca alkaloids: chemical, biochemical and cellular studies. (3/498)

A new semisynthetic anti-tumour bis-indol compound, KAR-2 [3'-(beta-chloroethyl)-2',4'-dioxo-3,5'-spiro-oxazolidino-4-dea cetoxy-vinblastine] with lower toxicity than vinca alkaloids used in chemotherapy binds to calmodulin but, in contrast to vinblastine, does not exhibit anti-calmodulin activity. To investigate whether the modest chemical modification of bis-indol structure is responsible for the lack of anti-calmodulin potency and for the different pharmacological effects, new derivatives have been synthesized for comparative studies. The synthesis of the KAR derivatives are presented. The comparative studies showed that the spiro-oxazolidino ring and the substitution of a formyl group to a methyl one were responsible for the lack of anti-calmodulin activities. The new derivatives, similar to the mother compounds, inhibited the tubulin assembly in polymerization tests in vitro, however their inhibitory effect was highly dependent on the organization state of microtubules; bundled microtubules appeared to be resistant against the drugs. The maximal cytotoxic activities of KAR derivatives in in vivo mice hosting leukaemia P388 or Ehrlich ascites tumour cells appeared similar to that of vinblastine or vincristine, however significant prolongation of life span could be reached with KAR derivatives only after the administration of a single dose. These studies plus data obtained using a cultured human neuroblastoma cell line showed that KAR compounds displayed their cytotoxic activities at significantly higher concentrations than the mother compounds, although their antimicrotubular activities were similar in vitro. These data suggest that vinblastine/vincristine damage additional crucial cell functions, one of which could be related to calmodulin-mediated processes.  (+info)

Graft-versus-leukemia effect and graft-versus-host disease can be differentiated by cytotoxic mechanisms in a murine model of allogeneic bone marrow transplantation. (4/498)

Allogeneic bone marrow transplantation (allo-BMT) is associated with both graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL) effect. In the present study, we examined the contribution of cytotoxic effector mechanisms, which are mediated by tumor necrosis factor-alpha (TNF-alpha), Fas ligand (FasL), or perforin, to GVHD and GVL effect in a murine BMT model. Bone marrow cells plus spleen cells (BMS) from wild-type, FasL-defective, or perforin-deficient donors were transferred into lethally irradiated recipients in the parent (C57BL/6) to F1 (C57BL/6 x DBA/2) BMT model with or without prior inoculation of DBA/2 leukemia L1210 or P815 mast cytoma cells. The effect of anti-TNF-alpha antibody administration was also examined. Whereas the defect or blockade of each cytotoxic pathway could ameliorate lethal acute GVHD, the GVL effect was differentially affected. The wild-type BMS recipients died of acute GVHD within 50 days without residual leukemia cells. The FasL-defective BMS recipients showed 60%< survival over 80 days without acute GVHD or residual leukemia cells. Administration of anti-TNF-alpha antibody resulted in early leukemia relapse and the recipients died within 25 days with massive leukemia infiltration in the liver. The perforin-deficient BMS recipients died within 60 days with residual leukemia cells. These results suggest that blockade of the Fas/FasL pathway could be used for ameliorating GVHD without impairing GVL effect in allo-BMT.  (+info)

Cutting edge: receptor-mediated endocytosis of heat shock proteins by professional antigen-presenting cells. (5/498)

Immunization with heat shock proteins (HSPs) induces Ag-specific CTL responses. The specificity of the immune response is based on peptides associated with HSPs. To investigate how exogenous HSP/peptide complexes gain access to the MHC class I-restricted Ag presentation pathway, we incubated the monocytic cell line P388D1 and the dendritic cell line D2SC/1 with gold-labeled HSPs gp96 and HSC70. We show that HSPs bind specifically to the surface of these APCs and are internalized spontaneously by receptor-mediated endocytosis, demonstrating the existence of specific receptors for HSPs on these cells. In addition, we observe colocalization of internalized HSPs and surface MHC class I molecules in early and late endosomal structures. These findings provide possible explanations for the immunogenicity of HSP/peptide complexes and for the transfer of HSP-associated peptides onto MHC class I molecules.  (+info)

Enhancement of the Listeria monocytogenes p60-specific CD4 and CD8 T cell memory by nonpathogenic Listeria innocua. (6/498)

The contact of T cells to cross-reactive antigenic determinants expressed by nonpathogenic environmental micro-organisms may contribute to the induction or maintenance of T cell memory. This hypothesis was evaluated in the model of murine Listeria monocytogenes infection. The influence of nonpathogenic L. innocua on the L. monocytogenes p60-specific T cell response was analyzed. We show that some CD4 T cell clones raised against purified p60 from L. monocytogenes cross-react with p60 purified from L. innocua. The L. monocytogenes p60-specific CD4 T cell clone 1A recognized the corresponding L. innocua p60 peptide QAAKPAPAPSTN, which differs only in the first amino acid residue. In vitro experiments revealed that after L. monocytogenes infection of APCs, MHC class I-restricted presentation of p60 occurs, while MHC class II-restricted p60 presentation is inhibited. L. innocua-infected cells presented p60 more weakly but equally well in the context of both MHC class I and MHC class II. In contrast to these in vitro experiments the infection of mice with L. monocytogenes induced a strong p60-specific CD4 and CD8 T cell response, while L. innocua infection failed to induce p60-specific T cells. L. innocua booster infection, however, expanded p60-specific memory T cells induced by previous L. monocytogenes infection. In conclusion, these findings suggest that infection with a frequently occurring environmental bacterium such as L. innocua, which is nonpathogenic and not adapted to intracellular replication, can contribute to the maintenance of memory T cells specific for a related intracellular pathogen.  (+info)

Regulation of delayed prostaglandin production in activated P388D1 macrophages by group IV cytosolic and group V secretory phospholipase A2s. (7/498)

Group V secretory phospholipase A2 (sPLA2) rather than Group IIA sPLA2 is involved in short term, immediate arachidonic acid mobilization and prostaglandin E2 (PGE2) production in the macrophage-like cell line P388D1. When a new clone of these cells, P388D1/MAB, selected on the basis of high responsivity to lipopolysaccharide plus platelet-activating factor, was studied, delayed PGE2 production (6-24 h) in response to lipopolysaccharide alone occurred in parallel with the induction of Group V sPLA2 and cyclooxygenase-2 (COX-2). No changes in the level of cytosolic phospholipase A2 (cPLA2) or COX-1 were observed, and Group IIA sPLA2 was not detectable. Use of a potent and selective sPLA2 inhibitor, 3-(3-acetamide 1-benzyl-2-ethylindolyl-5-oxy)propanesulfonic acid (LY311727), and an antisense oligonucleotide specific for Group V sPLA2 revealed that delayed PGE2 was largely dependent on the induction of Group V sPLA2. Also, COX-2, not COX-1, was found to mediate delayed PGE2 production because the response was completely blocked by the specific COX-2 inhibitor NS-398. Delayed PGE2 production and Group V sPLA2 expression were also found to be blunted by the inhibitor methylarachidonyl fluorophosphonate. Because inhibition of Ca2+-independent PLA2 by an antisense technique did not have any effect on the arachidonic acid release, the data using methylarachidonyl fluorophosphonate suggest a key role for the cPLA2 in the response as well. Collectively, the results suggest a model whereby cPLA2 activation regulates Group V sPLA2 expression, which in turn is responsible for delayed PGE2 production via COX-2.  (+info)

Apoptosis induction via microtubule disassembly by an antitumour compound, pironetin. (8/498)

We reported previously that pironetin and its derivatives were potent inhibitors of cell cycle progression at the M-phase and showed antitumour activity against a murine tumour cell line, P388 leukaemia, transplanted in mice. In this paper, we investigated the mechanism of action of pironetins in antitumour activity and cell cycle arrest at the M-phase. As reported previously for murine leukaemia P388 cells, pironetin showed antitumour activity in a dose-dependent manner in the human leukaemia cell line HL-60. Since DNA fragmentation was observed in both P388 and HL-60 cells, the antitumour activity of pironetin is thought to be due to the induction of apoptosis. Pironetin also induced the rapid phosphorylation of Bcl-2 before formation of the DNA ladder in HL-60 cells, as seen with several tubulin binders. These results suggest that the antitumour activity of pironetin is due to apoptosis caused by the phosphorylation of Bcl-2, and that pironetin targets the microtubules. Pironetin and demethylpironetin exhibited reversible disruption of the cellular microtubule network in normal rat fibroblast 3Y1 cells. However, epoxypironetin, which contains epoxide instead of the double bond of pironetin, showed only weak activity. Since the concentrations that inhibit cell cycle progression at the M-phase were the same as those for disruption of the microtubule network, it was suggested that the mitotic arrest induced by pironetin was the result of the loss of the mitotic spindle. These compounds also inhibited the microtubule-associated protein-induced and glutamate-induced tubulin assembly in vitro. Pironetin inhibited the binding of [3H]vinblastine, but not that of [3H]colchicine, to tubulin, and the Kd values revealed that the affinity of pironetin for tubulin is stronger than that of vinblastine. These results suggest that pironetins are novel antitumour agents which inhibit microtubule assembly.  (+info)

I'm sorry for any confusion, but "Leukemia P388" is not a widely recognized medical term or a specific type of leukemia. The term "P388" is often used to refer to a particular type of mouse leukemia that is commonly used in laboratory research for testing potential anti-cancer drugs.

Leukemia, in general, is a type of cancer that originates in the bone marrow and results in an overproduction of abnormal white blood cells (leukocytes). These abnormal cells crowd out the healthy cells in the bone marrow, leading to a weakened immune system and various complications.

There are many different types of leukemia, classified based on the type of white blood cell affected (myeloid or lymphocytic) and the speed of progression (acute or chronic). If you're looking for information about a specific type of leukemia, I would be happy to help if you could provide more details.

I'm sorry for any confusion, but "Sarcoma 180" is not a recognized medical term or an official classification of sarcomas in humans. It appears to be a term used primarily in research involving mice. Sarcoma 180 is a transplantable tumor that was first isolated from a mouse and has been used as a model for cancer research, particularly in studies involving immunotherapy and cancer treatment.

In general, sarcomas are cancers that develop from connective tissues such as bones, muscles, tendons, cartilages, nerves, and blood vessels. They can be further classified into various subtypes based on the specific type of tissue they originate from and their genetic characteristics. If you have any concerns about a specific medical condition or term, I would recommend consulting with a healthcare professional for accurate information.

Experimental leukemia refers to the stage of research or clinical trials where new therapies, treatments, or diagnostic methods are being studied for leukemia. Leukemia is a type of cancer that affects the blood and bone marrow, leading to an overproduction of abnormal white blood cells.

In the experimental stage, researchers investigate various aspects of leukemia, such as its causes, progression, and potential treatments. They may conduct laboratory studies using cell cultures or animal models to understand the disease better and test new therapeutic approaches. Additionally, clinical trials may be conducted to evaluate the safety and efficacy of novel treatments in human patients with leukemia.

Experimental research in leukemia is crucial for advancing our understanding of the disease and developing more effective treatment strategies. It involves a rigorous and systematic process that adheres to ethical guidelines and scientific standards to ensure the validity and reliability of the findings.

Antibiotics are a type of medication used to treat infections caused by bacteria. They work by either killing the bacteria or inhibiting their growth.

Antineoplastics, also known as chemotherapeutic agents, are a class of drugs used to treat cancer. These medications target and destroy rapidly dividing cells, such as cancer cells, although they can also affect other quickly dividing cells in the body, such as those in the hair follicles or digestive tract, which can lead to side effects.

Antibiotics and antineoplastics are two different classes of drugs with distinct mechanisms of action and uses. It is important to use them appropriately and under the guidance of a healthcare professional.

Leukemia is a type of cancer that originates from the bone marrow - the soft, inner part of certain bones where new blood cells are made. It is characterized by an abnormal production of white blood cells, known as leukocytes or blasts. These abnormal cells accumulate in the bone marrow and interfere with the production of normal blood cells, leading to a decrease in red blood cells (anemia), platelets (thrombocytopenia), and healthy white blood cells (leukopenia).

There are several types of leukemia, classified based on the specific type of white blood cell affected and the speed at which the disease progresses:

1. Acute Leukemias - These types of leukemia progress rapidly, with symptoms developing over a few weeks or months. They involve the rapid growth and accumulation of immature, nonfunctional white blood cells (blasts) in the bone marrow and peripheral blood. The two main categories are:
- Acute Lymphoblastic Leukemia (ALL) - Originates from lymphoid progenitor cells, primarily affecting children but can also occur in adults.
- Acute Myeloid Leukemia (AML) - Develops from myeloid progenitor cells and is more common in older adults.

2. Chronic Leukemias - These types of leukemia progress slowly, with symptoms developing over a period of months to years. They involve the production of relatively mature, but still abnormal, white blood cells that can accumulate in large numbers in the bone marrow and peripheral blood. The two main categories are:
- Chronic Lymphocytic Leukemia (CLL) - Affects B-lymphocytes and is more common in older adults.
- Chronic Myeloid Leukemia (CML) - Originates from myeloid progenitor cells, characterized by the presence of a specific genetic abnormality called the Philadelphia chromosome. It can occur at any age but is more common in middle-aged and older adults.

Treatment options for leukemia depend on the type, stage, and individual patient factors. Treatments may include chemotherapy, targeted therapy, immunotherapy, stem cell transplantation, or a combination of these approaches.

Acute myeloid leukemia (AML) is a type of cancer that originates in the bone marrow, the soft inner part of certain bones where new blood cells are made. In AML, the immature cells, called blasts, in the bone marrow fail to mature into normal blood cells. Instead, these blasts accumulate and interfere with the production of normal blood cells, leading to a shortage of red blood cells (anemia), platelets (thrombocytopenia), and normal white blood cells (leukopenia).

AML is called "acute" because it can progress quickly and become severe within days or weeks without treatment. It is a type of myeloid leukemia, which means that it affects the myeloid cells in the bone marrow. Myeloid cells are a type of white blood cell that includes monocytes and granulocytes, which help fight infection and defend the body against foreign invaders.

In AML, the blasts can build up in the bone marrow and spread to other parts of the body, including the blood, lymph nodes, liver, spleen, and brain. This can cause a variety of symptoms, such as fatigue, fever, frequent infections, easy bruising or bleeding, and weight loss.

AML is typically treated with a combination of chemotherapy, radiation therapy, and/or stem cell transplantation. The specific treatment plan will depend on several factors, including the patient's age, overall health, and the type and stage of the leukemia.

Fermentation is a metabolic process in which an organism converts carbohydrates into alcohol or organic acids using enzymes. In the absence of oxygen, certain bacteria, yeasts, and fungi convert sugars into carbon dioxide, hydrogen, and various end products, such as alcohol, lactic acid, or acetic acid. This process is commonly used in food production, such as in making bread, wine, and beer, as well as in industrial applications for the production of biofuels and chemicals.

Chronic lymphocytic leukemia (CLL) is a type of cancer that starts from cells that become certain white blood cells (called lymphocytes) in the bone marrow. The cancer (leukemia) cells start in the bone marrow but then go into the blood.

In CLL, the leukemia cells often build up slowly. Many people don't have any symptoms for at least a few years. But over time, the cells can spread to other parts of the body, including the lymph nodes, liver, and spleen.

The "B-cell" part of the name refers to the fact that the cancer starts in a type of white blood cell called a B lymphocyte or B cell. The "chronic" part means that this leukemia usually progresses more slowly than other types of leukemia.

It's important to note that chronic lymphocytic leukemia is different from chronic myelogenous leukemia (CML). Although both are cancers of the white blood cells, they start in different types of white blood cells and progress differently.

Leukemia, lymphoid is a type of cancer that affects the lymphoid cells, which are a vital part of the body's immune system. It is characterized by the uncontrolled production of abnormal white blood cells (leukocytes or WBCs) in the bone marrow, specifically the lymphocytes. These abnormal lymphocytes accumulate and interfere with the production of normal blood cells, leading to a decrease in red blood cells (anemia), platelets (thrombocytopenia), and healthy white blood cells (leukopenia).

There are two main types of lymphoid leukemia: acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL). Acute lymphoblastic leukemia progresses rapidly, while chronic lymphocytic leukemia has a slower onset and progression.

Symptoms of lymphoid leukemia may include fatigue, frequent infections, easy bruising or bleeding, weight loss, swollen lymph nodes, and bone pain. Treatment options depend on the type, stage, and individual patient factors but often involve chemotherapy, radiation therapy, targeted therapy, immunotherapy, or stem cell transplantation.

Chronic myelogenous leukemia (CML), BCR-ABL positive is a specific subtype of leukemia that originates in the bone marrow and involves the excessive production of mature granulocytes, a type of white blood cell. It is characterized by the presence of the Philadelphia chromosome, which is formed by a genetic translocation between chromosomes 9 and 22, resulting in the formation of the BCR-ABL fusion gene. This gene encodes for an abnormal protein with increased tyrosine kinase activity, leading to uncontrolled cell growth and division. The presence of this genetic abnormality is used to confirm the diagnosis and guide treatment decisions.

Medical Definition:

Murine leukemia virus (MLV) is a type of retrovirus that primarily infects and causes various types of malignancies such as leukemias and lymphomas in mice. It is a complex genus of viruses, with many strains showing different pathogenic properties.

MLV contains two identical single-stranded RNA genomes and has the ability to reverse transcribe its RNA into DNA upon infection, integrating this proviral DNA into the host cell's genome. This is facilitated by an enzyme called reverse transcriptase, which MLV carries within its viral particle.

The virus can be horizontally transmitted between mice through close contact with infected saliva, urine, or milk. Vertical transmission from mother to offspring can also occur either in-utero or through the ingestion of infected breast milk.

MLV has been extensively studied as a model system for retroviral pathogenesis and tumorigenesis, contributing significantly to our understanding of oncogenes and their role in cancer development. It's important to note that Murine Leukemia Virus does not infect humans.

Precursor Cell Lymphoblastic Leukemia-Lymphoma (previously known as Precursor T-lymphoblastic Leukemia/Lymphoma) is a type of cancer that affects the early stages of T-cell development. It is a subtype of acute lymphoblastic leukemia (ALL), which is characterized by the overproduction of immature white blood cells called lymphoblasts in the bone marrow, blood, and other organs.

In Precursor Cell Lymphoblastic Leukemia-Lymphoma, these abnormal lymphoblasts accumulate primarily in the lymphoid tissues such as the thymus and lymph nodes, leading to the enlargement of these organs. This subtype is more aggressive than other forms of ALL and has a higher risk of spreading to the central nervous system (CNS).

The medical definition of Precursor Cell Lymphoblastic Leukemia-Lymphoma includes:

1. A malignant neoplasm of immature T-cell precursors, also known as lymphoblasts.
2. Characterized by the proliferation and accumulation of these abnormal cells in the bone marrow, blood, and lymphoid tissues such as the thymus and lymph nodes.
3. Often associated with chromosomal abnormalities, genetic mutations, or aberrant gene expression that contribute to its aggressive behavior and poor prognosis.
4. Typically presents with symptoms related to bone marrow failure (anemia, neutropenia, thrombocytopenia), lymphadenopathy (swollen lymph nodes), hepatosplenomegaly (enlarged liver and spleen), and potential CNS involvement.
5. Diagnosed through a combination of clinical evaluation, imaging studies, and laboratory tests, including bone marrow aspiration and biopsy, immunophenotyping, cytogenetic analysis, and molecular genetic testing.
6. Treated with intensive multi-agent chemotherapy regimens, often combined with radiation therapy and/or stem cell transplantation to achieve remission and improve survival outcomes.

Leukemia, T-cell is a type of cancer that affects the T-cells or T-lymphocytes, which are a type of white blood cells responsible for cell-mediated immunity. It is characterized by an excessive and uncontrolled production of abnormal T-cells in the bone marrow, leading to the displacement of healthy cells and impairing the body's ability to fight infections and regulate immune responses.

T-cell leukemia can be acute or chronic, depending on the rate at which the disease progresses. Acute T-cell leukemia progresses rapidly, while chronic T-cell leukemia has a slower course of progression. Symptoms may include fatigue, fever, frequent infections, weight loss, easy bruising or bleeding, and swollen lymph nodes. Treatment typically involves chemotherapy, radiation therapy, stem cell transplantation, or targeted therapy, depending on the type and stage of the disease.

Acute Monocytic Leukemia (AML-M5) is a subtype of acute myeloid leukemia (AML), which is a type of cancer affecting the blood and bone marrow. In AML-M5, there is an overproduction of abnormal monocytes, a type of white blood cell that normally helps fight infection and is involved in the body's immune response. These abnormal monocytes accumulate in the bone marrow and interfere with the production of normal blood cells, leading to symptoms such as fatigue, frequent infections, and easy bruising or bleeding. The disease progresses rapidly without treatment, making it crucial to begin therapy as soon as possible after diagnosis.

The Moloney murine leukemia virus (Mo-MLV) is a type of retrovirus, specifically a gammaretrovirus, that is commonly found in mice. It was first discovered and isolated by John Moloney in 1960. Mo-MLV is known to cause various types of cancerous conditions, particularly leukemia, in susceptible mouse strains.

Mo-MLV has a single-stranded RNA genome that is reverse transcribed into double-stranded DNA upon infection of the host cell. This viral DNA then integrates into the host's genome and utilizes the host's cellular machinery to produce new virus particles. The Mo-MLV genome encodes for several viral proteins, including gag (group-specific antigen), pol (polymerase), and env (envelope) proteins, which are essential for the replication cycle of the virus.

Mo-MLV is widely used in laboratory research as a model retrovirus to study various aspects of viral replication, gene therapy, and oncogenesis. It has also been engineered as a vector for gene delivery applications due to its ability to efficiently integrate into the host genome and deliver large DNA sequences. However, it is important to note that Mo-MLV and other retroviruses have the potential to cause insertional mutagenesis, which can lead to unintended genetic alterations and adverse effects in some cases.

ran an in vivo study on arglabin and reported its ability to inhibit DNA synthesis of the P388 lymphocytic leukemia cells. In ... "Sesquiterpene Lactone Arglabin Influences DNA Synthesis in P388 Leukemia Cells in vivo". Pharmaceutical Chemistry Journal. 38 ( ... a Source To Discover Agents That Selectively Inhibit Acute Myelogenous Leukemia Stem and Progenitor Cells". Journal of ... 2012, Yindgai Gao and Yue Chen tested arglabin for biological activity against acute myelogenous leukemia (AML). Their results ...
Additionally, nardosinone has demonstrated cytotoxic activity against cultured P-388 lymphocytic leukemia cells. Schulte KE, ...
For example, the response of mice with P-388 lymphocytic leukemia to injections of debromoaplysiatoxin. The result was that the ... Debromoaplysiatoxin has activity against P-388 mouse lymphatic leukaemia and was found to cause dermatitis. It has been found ...
In cell cultures, it has shown cytotoxicity against the experimental lymphocytic leukemia P388 cell line. It exhibits strong ...
The sterol is cytotoxic to mouse P388 leukemia cells and A549 human alveolar epithelial cells grown in culture. Bills CE, ...
When administered orally the results showed prolongation of life expectancy and curing of L1210 and P388 leukemia in lab rats. ... Along with anti-septic properties, ambazone has also shown its ability to fight forms of leukemia in lab rats. ...
500nM against P388 leukemia cells). It is an antineoplastic antibiotic and an intercalating agent. Becatecarin (BMS-181176) is ...
... where it was found to be cytotoxic against P388 murine leukemia cells (IC50 8 nM), and has later been found to have strong ...
... leukemia L5178 MeSH C04.557.337.372.782 - leukemia p388 MeSH C04.557.337.385 - leukemia, feline MeSH C04.557.337.415 - leukemia ... leukemia L1210 MeSH C04.619.531.602 - leukemia L5178 MeSH C04.619.531.782 - leukemia p388 MeSH C04.619.857.573 - sarcoma 37 ... leukemia, b-cell, acute MeSH C04.557.337.428.500.125 - leukemia, B-Cell, chronic MeSH C04.557.337.428.500.500 - leukemia, pre-b ... leukemia, T-Cell, chronic MeSH C04.557.337.428.580 - leukemia, t-cell MeSH C04.557.337.428.580.100 - leukemia, t-cell, acute ...
... leukemia P388, sarcoma 180, Ehrlich Ascites carcinoma, Walker carcinosarcoma-256, and light activity against leukemia L-1210 in ...
A high number of white cells in the blood indicates leukemia, so a new anti-cancer drug had been discovered. These two ... Hemiasterlin A and hemiasterlin B show potent activity against the P388 cell line and inhibit cell division by binding to the ... Vincristine is mainly used to treat acute leukemia and other lymphomas. Vinorelbine was developed under the direction of the ...
The expression of MDR-1/P-glycoprotein in the P388/ADR, P388 and HCT-15 cell lines is examined using the WB technique. WB has ... of Idarubicin and Doxorubicin Solid Lipid Nanoparticles to Overcome Pgp-Mediated Multiple Drug Resistance in Leukemia". Journal ...
Pengujian aktivitas sitotoksik terhadap sel murin leukemia P388 dari masing-masing senyawa oligostilbenoid menunjukkan nilai ... OLIGOMER RESVERATROL DARI KULIT KAYU DIPTEROCARPUS RETUSUS BLUME DAN EFEK SITOTOKSIKNYA TERHADAP SEL MURIN LEUKEMIA P388 ... OLIGOMER COMPOUNDS FROM THE TREE BARK OF DIPTEROCARPUS RETUSUS BLUME AND CYTOTOXIC EFFECT AGAINST MURINE LEUKAEMIA P388. ...
ran an in vivo study on arglabin and reported its ability to inhibit DNA synthesis of the P388 lymphocytic leukemia cells. In ... "Sesquiterpene Lactone Arglabin Influences DNA Synthesis in P388 Leukemia Cells in vivo". Pharmaceutical Chemistry Journal. 38 ( ... a Source To Discover Agents That Selectively Inhibit Acute Myelogenous Leukemia Stem and Progenitor Cells". Journal of ... 2012, Yindgai Gao and Yue Chen tested arglabin for biological activity against acute myelogenous leukemia (AML). Their results ...
Four transplantable rodent tumors (L1210 lymphoid leukemia, P388 lymphocytic leukemia, B16 melanoma, and Walker 256 ... Three transplantable rodent tumors (osteogenic sarcoma, Lewis lung carcinoma, and P388 leukemia). No antitumor activity at 20% ... Two human acute myeloid leukemia cell lines (KG-1 and HL-60). A 50% inhibition of colony formation by both normal and leukemic ... None of the solid tumors or leukemias that were investigated responded to amygdalin at any dose that was tested. No ...
Chemotherapy: Tumor response to chemotherapy in the P-388 mouse leukemia model is not affected by ondansetron. In humans, ...
However, these antitumor effects were reported to be four times more potent in P-388 mouse leukemia (Cañedo et al., 2000; ... nov which showed cytotoxicity against five cancer cell lines namely mouse lymphoma (P388), human leukemia (HL60), human lung ... as well as P-388 mouse leukemia (Malet-Cascón et al., 2003; Rodríguez et al., 2003). A macrolactone compound called IB-96212 ( ... Cyanogrisides F (62) and G (63) have shown cytotoxicity against HCT-116 and leukemia HL-60 cell lines (Fu et al., 2014). In ...
In vivo development and in vitro characterization of a subclone of murine P388 leukemia resistant to bis(diphenylphosphine) ... In vivo development and in vitro characterization of a subclone of murine P388 leukemia resistant to bis(diphenylphosphine) ... In vivo development and in vitro characterization of a subclone of murine P388 leukemia resistant to bis(diphenylphosphine) ... In vivo development and in vitro characterization of a subclone of murine P388 leukemia resistant to bis(diphenylphosphine) ...
The in vivo antitumoral/antileukemic activity was evaluated using the following panel of tumor lines: P-388 leukemia, sarcoma ( ...
Phenylahistin also showed antitumor activity against P388 leukemia and Lewis lung carcinoma cells in vivo.. ...
... he strong cytotoxic effect of Thujaplicin on murine P388 lymphocytic leukemia cell line [CLL, chronic lymphocytic leukemia] ...
... he strong cytotoxic effect of Thujaplicin on murine P388 lymphocytic leukemia cell line [CLL, chronic lymphocytic leukemia] ...
Rapid kinetics of the interaction between daunomycin and drug-sensitive or drug-resistant P388 leukemia cells. Soto, F., ... Possible coexistence of two independent mechanisms contributing to anthracycline resistance in leukaemia P388 cells. Soto, F., ...
Anticancer activity tests against P-388 murine leukemia cells revealed that compound 1 has an IC50of 2.35 µg/mL, confirming ... with different techniques to gain more complete data and then tested for anticancer activity test against P-388 murine leukemia ...
The use of bromelain in cancer has its roots in a laboratory study of several tumor cell lines - P-388 leukemia, sarcoma (S-37 ...
Vero Cells, Tumor Cells, Cultured, Animals, Lagomorpha, Mice, Toxoplasma, Toxoplasmosis, Animal, Leukemia P388, Parasitology, ...
Bioassay-guided (murine P388 lymphocytic leukemia and human cancer cell lines) separation of an ethyl acetate extract prepared ... N2 - Bioassay-guided (murine P388 lymphocytic leukemia and human cancer cell lines) separation of an ethyl acetate extract ... AB - Bioassay-guided (murine P388 lymphocytic leukemia and human cancer cell lines) separation of an ethyl acetate extract ... abstract = "Bioassay-guided (murine P388 lymphocytic leukemia and human cancer cell lines) separation of an ethyl acetate ...
It has an inhibitory effect on P388 leukemia cells and can prolong survival. One of its mechanisms of action is to inhibit the ...
Enhanced efflux of actinomycin d, vincristine, and vinblastine in adriamycin-resistant subline of p388 leukemia. ...
Tumor response to chemotherapy in the P-388 mouse leukemia model is not affected by ondansetron. In humans, carmustine, ... Tumor response to chemotherapy in the P-388 mouse leukemia model is not affected by ondansetron. In humans, carmustine, ...
Tumor response to chemotherapy in the P-388 mouse leukemia model is not affected by ondansetron. In humans, carmustine, ... Tumor response to chemotherapy in the P-388 mouse leukemia model is not affected by ondansetron. In humans, carmustine, ...
Compound 3 exhibited modest cytotoxicity against P388 murine leukemia cells with an IC50 value of 19 µM. ...
Multifactorial resistance to antineoplastic agents in drug-resistant P388 murine leukemia, Chinese hamster ovary, and human ... Mitoxantrone and 5‐azacytidine for refractory/relapsed ANLL or CML in blast crisis: A leukemia intergroup study Journal ... Relation between platinum-DNA adducts and complete remission in adult acute nonlymphocytic leukemia Journal Articles ...
Test of Dihidroisocoumarin Activity Against Murine Leukemia Cells P-388 From the Stem Bark Extract of Shorea Singkawang (Miq) . ...
The in vivo antitumor effect was evaluated by the number of survival days of mouse leukemia P388-bearing female CDF1 mice. The ... obliquus sclerotia against mouse leukemia P388 cells was assessed. METHODS AND RESULTS:. Cell viability was measured by MTT ... The intraperitoneal administration of 10 mg/kg Inotodiol prolonged the number of survival days of the P388-bearing mice. ... DNA fragmentation and caspase-3/7 activation were observed in the P388 cells treated with Inotodiol (30 microM). A caspase-3 ...
... of methotrexate and retinyl palmitate enhanced antitumor activity in mice bearing ascites sarcoma 180 or P388 leukemia. ... Effects of vitamin A on survival in patients with chronic myelogenous leukemia: a SWOG randomized trial. Leuk Res 1995;19(9): ... Outcome of childhood acute promyelocytic leukemia with all-trans-retinoic acid and chemotherapy. J Clin Oncol 2004;22(8):1404- ... Acne vulgaris, acute promyelocytic leukemia, alcohol withdrawal support, Alzheimer's disease, anemia (associated with ...
The inhibition of methanol extract of noni fruits and scopoletin against murine leukemia P388 cells using MTT assay showed IC50 ...
Overcoming of vincristine resistance in P388 leukemia in vivo and in vitro though enhanced cytotoxicity of vincristine and vin- ... Cleavage of Bcl-2 is an early event in chemotherapy-induced apoptosis of human myeloid leukemia cells // Leukemia. 1999. - Vol ... And leukemia // Cell. 1998. - Vol. 94. - P. 912.. 110. Evan G., Littlewood T. A matter of life and death // Science. 1998. - ... Xie P., Chan F.S., Ip N.Y., Leung M.F. Induction of gpl 30 and LIF by differentiation inducers in human myeloid leukemia K562 ...
This isoprenylatedflavanoid also showed potent cytotoxic activity against various cell lines like murine leukemia P388, ...
... was found to possess potent anticancer activities in both the in vivo hollow fiber assay and the P-388 lymphocytic leukemia ... The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic ... Synergistic effect of inhibiting translation initiation in combination with cytotoxic agents in acute myelogenous leukemia ... which is approved for the treatment of chronic myeloid leukemia [27]. ...
  • T]he strong cytotoxic effect of Thujaplicin on murine P388 lymphocytic leukemia cell line [CLL, chronic lymphocytic leukemia] should be emphasized. (oil-testimonials.com)
  • Bioassay-guided (murine P388 lymphocytic leukemia and human cancer cell lines) separation of an ethyl acetate extract prepared from the inky cap fungus Coprinus cinereus led to the isolation of three new sesquiterpenes, 7,7a-diepicoprinastatin 1 (1), 14-hydroxy-5-desoxy-2S,3S,9R-illudosin (2), and 4,5-dehydro-5-deoxyarmillol (3), together with the known armillol (4). (elsevierpure.com)
  • In vivo development and in vitro characterization of a subclone of murine P388 leukemia resistant to bis(diphenylphosphine)ethane. (aspetjournals.org)
  • Cyclobutane 2 led to modest inhibition of the murine P388 leukemia cell line. (elsevierpure.com)
  • The compound 1 was further characterized with different techniques to gain more complete data and then tested for anticancer activity test against P-388 murine leukemia cells. (ijournalse.org)
  • Anticancer activity tests against P-388 murine leukemia cells revealed that compound 1 has an IC 50 of 2.35 µg/mL, confirming that the compound is categorized as an active anticancer agent and suggesting that the compound has promising potential that deserves further investigations. (ijournalse.org)
  • It has an inhibitory effect on P388 leukemia cells and can prolong survival. (focusherb.com)
  • Its main anti-tumor activity is concentrated on neuroectodermal tumors, liver cancer, lung squamous cell carcinoma, skin Merkel cell carcinoma, gastric cancer, leukemia and other tumors. (focusherb.com)
  • Intracellular metabolism of 5,10-dideazatetrahydrofolic acid in human leukemia cell lines. (aspetjournals.org)
  • The in vivo antitumoral/antileukemic activity was evaluated using the following panel of tumor lines: P-388 leukemia, sarcoma (S-37), Ehrlich ascitic tumor (EAT), Lewis lung carcinoma (LLC), MB-F10 melanoma and ADC-755 mammary adenocarcinoma. (greenmedinfo.com)
  • The coordinated gold compound, 2,3,4,6-tetra-O-acetyl-1-thio-beta-D-glucopyranosato-S-triethylphosphine-gold (auranofin) was found to be effective in increasing the life span of C57BL x DBA/2 F1 mice inoculated with the lymphocytic leukemia P388. (nih.gov)
  • 770-fold from the P-388 lymphocytic leukemia tumor cell line. (nih.gov)
  • 13. Doxorubicin cytotoxicity to P388 lymphocytic leukemia as determined by alkaline elution and established assays. (nih.gov)
  • An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene. (nih.gov)
  • T]he strong cytotoxic effect of Thujaplicin on murine P388 lymphocytic leukemia cell line [CLL, chronic lymphocytic leukemia] should be emphasized. (oil-testimonials.com)
  • Continuation of a detailed investigation of cancer cell growth inhibitory (P388 lymphocytic leukemia) fractions (trace) from H. erecta has revealed the presence (10 -5 to 10 -7 % yield) of cytotoxic pentacyclic sesterterpenes. (elsevierpure.com)
  • 1. [In vitro evaluation of the chemosensitivity of an experimental murine leukemia rendered resistant in vivo to adriamycin]. (nih.gov)
  • 2. [A short term test suitable for in vitro prediction of the drug sensitivity of human leukemias: a preliminary study on murine experimental neoplasms]. (nih.gov)
  • 4. Mechanism of acquired resistance to methotrexate in P388 murine leukemia cells and in their doxorubicin-resistant subline. (nih.gov)
  • 7. Murine splenocyte migration inhibition assay I. Detection of differential responses to murine leukemia P388 and its adriamycin-resistant subline P388/ADR. (nih.gov)
  • 9. Reversal of acquired resistance to doxorubicin in P388 murine leukemia cells by perhexiline maleate. (nih.gov)
  • 10. Differential effect of collaterally sensitive antimetabolites on P388 murine leukemia sensitive and resistant to adriamycin in vitro. (nih.gov)
  • 18. Anthracycline resistance in P388 murine leukemia and its circumvention by calcium antagonists. (nih.gov)
  • Purification Of Active Compounds From Kecapi Leaves That Have Potential As Anticancer Fon IN Vitro On Murine Cells Leukemia A P-388. (uisu.ac.id)
  • Using a Topo I-deficient murine B lymphoma-derived subclone (P388-45/C) selected for its resistance to high dosage of the antitumor drug camptothecin, we show that Topo I depletion results in the hypophosphorylation of SR proteins and impairs exonic splicing enhancer (ESE)-dependent but not constitutive splicing. (hal.science)
  • The cell inhibition activities of several Annonaceous acetogenins, covering the three major structural classes of bis-adjacent, bis-non-adjacent, and single tetrahydrofuran (THF) ring compounds and their respective ketolactone rearrangement products, were tested in an in vitro disk diffusion assay against three murine (P388, PO3, and M17/Adr) and two human (H8 and H125) cancerous cell lines as well as a non-cancerous immortalized rat GI epithelial cell line (I18). (cancer.org)
  • DMAB was active in the National Cancer Institute in vivo anticancer drug screen for tumor model L1210 leukemia in BDF1 mice. (nih.gov)
  • Esophageal cancer chemotherapy drug etoposide injection can cure more than half of L1210 leukemia in mice, on the S37, S180 tumor inhibition rate of 61% - 72%, so that the survival of mice suffering from leukemia P1534 compared with the control group increased by 83% - 110% of mice Lewis lung cancer lung metastasis was inhibited. (cancerlive.net)
  • The metallocene dihalides are a relatively new class of small, hydrophobic organometallic anticancer agents that exhibit antitumour properties against numerous cell lines including leukemias P388 and L1210, colon 38 and Lewis lung carcinomas, B16 melanoma, solid and fluid Ehrlich ascites tumours and several human colon and lung carcinomas transplanted into athymic mice. (eurekaselect.com)
  • 14. In vivo circumvention of vincristine resistance in mice with P388 leukemia using a novel compound, AHC-52. (nih.gov)
  • In vivo administration of PDX-101 increased median survival in mice carrying P388 leukemia cells from 9 to 16 days. (medscape.com)
  • As many consider P388 an "artificial" model (an "in vivo test tube"), further studies were performed with A2780 human xenografts in mice. (medscape.com)
  • When these analogues were separated into mitomycin C and mitomycin A subsets, the former gave a correlation only with E½, whereas the latter (which differ little in their E½ values) gave a correlation only with log P. These correlations are in contrast to those made in the P388 leukemia assay in mice wherein the most active mitomycin C and mitomycin A analogues were the most hydrophilic ones. (arizona.edu)
  • When the compounds were injected i.p., alpha- and gamma-tocotrienols were effective against sarcoma 180, Ehrlich carcinoma, and IMC carcinoma, and gamma-tocotrienol showed a slight life-prolonging effect in mice with Meth A fibrosarcoma, but thetocotrienols had no antitumor activity against P388 leukemia at doses of 5-40 mg/kg/d. (tocotrienolresearch.org)
  • while the 3-acethyl-ursolic [3-acethyl-oleanolic] acids with IC 50 = 37.9 µg/mL showed two-fold more potent then their parent triterpenes (IC 50 = 53.5 µg/mL) in the inhibition of P388 leukemia cell growth. (ugm.ac.id)
  • Employing P388 leukemia and human tumor cell line-guided bioassay techniques, two new moderate inhibitors of cancer cells were isolated and named sesterstatins 4 (1a, P388 ED 50 4.9 μg/mL) and 5 (1b, DU-145 prostate GI 50 1.9 μg/mL). (elsevierpure.com)
  • 6. Resistance to adriamycin: relationship of cytotoxicity to drug uptake and DNA single- and double-strand breakage in cloned cell lines of adriamycin-sensitive and -resistant P388 leukemia. (nih.gov)
  • 12. Intracellular adriamycin levels and cytotoxicity in adriamycin-sensitive and adriamycin-resistant P388 mouse leukemia cells. (nih.gov)
  • 3. In vivo characteristics of resistance and cross-resistance of an adriamycin-resistant subline of P388 leukemia. (nih.gov)
  • Overexpression of the multidrug resistance proteins P-glycoprotein (Pgp), multidrug resistance protein (MRP-1), breast cancer resistance protein (BCRP), and lung resistance protein (LRP) is associated with treatment failure in acute myeloid leukemia (AML) and other malignancies. (aacrjournals.org)
  • Leucemia linfocítica experimental inducida originalmente en ratones DBA/2 mediante una clase de pintura que contiene metilcolantreno. (bvsalud.org)
  • Because the efflux transporter P-glycoprotein (P-gp) is involved in the absorption, distribution, and excretion of many drugs and often participates in drug-drug interactions, we studied the effect of a crude kava extract and the main kavalactones kavain, dihydrokavain, methysticin, dihydromethysticin, yangonin, and desmethoxyyangonin on the P-gp-mediated efflux of calcein-acetoxymethylester in the P-gp-overexpressing cell line P388/dx and the corresponding cell line P388. (nih.gov)
  • Our results indicate that NBPQD is able to alleviate leukemia and it is worthy of further characterization as a potential anti-leukemic drug. (japsonline.com)
  • Causes of leukemia are diverse and they could be familial, infectious, physical, or chemical depending on the cell type and the individual variations from one patient to another ( Pui, 1995 ). (japsonline.com)