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> Disorders > Neoplastic Process > Leukemia

Leukemia

Leukemia: A group of malignant neoplasmatic disorders characterized by an uncontrolled proliferation and accumulation of immature white blood cells.
This results in impaired functions of the hematopoietic and lymphoid systems.
Leukemias are classified by the speed of progression and cell type involved (e.g. acute, chronic, lymphoid, myeloid).
Effective treatment and management of Leukemia requires a thorough understanding of the underlying mechanisms and optimal research protocols.
PubCompare.ai offers an AI-powered platform to streamline your Leukemia research, locate the best protocols, and enhance the reproducibility and accuracy of your findings.

Most cited protocols related to «Leukemia»

1
Identifying Mut-Driver Genes Through Mutation Patterns
Cited 267 times
If mutation frequency, corrected for mutation context, gene length, and other parameters, cannot reliably identify modestly mutated driver genes, what can? In our experience, the best way to identify Mut-driver genes is through their pattern of mutation rather than through their mutation frequency. The patterns of mutations in well-studied oncogenes and tumor suppressor genes are highly characteristic and nonrandom. Oncogenes are recurrently mutated at the same amino acid positions, whereas tumor suppressor genes are mutated through protein-truncating alterations throughout their length (Fig. 4 and table S2A).
On the basis of these mutation patterns rather than frequencies, we can determine which of the 18,306 mutated genes containing a total of 404,863 subtle mutations that have been recorded in the Catalogue of Somatic Mutations in Cancer (COSMIC) database (30 (link)) are Mut-driver genes and whether they are likely to function as oncogenes or tumor suppressor genes. To be classified as an oncogene, we simply require that >20% of the recorded mutations in the gene are at recurrent positions and are missense (see legend to table S2A). To be classified as a tumor suppressor gene, we analogously require that >20% of the recorded mutations in the gene are inactivating. This “20/20 rule” is lenient in that all well-documented cancer genes far surpass these criteria (table S2A).
The following examples illustrate the value of the 20/20 rule. When IDH1 mutations were first identified in brain tumors, their role in tumorigenesis was unknown (2 (link), 31 (link)). Initial functional studies suggested that IDH1 was a tumor suppressor gene and that mutations inactivated this gene (32 (link)). However, nearly all of the mutations in IDH1 were at the identical amino acid, codon 132 (Fig. 4). As assessed by the 20/20 rule, this distribution unambiguously indicated that IDH1 was an oncogene rather than a tumor suppressor gene, and this conclusion was eventually supported by biochemical experiments (33 (link), 34 (link)). Another example is provided by mutations in NOTCH1. In this case, some functional studies suggested that NOTCH1 was an oncogene, whereas others suggested it was a tumor suppressor gene (35 (link), 36 (link)). The situation could be clarified through the application of the 20/20 rule to NOTCH1 mutations in cancers. In “liquid tumors” such as lymphomas and leukemias, the mutations were often recurrent and did not truncate the predicted protein (37 (link)). In squamous cell carcinomas, the mutations were not recurrent and were usually inactivating (38 (link)–40 (link)). Thus, the genetic data clearly indicated that NOTCH1 functions differently in different tumor types. The idea that the same gene can function in completely opposite ways in different cell types is important for understanding cell signaling pathways.
Vogelstein B., Papadopoulos N., Velculescu V.E., Zhou S., Diaz LA J.r, & Kinzler K.W. (2013). Cancer Genome Landscapes. Science (New York, N.Y.), 339(6127), 1546-1558.
Publication 2013
Amino Acids Ataxia Telangiectasia Mutated Proteins Brain Neoplasms Cells Codon Cosmic composite resin Diploid Cell Gene, Cancer Genes Leukemia Lymphoma Malignant Neoplasms Mutation Neoplasms Neoplastic Cell Transformation Oncogenes Proteins Reproduction Signal Transduction Pathways Squamous Cell Carcinoma Tumor Suppressor Genes
2
Childhood Cancer Survivor Study Cohort
Cited 69 times
The CCSS cohort consists of previously untreated patients diagnosed prior to 21 years of age with leukemia, lymphoma, central nervous system cancer, neuroblastoma, bone or soft tissue sarcoma, or kidney cancer, who survived for at least five years after the date of diagnosis. Survivors were diagnosed between January 1, 1970 and December 31, 1986 at one of 26 participating institutions. The study design, cohort characteristics and outcomes ascertained are presented in detail elsewhere [12 (link)–14 (link)]. The CCSS was approved by the Institutional Review Board at each participating institution, and informed consent for participation was obtained from all subjects who were 18 or more years of age, or their parents, if the subject was less than 18 years of age.
Green D.M., Nolan V.G., Goodman P.J., Whitton J.A., Srivastava D., Leisenring W.M., Neglia J.P., Sklar C.A., Kaste S.C., Hudson M.M., Diller L.R., Stovall M., Donaldson S.S, & Robison L.L. (2013). The Cyclophosphamide Equivalent Dose as an Approach for Quantifying Alkylating Agent Exposure. A Report from the Childhood Cancer Survivor Study. Pediatric blood & cancer, 61(1), 53-67.
Publication 2013
Bones Cancer of Kidney Ethics Committees, Research Leukemia Lymphoma Nervous System Neoplasms Neuroblastoma Parent Patients Sarcoma Survivors
3
Comprehensive Hematological Sampling for Research
Cited 43 times
Multiple types of biological samples were collected from healthy volunteers and patients with suspicion or diagnosis of different types of hematological malignancies and other non-clonal hematological and non-hematological disorders, as specified later in each section of this paper. The collected samples concerned peripheral blood (PB), bone marrow (BM), fine needle aspirates (FNA), biopsies from lymphoid and non-lymphoid tissues, cerebrospinal fluid (CSF) and vitreous samples. For all patients with a hematological malignancy, the diagnosis was established according to the WHO criteria.3 Informed consent procedures and forms were proposed and approved at the first EuroFlow meeting (see the Editorial in this Leukemia issue). Informed consent was given by donors or their guardians (for example, parents) in case of children according to the guidelines of the local Medical Ethics Committees and in line with the Declaration of Helsinki Protocol. All participants obtained approval or no-objection from the local Medical Ethics Committees for secondary use of remaining diagnostic material for the EuroFlow studies, which also allows the inclusion of anonymized flow cytometric results into a central (public) database to define reference values for normal, reactive, regenerating and malignant cell samples.
van Dongen J.J., Lhermitte L., Böttcher S., Almeida J., van der Velden V.H., Flores-Montero J., Rawstron A., Asnafi V., Lécrevisse Q., Lucio P., Mejstrikova E., Szczepański T., Kalina T., de Tute R., Brüggemann M., Sedek L., Cullen M., Langerak A.W., Mendonça A., Macintyre E., Martin-Ayuso M., Hrusak O., Vidriales M.B, & Orfao A. (2012). EuroFlow antibody panels for standardized n-dimensional flow cytometric immunophenotyping of normal, reactive and malignant leukocytes. Leukemia, 26(9), 1908-1975.
Publication 2012
Aspiration Biopsy, Fine-Needle Biopharmaceuticals Biopsy BLOOD Bone Marrow Cells Cerebrospinal Fluid Child Clone Cells Diagnosis Donors Flow Cytometry Healthy Volunteers Hematological Disease Hematologic Neoplasms Legal Guardians Leukemia Lymph Lymphoid Tissue Parent Patients Regional Ethics Committees Specimen Collection
4
Cloning and Expression of PH Domain Proteins
Cited 37 times
The PH domains of PLCδ1 (1–170), Bruton's tyrosine kinase (1–177), Akt protein kinase (1–167), and dynamin (508–652) were amplified with the Advantage Klentaq polymerase mix (CLONTECH Labs, Inc., Palo Alto, CA) from human cDNAs (marathon cDNA from brain and K562 leukemia cells; CLONTECH Labs, Inc.) with the following primer pairs:
PLCδ: 5′-GGCATGGACTCGGGCCGGGACTTCCTG-3′, 5′-AAGATCTTCCGGGCATAGCTGTCG-3′;
Btk: 5′-CCAAGTCCTGGCATCTCAATGCATCTG-3′,
5′-TGGAGACTGGTGCTGCTGCTGGCTC-3′;
Akt: 5′-GTCAGCTGGTGCATCAGAGGCTGTG-3′,
5′-CACCAGGATCACCTTGCCGAAAGTGCC-3′;
Dyn: 5′-ATGCTCAGCAGAGGAGCAACCAGATG-3′,
5′-GAGTCCACAAGATTCCGGATGGTCTC-3′.
The amplified products were subcloned into the PGEM-Easy T/A cloning vector (Promega Corp., Madison, WI) and sequenced with dideoxy sequencing (thermosequenase; Amersham Corp.). A second amplification reaction was performed from these plasmids with nested primers that contained restriction sites for appropriate cloning into the pEGFP-N1 (PLCδ, Btk, and Akt) or pEGFP-C1 (dynamin) plasmids (CLONTECH Labs, Inc.) to preserve the reading frame. Plasmids were transfected into COS-7 cells or NIH-3T3 cells and cell lysates were resolved by SDS-PAGE followed by Western blot analysis for the presence of the GFP fusion proteins using a polyclonal antibody against GFP (CLONTECH Labs, Inc.).
Mutations were created in the PHPLCδ–GFP fusion plasmid by the QuickChange™ mutagenesis kit (Stratagene, La Jolla, CA). For practical purposes, a SalI site was introduced into the PH domain sequence which changed S34 to a T but this substitution did not change any characteristic compared with the wild-type protein. All mutations were confirmed by dideoxy sequencing and the expression of the fusion protein by Western blot analysis.
Várnai P, & Balla T. (1998). Visualization of Phosphoinositides That Bind Pleckstrin Homology Domains: Calcium- and Agonist-induced Dynamic Changes and Relationship to Myo-[3H]inositol-labeled Phosphoinositide Pools. The Journal of Cell Biology, 143(2), 501-510.
Publication 1998
Brain Cells Cloning Vectors COS-7 Cells DNA, Complementary Dynamins Homo sapiens Immunoglobulins K562 Cells Leukemia Marathon composite resin Mutagenesis Mutation NIH 3T3 Cells Oligonucleotide Primers Plasmids Pleckstrin Homology Domains Promega prostaglandin M Protein Kinases Proteins Reading Frames SDS-PAGE Tyrosine Kinase, Agammaglobulinaemia Western Blot
5
Comprehensive Genetic Profiling Protocol
Cited 34 times
Genetic profiling included cytogenetic analyses and sequencing of 111 genes (Table S2 in the Supplementary Appendix). Sequencing data have been deposited in the European Genome-Phenome Archive (www.ebi.ac.uk/ega) under accession number EGAS00001000275. We based our analysis on variants that we classified as driver mutations, using widely accepted genetic criteria.12 (link) Recurrent fusion genes, aneuploidies, and leukemia gene mutations, including base substitutions and small (<200-bp) insertions or deletions (indels), were all included as drivers.
Papaemmanuil E., Gerstung M., Bullinger L., Gaidzik V.I., Paschka P., Roberts N.D., Potter N.E., Heuser M., Thol F., Bolli N., Gundem G., Van Loo P., Martincorena I., Ganly P., Mudie L., McLaren S., O’Meara S., Raine K., Jones D.R., Teague J.W., Butler A.P., Greaves M.F., Ganser A., Döhner K., Schlenk R.F., Döhner H, & Campbell P.J. (2016). Genomic Classification and Prognosis in Acute Myeloid Leukemia. The New England journal of medicine, 374(23), 2209-2221.
Publication 2016
Aneuploidy Cytogenetic Analysis Europeans Gene Deletion Genes Genome INDEL Mutation Insertion Mutation Leukemia Mutation Reproduction

Most recents protocols related to «Leukemia»

1
Tucaresol Combination Therapy Evaluation
Not available on PMC !

Example 1

1) Tucaresol

Tucaresol (0-1200 μM) is exposed for 72 hours to a panel of human liquid, hematological, and solid tumors such as multiple myeloma, leukemia, colorectal, non-small cell lung cancer (squamous and adenocarcinoma), hepatocellular, renal, pancreatic and breast cancer cell lines, and human non-tumor such as HUVEC, PBMC, skin fibroblast cells lines. Tucaresol is studied either alone or in combination with standard-of-care agents (1-100 μM). All cell lines are grown in standard serum-containing media with an exposure time of 24-144 hours. Cell viability is measured using, for example, the Cell TiterGlo® Viability Assay. The potency (IC50) and efficacy (% cell kill) are determined from the percent cell growth of the vehicle control.

2) Tucaresol Plus PD-1 Antibody

Tucaresol (0-1200 μM) in the presence of a PD-1 antibody is exposed for 72 hours to a panel of human liquid, hematological, and solid tumor such as multiple myeloma, leukemia, colorectal, non-small cell lung cancer (squamous and adenocarcinoma), hepatocellular, renal, pancreatic and breast cancer cell lines, and human non-tumor such as HUVEC, PBMC, skin fibroblast cells lines, and the viability of the cell lines are measured as described above. The viability of the cell lines in the presence of tucaresol plus PD-1 antibody is compared to the viability of the cell lines in the presence of a CTLA-4 antibody plus the PD-1 antibody or PD-1 antibody alone.

3) CTLA-4 Antibody Plus PD-1 Antibody

CTLA-4 antibody in the presence of a PD-1 antibody is exposed for 72 hours to a panel of human liquid, hematological, and solid tumor such as multiple myeloma, leukemia, colorectal, non-small cell lung cancer (squamous and adenocarcinoma), hepatocellular, renal, pancreatic and breast cancer cell lines, and human non-tumor such as HUVEC, PBMC, skin fibroblast cells lines, and the viability of the cell lines are measured as described above.

4) Tucaresol Plus Plinabulin

Tucaresol (0-1200 μM) in the presence of Plinabulin is exposed for 72 hours to a panel of human liquid, hematological, and solid tumor such as multiple myeloma, leukemia, colorectal, non-small cell lung cancer (squamous and adenocarcinoma), hepatocellular, renal, pancreatic and breast cancer cell lines, and human non-tumor such as HUVEC, PBMC, skin fibroblast cells lines, and the viability of the cell lines are measured as described above.

The viability of the cell lines in the presence of tucaresol, tucaresol plus PD-1 antibody, CTLA-4 antibody plus the PD-1 antibody, and tucaresol plus plinabulin are compared.

US11857522B2. Compositions containing tucaresol or its analogs (2024-01-02). BeyondSpring Pharmaceuticals, Inc. [US]. Inventors: Ramon Mohanlal [US], Lan Huang [US], George Kenneth Lloyd [US].
Patent 2024
Adenocarcinoma Biological Assay Cell Lines Cells Cell Survival Cytotoxic T-Lymphocyte Antigen 4 Fibroblasts Homo sapiens Immunoglobulins Kidney Leukemia MCF-7 Cells Multiple Myeloma Neoplasms Non-Small Cell Lung Carcinoma Pancreas plinabulin Serum Skin tucaresol
2
Bioactivity Validation of Compounds 3 and 7
Not available on PMC !

Example 19

To confirm bioactivity of 3 and 7, experiments were performed with the HH cell line, a mature T cell line derived from peripheral blood of a patient with aggressive cutaneous T cell leukemia/lymphoma (ATCC® CRL-2105™) which been demonstrated to only express the IL-2Rβ/γ. One of the earliest events in cytokine mediated activation of lymphocytes such as CD8+ T cells and NK cells is Janus Associated Kinase mediated phosphorylation and activation of Signal transducer and activator of transcription (pSTAT5). Thus, pSTAT5 was used to measure biological activity of 3 and 7 alongside 12. 3 demonstrated clear bioactivity in IL-2Rβ/γ expressing HH cells (EC50: 773 ng/ml) that was approximately 3.5 fold lower than 12 (EC50: 233 ng/ml). Additionally, 7 induced bioactivity (EC50: 756 ng/ml) very similar to 3, demonstrating that 7 retains bioactivity after being released from prodrug 5 even after accelerated (stress) conditions.

US11879001B2. Conjugate comprising an IL-2 moiety (2024-01-23). ASCENDIS PHARMA ONCOLOGY DIVISION A/S [DK]. Inventors: Nina Gunnarsson [DK], Matiss Maleckis [DK], David B. Rosen [US].
Patent 2024
Biopharmaceuticals BLOOD CD8-Positive T-Lymphocytes Cell Lines Cells Cytokine IL19 protein, human Kinase, Janus Leukemia Lymphocyte Activation Lymphoma, T-Cell, Cutaneous Natural Killer Cells Patients Phosphorylation Prodrugs Transcription, Genetic Transducers
3
Evaluating Tucaresol and Checkpoint Inhibitors in Xenograft Models
Not available on PMC !

Example 7

Five groups including tucaresol, tucaresol plus PD-1 or PD-L1 antibody, tucaresol plus CTLA-4 antibody, CTLA-4 antibody plus PD-1 or PD-L1 antibody, and tucaresol plus plinabulin are tested to determine their effect in an animal xenograft model.

The combined treatment with tucaresol and the checkpoint inhibitor(s) is tested in comparison with the treatment with tucaresol alone, the treatment with checkpoint inhibitor alone, or combination of checkpoint inhibitors. The tests are performed using seven to ten-week old athymic (nu/nu) mice that were injected subcutaneously with human tumor cell lines (of either solid or liquid tumor origin, for example of breast, lung, colon, brain, liver, leukemia, myeloma, lymphoma, sarcoma, pancreatic or renal origin). Six to ten testing groups are prepared, and each group includes 10 mice.

Each treatment starts at tumor size between 40-150 mm3 and continues until Day 24-56, when the animals are necropsied. To determine the efficacy of each treatment, the following data are collected: mortality; the body weight of the mice assessed twice weekly both prior to treatments; the rate of tumor growth as determined by the tumor size measurement (twice every week); the tumor growth index; overall survival rate; the tumor weight at necropsy; and the time required to increase tumor size 10 fold.

US11857522B2. Compositions containing tucaresol or its analogs (2024-01-02). BeyondSpring Pharmaceuticals, Inc. [US]. Inventors: Ramon Mohanlal [US], Lan Huang [US], George Kenneth Lloyd [US].
Patent 2024
Animal Model Animals Autopsy Body Weight Brain Breast CD274 protein, human Cell Cycle Checkpoints Cell Line, Tumor Colon Combined Modality Therapy CTLA4 protein, human Genes, Neoplasm GZMB protein, human Heterografts Homo sapiens Immunoglobulins inhibitors Kidney Leukemia Liver Lung Lymphoma Mice, Nude Multiple Myeloma Mus Neoplasms Pancreas plinabulin Sarcoma Thymic aplasia tucaresol
4
Colocalization of Antibodies in B-cells
Not available on PMC !

Example 4

To determine where 2F2-grafted “humanized” antibodies and antibody variants are delivered upon internalization into the cell, colocalization studies of the anti-CD79b antibodies internalized into B-cell lines may be assessed in Ramos cell lines. LAMP-1 is a marker for late endosomes and lysosomes (Kleijmeer et al., Journal of Cell Biology, 139(3): 639-649 (1997); Hunziker et al., Bioessays, 18:379-389 (1996); Mellman et al., Annu. Rev. Dev. Biology, 12:575-625 (1996)), including MHC class II compartments (MIICs), which is a late endosome/lysosome-like compartment. HLA-DM is a marker for MIICs.

Ramos cells are incubated for 3 hours at 37° C. with 1 μg/ml 2F2-grafted “humanized” antibodies and antibody variants, FcR block (Miltenyi) and 25 μg/ml Alexa647-Transferrin (Molecular Probes) in complete carbonate-free medium (Gibco) with the presence of 10 μg/ml leupeptin (Roche) and 5 μM pepstatin (Roche) to inhibit lysosomal degradation. Cells are then washed twice, fixed with 3% paraformaldehyde (Electron Microscopy Sciences) for 20 minutes at room temperature, quenched with 50 mM NH4Cl (Sigma), permeabilized with 0.4% Saponin/2% FBS/1% BSA for 20 minutes and then incubated with 1 μg/ml Cy3 anti-mouse (Jackson Immunoresearch) for 20 minutes. The reaction is then blocked for 20 minutes with mouse IgG (Molecular Probes), followed by a 30 minute incubation with Image-iT FX Signal Enhancer (Molecular Probes). Cells are finally incubated with Zenon Alexa488-labeled mouse anti-LAMP1 (BD Pharmingen), a marker for both lysosomes and MIIC (a lysosome-like compartment that is part of the MHC class II pathway), for 20 minutes, and post-fixed with 3% PFA. Cells are resuspended in 20 μl saponin buffer and allowed to adhere to poly-lysine (Sigma) coated slides prior to mounting a coverglass with DAPI-containing VectaShield (Vector Laboratories). For immunofluorescence of the MIIC or lysosomes, cells are fixed, permeabilized and enhanced as above, then co-stained with Zenon labeled Alexa555-HLA-DM (BD Pharmingen) and Alexa488-Lamp1 in the presence of excess mouse IgG as per the manufacturer's instructions (Molecular Probes).

Accordingly, colocalization of 2F2-grafted “humanized” antibodies or antibody variants with MIIC or lysosomes of B-cell lines as assessed by immunofluorescence may indicate the molecules as excellent agents for therapy of tumors in mammals, including B-cell associated cancers, such as lymphomas (i.e. Non-Hodgkin's Lymphoma), leukemias (i.e. chronic lymphocytic leukemia), and other cancers of hematopoietic cells.

US11866496B2. Humanized anti-CD79B antibodies and immunoconjugates and methods of use (2024-01-09). Genentech, Inc. [US]. Inventors: Yvonne Chen [US], Mark Dennis [US], Kristi Elkins [US], Jagath Reddy Junutula [US], Andrew Polson [US], Bing Zheng [US].
Patent 2024
Alexa Fluor 647 Anti-Antibodies Antibodies, Monoclonal, Humanized B-Lymphocytes Buffers Carbonates CD79B protein, human Cell Lines Cells Chronic Lymphocytic Leukemia Cloning Vectors DAPI Electron Microscopy Endosomes Genes, MHC Class II Hematopoietic Neoplasms Immunofluorescence Immunoglobulins Leukemia leupeptin Lymphoma Lymphoma, Non-Hodgkin Lysine lysosomal-associated membrane protein 1, human Lysosomes Malignant Neoplasms Mammals Molecular Probes Mus Neoplasms paraform pepstatin Poly A Saponin Therapeutics Transferrin
5
COVID-19 Severity Grading and Disease Status
Confirmed cases of COVID-19 were defined by a positive reverse transcription polymerase chain reaction (RT-PCR) assay of a specimen collected on a nasopharyngeal swab.
The severity of COVID-19 at admission is graded according to the China Center for Disease Control and Prevention definitions (17 (link)).
Disease status at the time of SARS-CoV-2 detection was defined according to each specific disease’s revised criteria for leukemia, myeloproliferative neoplasm, multiple myeloma, and lymphoma. The ISI was calculated as previously described (4 (link)).
Busca A., Salmanton-García J., Marchesi F., Farina F., Seval G.C., Van Doesum J., De Jonge N., Bahr N.C., Maertens J., Meletiadis J., Fracchiolla N.S., Weinbergerová B., Verga L., Ráčil Z., Jiménez M., Glenthøj A., Blennow O., Tanase A.D., Schönlein M., Prezioso L., Khanna N., Duarte R.F., Žák P., Nucci M., Machado M., Kulasekararaj A., Espigado I., De Kort E., Ribera-Santa Susana J.M., Marchetti M., Magliano G., Falces-Romero I., Ilhan O., Ammatuna E., Zompi S., Tsirigotis P., Antoniadou A., Zambrotta G.P., Nordlander A., Karlsson L.K., Hanakova M., Dragonetti G., Cabirta A., Berg Venemyr C., Gräfe S., Van Praet J., Tragiannidis A., Petzer V., López-García A., Itri F., Groh A., Gavriilaki E., Dargenio M., Rahimli L., Cornely O.A, & Pagano L. (2023). Outcome of COVID-19 in allogeneic stem cell transplant recipients: Results from the EPICOVIDEHA registry. Frontiers in Immunology, 14, 1125030.
Publication 2023
Biological Assay COVID 19 Leukemia Lymphoma Multiple Myeloma Myeloproliferative Disorders Nasopharynx Reverse Transcriptase Polymerase Chain Reaction

Top products related to «Leukemia»

1
Fetal bovine serum (fbs) by Thermo Fisher Scientific
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
2
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RPMI 1640 medium is a commonly used cell culture medium developed at Roswell Park Memorial Institute. It is a balanced salt solution that provides essential nutrients, vitamins, and amino acids to support the growth and maintenance of a variety of cell types in vitro.
3
Rpmi 1640 by Thermo Fisher Scientific
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RPMI 1640 is a common cell culture medium used for the in vitro cultivation of a variety of cells, including human and animal cells. It provides a balanced salt solution and a source of essential nutrients and growth factors to support cell growth and proliferation.
4
Penicillin streptomycin by Thermo Fisher Scientific
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Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.
5
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Penicillin is a type of antibiotic used in laboratory settings. It is a broad-spectrum antimicrobial agent effective against a variety of bacteria. Penicillin functions by disrupting the bacterial cell wall, leading to cell death.
6
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Streptomycin is a broad-spectrum antibiotic used in laboratory settings. It functions as a protein synthesis inhibitor, targeting the 30S subunit of bacterial ribosomes, which plays a crucial role in the translation of genetic information into proteins. Streptomycin is commonly used in microbiological research and applications that require selective inhibition of bacterial growth.
7
Thp 1 by American Type Culture Collection
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The THP-1 is a human acute monocytic leukemia cell line. It is a commonly used model for studying monocyte and macrophage biology.
8
Dulbecco modified eagle medium (dmem) by Thermo Fisher Scientific
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DMEM (Dulbecco's Modified Eagle's Medium) is a cell culture medium formulated to support the growth and maintenance of a variety of cell types, including mammalian cells. It provides essential nutrients, amino acids, vitamins, and other components necessary for cell proliferation and survival in an in vitro environment.
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L glutamine by Thermo Fisher Scientific
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L-glutamine is an amino acid that is commonly used as a dietary supplement and in cell culture media. It serves as a source of nitrogen and supports cellular growth and metabolism.
10
Hl 60 by American Type Culture Collection
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The HL-60 is a human promyelocytic leukemia cell line. It is a well-established in vitro model system for studying cellular differentiation and hematopoiesis.

More about "Leukemia"

Hematological malignancies, blood cancers, myeloid leukemia, lymphoid leukemia, CML, AML, ALL, haematopoiesis, haematologic stem cells, haemopoiesis, haemocytes, haemato-oncology, haemoblastosis, haemocytoblast, haemopathy, haemotroph, haematopathology, haemocytoblastosis, haemocytogenesis, haemocytopoiesis, haemocytotherapy, haemography, haemokonia, haemology, haemolysis, haemophilia, haemoplasma, haemoptysis, haemopoiesis, haemorrhagia, haemosiderin, haemostasis