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> Disorders > Neoplastic Process > Chronic Lymphocytic Leukemia

Chronic Lymphocytic Leukemia

Chronic lymphocytic leukemia (CLL) is a type of slow-growing blood cancer that primarily affects older adults.
It is characterized by the accumulation of mature-appearing lymphocytes in the blood, bone marrow, and lymphoid tissues.
CLL often progresses slowly, and some individuals may not require treatment for many years.
However, in some cases, the disease can progress more rapidly and require immediate treatment.
Effective management of CLL requires a careful balance between monitoring the disease and providing timely interventions when necessary.
Researchers and clinicians are continually working to improve the understanding and treatment of this complex hematologic malignancy.

Most cited protocols related to «Chronic Lymphocytic Leukemia»

1
Diffusional Kurtosis Estimator: A Rapid MRI Protocol
Cited 105 times
In the first stage of processing, the DWI’s are optionally smoothed using a Gaussian kernel to reduce the impact of noise and misregistration. Next, D and W are estimated using the CLLS-QP algorithm, and finally, the scalar measures are obtained from the tensors. The pipeline was implemented in-house in the MATLAB environment (http://www.mathworks.com). The program, designated as Diffusional Kurtosis Estimator (DKE), is available upon request from the corresponding author.
The parameters used with DKE were as follows: the full width at half maximum of the Gaussian kernel was 3.375 mm; Kmin = 0; and C = 3. The tensors were also estimated using the UNLS, ULLS and CLLS-H algorithms following smoothing of DWI’s. Three processing protocols were considered where different subsets of the acquired DWI’s were used to estimate the parametric maps. In the reference protocol, the maps were obtained using all of the available DWI’s. In the standard protocol, the maps were estimated using NEX = 11 for b = 0 images, and NEX = 1 for b = 1000, 2000 s/mm2 DWI’s. Finally, in the fast protocol, the maps were obtained with NEX = 11 for b = 0 images, and NEX = 1 with 15 of b = 1000 s/mm2 and all of b = 2000 s/mm2 DWI’s. We used the maps obtained using the reference protocol and ULLS as baseline for evaluating the maps estimated with the other protocols. The standard protocol is currently used for clinical research acquisitions, and the fast protocol was conjured up as a potential candidate for future clinical research acquisitions. The estimated acquisition time for the fast protocol is 5:54 minutes.
Tabesh A., Jensen J.H., Ardekani B.A, & Helpern J.A. (2010). Estimation of Tensors and Tensor-Derived Measures in Diffusional Kurtosis Imaging. Magnetic Resonance in Medicine, 65(3), 823-836.
Publication 2010
Chronic Lymphocytic Leukemia Diffusion Microtubule-Associated Proteins
2
Quantifying Synergistic Drug Interactions
Cited 51 times
To demonstrate the performance of the ZIP-based delta scoring, we considered a recent cancer drug screen study involving ibrutinib in combination with 466 compounds for the activated B-cell-like subtype (ABC) of diffuse large B-cell lymphoma (DLBCL) [14] (link). Ibrutinib is a small molecule targeting Bruton's tyrosine kinase (BTK) approved for the treatment of mantle cell lymphoma and chronic lymphocytic leukemia [16] (link). In this study, a high-throughput drug combination screening was used to identify other compounds that can synergistically interact with ibrutinib to improve its anticancer efficacy and circumvent drug resistance. For each drug pair, a 6 × 6 dose–response matrix design was utilized, where the drug effect was measured as percentage of cell viability using TMD8 cancer cell line. The raw combination data was provided by the authors via personal communication, but can now be downloaded from https://tripod.nih.gov/matrix-client/rest/matrix/export/241. We transformed the original percentage viability data into the percentage inhibition data before applying the drug combination analysis to be compatible with the mathematical formulation defined in the Methods section.
We ran the ZIP model on the drug combination data and calculated a summary delta score Δ for each drug pair by taking the average of all the delta scores over its dose combinations, i.e., Δ=1n∑i=1nδ, where n is the number of dose combinations and n = 25 for a 6 × 6 dose–response matrix (monotherapy responses were removed). We compared the summary delta scores with the other scores derived from the HSA-, Bliss- and Loewe-based models. For HSA and Bliss, there were existing scores implemented in the original study [14] (link), which were based on the following methods: 1) NumExcess is the number of wells in the dose matrix that produced higher effect than both of the individual drug effects; 2) ExcessHSA is the sum of differences between the combination effect and the expected HSA effect; 3) MedianExcess is the median of the HSA excess; 4) ExcessCRX is an extension of the HSA model that was adjusted by dilution factors; 5) LS3 × 3 is the ExcessHSA applied to a 3 × 3 block showing the best HSA synergy in the dose matrix; 6) Beta (β) is the interaction parameter minimizing the deviance from the Bliss independence model over all dose combinations defined as argminβ∑1−yc−β1−y11−y22 ; and 7) Gamma (γ) is a combination of HSA and Bliss models minimizing argminγ∑1−yc−γmax1−y1,1−y22. For the Loewe-based models, we calculated the two common interaction indices CI (Eq. (8)) and alpha(a) (Eq. (9)). The CI was calculated using an R package SYNERGY [13] (link) and the alpha score was estimated using the R package drc[12] .
Yadav B., Wennerberg K., Aittokallio T, & Tang J. (2015). Searching for Drug Synergy in Complex Dose–Response Landscapes Using an Interaction Potency Model. Computational and Structural Biotechnology Journal, 13, 504-513.
Publication 2015
B-Lymphocytes Cell Lines Cell Survival Chronic Lymphocytic Leukemia Diffuse Large B-Cell Lymphoma Drug Combinations Gamma Rays ibrutinib Malignant Neoplasms Mantle-Cell Lymphoma Pharmaceutical Preparations Psychological Inhibition Resistance, Drug Technique, Dilution Tyrosine Kinase, Agammaglobulinaemia
3
MILE Microarray Protocol Validation
Cited 30 times
There were two stages in the MILE prephase study: protocol training and proficiency testing. As part of the initial protocol training each participating laboratory was provided with identical equipment, including reagent kits, enzymes, spectrophotometer, and heat block instruments, and eight microarray experiments were performed at each centre with an on-site trainer in the respective laboratory being trained. The eight samples analysed during the training course were represented by MCF-7 (breast adenocarcinoma) and HepG2 (liver carcinoma) cell line total RNA (Ambion, Austin, TX, USA) with 1·0 μg and 5·0 μg input of total RNA, respectively, and four leukaemia patient sample lysates prepared from mononuclear cells obtained after Ficoll density purification. Patient lysates comprised cells of one chronic myeloid leukaemia (CML), one chronic lymphocytic leukaemia (CLL), and two replicate lysates of an AML patient sample (containing a translocation t(8;21), French-American-British (FAB) type M2). The total RNA from the patient lysates was extracted at each centre as part of the training programme, making these samples a test of the entire microarray process workflow post sample acquisition (RNeasy kit, Qiagen, Hilden, Germany). Subsequently, after the training phase and for operator proficiency testing, each laboratory independently performed four microarray experiments each for MCF-7 and HepG2 cell lines with inputs of 1·5 μg, 3·0 μg, 5·0 μg, and 8·0 μg total RNA. In total, 204 microarray profiles were included in the analysis (for details see Appendix SI and SII). The three anonymous replicate patient lysates were provided by the Laboratory for Leukaemia Diagnostics in Munich, Germany. All patients gave their informed consent for participation after having been advised of the purpose and investigational nature of the study. The study design adhered to the tenets of the Declaration of Helsinki and was approved by the ethics committees of the participating institutions before its initiation. Details on the microarray analysis workflow, image analysis, quality reports, as well as statistical methods are given in Appendix SI.
Kohlmann A., Kipps T.J., Rassenti L.Z., Downing J.R., Shurtleff S.A., Mills K.I., Gilkes A.F., Hofmann W.K., Basso G., Dell’Orto M.C., Foà R., Chiaretti S., De Vos J., Rauhut S., Papenhausen P.R., Hernández J.M., Lumbreras E., Yeoh A.E., Koay E.S., Li R., Liu W.M., Williams P.M., Wieczorek L, & Haferlach T. (2008). An international standardization programme towards the application of gene expression profiling in routine leukaemia diagnostics: the Microarray Innovations in LEukemia study prephase. British Journal of Haematology, 142(5), 802-807.
Publication 2008
Adenocarcinoma austin Breast Cell Lines Cells Chronic Lymphocytic Leukemia Diagnosis DNA Replication Enzymes Ficoll Hepatocellular Carcinomas Hep G2 Cells Institutional Ethics Committees Leukemia Leukemias, Chronic Granulocytic Microarray Analysis Patients Translocation, Chromosomal
4
Molecular Profiling of Brain Tumors
Cited 24 times
DNA was extracted from samples of primary brain tumor and xenografts and from patient-matched normal blood lymphocytes obtained from the Tissue Bank at the Preston Robert Tisch Brain Tumor Center at Duke University and collaborating centers, as described previously.17 (link) All analyzed brain tumors were subjected to consensus review by two neuropathologists. Table 1 lists the types of brain tumors we analyzed. The samples from glioblastomas included 138 primary tumors and 13 secondary tumors. Of the 138 primary tumors, 15 were from patients under the age of 21 years. Secondary glioblastomas were categorized as WHO grade IV on the basis of histologic criteria but had been categorized as WHO grade II or III at least 1 year earlier. Of the 151 tumors, 63 had been analyzed in our previous genomewide mutation analysis of glioblastomas. None of the lower-grade tumors were included in that analysis.16 (link)
In addition to brain tumors, we analyzed 35 lung cancers, 57 gastric cancers, 27 ovarian cancers, 96 breast cancers, 114 colorectal cancers, 95 pancreatic cancers, and 7 prostate cancers, along with 4 samples from patients with chronic myelogenous leukemia, 7 from patients with chronic lymphocytic leukemia, 7 from patients with acute lymphoblastic leukemia, and 45 from patients with acute myelogenous leukemia. All samples were obtained in accordance with the Health Insurance Portability and Accountability Act. Acquisition of tissue specimens was approved by the institutional review board at the Duke University Health System and at each of the participating institutions.
Exon 4 of the IDH1 gene was amplified with the use of a polymerase-chain-reaction (PCR) assay and sequenced in DNA from the tumor and lymphocytes from each patient, as described previously.16 (link) In all gliomas and medulloblastomas without an R132 IDH1 mutation, exon 4 of the IDH2 gene (which contains the IDH2 residue equivalent to R132 of IDH1) was sequenced and analyzed for somatic mutations. In addition, we evaluated all astrocytomas and oligodendrogliomas of WHO grade I to grade III, all secondary glioblastomas, and 96 primary glioblastomas without R132 IDH1 mutations or R172 IDH2 mutations for alterations in the remaining coding exons of IDH1 and IDH2. All coding exons of TP53 and PTEN were also sequenced in the panel of diffuse astrocytomas, oligodendrogliomas, anaplastic oligodendrogliomas, anaplastic astrocytomas, and glioblastomas. EGFR amplification and the CDKN2A-CDKN2B deletion were analyzed with the use of quantitative real-time PCR in the same tumors.18 (link) We evaluated samples of oligodendrogliomas and anaplastic oligodendrogliomas for loss of heterozygosity at 1p and 19q, as described previously.15 (link),19 (link)
Yan H., Parsons D.W., Jin G., McLendon R., Rasheed B.A., Yuan W., Kos I., Batinic-Haberle I., Jones S., Riggins G.J., Friedman H., Friedman A., Reardon D., Herndon J., Kinzler K.W., Velculescu V.E., Vogelstein B, & Bigner D.D. (2009). IDH1 and IDH2 Mutations in Gliomas. The New England journal of medicine, 360(8), 765-773.
Publication 2009
7-chloro-8-hydroxy-1-(3'-iodophenyl)-3-methyl-2,3,4,5-tetrahydro-1H-3-benzazepine Anaplastic Oligodendroglioma Astrocytoma Astrocytoma, Anaplastic Biological Assay BLOOD Brain Neoplasms Brain Tumor, Primary CDKN2A Gene Chronic Lymphocytic Leukemia Colorectal Carcinoma Deletion Mutation Diploid Cell EGFR protein, human Ethics Committees, Research Exons Gastric Cancer Genes Glioblastoma Glioma Grade II Astrocytomas Heterografts IDH2, human Leukemia, Myelocytic, Acute Leukemias, Chronic Granulocytic Loss of Heterozygosity Lung Cancer Lymphocyte Malignant Neoplasm of Breast Medulloblastoma Mutation Neoplasms Neuropathologist Oligodendroglioma Ovarian Cancer Pancreatic Cancer Patients Polymerase Chain Reaction Precursor Cell Lymphoblastic Leukemia Lymphoma Prostate Cancer PTEN protein, human Real-Time Polymerase Chain Reaction Tissues TP53 protein, human
5
Transcriptome Assembly and Quantification
Cited 21 times
We used Mandalorion version II34 (link) and FLAIR v1.4 to assemble isoforms on the SIRV and simulated data with tuned read support threshold parameters. FLAIR was run with the default settings. Mandalorion was run with the parameters on the GitHub ‘-u 5 -d 30 -s 200 -r 0.05 -i 0 -I 100 -t 0 -T 60’ varying -R (minimum number of reads for an isoform to be reported). Consensus isoform sequences were aligned to the genome with minimap2 and converted to gtf prior to running GFFCompare48 (link). Pinfish was run with default parameters, adjusting the minimum cluster size parameter only. For running FLAIR on the PromethION CLL/B cell data, the following FLAIR collapse algorithm was followed: to assemble the first-pass assembly, transcription start sites and transcription end sites are determined by the density of the read start and end coordinates. We compared 100-nt windows of end sites and picked the most frequently represented site in each window (-n best_only). The final nanopore-specific reference isoform assembly is made by aligning raw reads to the first-pass assembly transcript sequence using minimap2, keeping only the first-pass isoforms with a minimum number of three supporting reads with MAPQ ≥ 1. All pass reads, including reads that did not contain sequenced adapters on both ends, were used when running FLAIR as FLAIR is equipped to deal with truncated reads; information can be gleaned from truncated reads of sufficient length to be assigned to an isoform and the reads that are too short for a unique assignment are excluded from the isoform quantification.
Tang A.D., Soulette C.M., van Baren M.J., Hart K., Hrabeta-Robinson E., Wu C.J, & Brooks A.N. (2020). Full-length transcript characterization of SF3B1 mutation in chronic lymphocytic leukemia reveals downregulation of retained introns. Nature Communications, 11, 1438.
Publication 2020
Chronic Lymphocytic Leukemia Consensus Sequence Genome Protein Isoforms Shock Transcription, Genetic Transcription Initiation Site

Most recents protocols related to «Chronic Lymphocytic Leukemia»

1
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
2
MCC-Spain Multicancer Cohort Study
The MCC-Spain study (http://www.mccspain.org) is a multicase–control study conducted in different provinces in Spain between 2008 and 2013. MCC-Spain included breast, colorectal, prostate, and gastroesophageal cancer, as well as chronic lymphocytic leukemia cases, along with a common pool of population-based controls.30 (link) Cases were histologically confirmed incident prostate cancer patients [International Classification of Diseases, Tenth Revision (ICD)-10 C61 and D07.5], identified through active searches that included periodic visits to hospital departments, and were interviewed closely after diagnosis (median of 58 d). Controls were selected from the general population, identified from the lists of randomly selected family practitioners in primary health centers, and were frequency matched to cases by age for each region (12 recruitment areas).30 (link) Inclusion criteria required participants to be 20–85 y old, to have the ability to understand and answer the questionnaire, and to have lived for at least 6 months in the study area. The study protocol was approved by the ethics committee at all collaborating institutions, and each participant signed an informed consent form prior to enrollment. The overall response rate (subjects interviewed divided by subjects interviewed plus refusals) was 72% for prostate cancer cases and 53% for controls, leading to 996 prostate cancer cases and 1,281 controls recruited in the areas included in the present analysis (Asturias, Barcelona, Cantabria, Madrid, and Valencia).
Donat-Vargas C., Kogevinas M., Castaño-Vinyals G., Pérez-Gómez B., Llorca J., Vanaclocha-Espí M., Fernandez-Tardon G., Costas L., Aragonés N., Gómez-Acebo I., Moreno V., Pollan M, & Villanueva C.M. (2023). Long-Term Exposure to Nitrate and Trihalomethanes in Drinking Water and Prostate Cancer: A Multicase–Control Study in Spain (MCC-Spain). Environmental Health Perspectives, 131(3), 037004.
Publication 2023
Breast Chronic Lymphocytic Leukemia Diagnosis Ethics Committees Malignant Neoplasms Patients Prostate Prostate Cancer
3
Hematopoietic Stem Cell Transplantation
Wherever appropriate, the absolute numbers of transplanted patients, number of transplants or transplant rates are shown for specific countries, indications, or transplant techniques. Myeloid malignancy include acute myeloid leukemia (AML), myelodysplastic or myelodysplastic/myeloproliferative neoplasia (MDS or MDS/MPN overlap), myeloproliferative neoplasm (MPN), and chronic myeloid leukemia (CML). Lymphoid malignancy include acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), Hodgkin lymphoma (HL), non-Hodgkin lymphoma (NHL) and plasma cell disorders (PCD) (including multiple myeloma (MM) and others). Non-malignant disorders include bone marrow failure (BMF: severe aplastic anemia (SAA) and other BMF), thalassemia and sickle cell disease (HG), primary immune deficiencies (PID), inherited diseases of metabolism (IDM), and autoimmune diseases (AID). Others include histiocytosis and other rare disorders.
Passweg J.R., Baldomero H., Ciceri F., Corbacioglu S., de la Cámara R., Dolstra H., Glass B., Greco R., McLornan D.P., Neven B., de Latour R.P., Perić Z., Ruggeri A., Snowden J.A, & Sureda A. (2023). Hematopoietic cell transplantation and cellular therapies in Europe 2021. The second year of the SARS-CoV-2 pandemic. A Report from the EBMT Activity Survey. Bone Marrow Transplantation, 58(6), 647-658.
Publication 2023
Anemia, Sickle Cell Aplastic Anemia Autoimmune Diseases Cell Dyscrasia, Plasma Chronic Lymphocytic Leukemia Grafts Histiocytosis Hodgkin Disease Leukemia, Myelocytic, Acute Leukemias, Chronic Granulocytic Lymph Lymphoma, Non-Hodgkin, Familial Malignant Neoplasms Metabolic Diseases Multiple Myeloma Myeloproliferative Disorders Pancytopenia Patients Precursor Cell Lymphoblastic Leukemia Lymphoma Primary Immune Deficiency Disorder Rare Diseases Thalassemia
4
Retrospective Analysis of Mature B-cell Neoplasms
Flow cytometric results from patients who were diagnosed with mature B-cell neoplasms from October 2015 to October 2020, were reviewed retrospectively. Each case represented a primary diagnosis of lymphoma that was made based on an incisional or excisional tissue biopsy or fine-needle aspiration biopsy specimens. Histologic slides including immunohistochemical slides, were reviewed without knowledge of the flow cytometric results to confirm the initial diagnoses in all available cases. The diagnosis was made according to the World Health Organization (WHO) 2008 classification (12 (link)), WHO 2017 classification,and WHO 2022 classification (2 , 3 (link), 13 (link)). These patients included 119 patients with DLBCL, 25 patients with Burkitt lymphoma, 67 patients with MCL, 76 patients with follicular lymphoma (FL), 30 patients with marginal zone lymphoma (MZL), 32 patients with lymphoplasmacytic lymphoma (LPL)/Waldenstrom’s macroglobulinemia (WM), 159 patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL), 5 patients with hairy cell leukemia, 4 patients with mucosa-associated lymphoid tissue lymphoma (MALT-L), and 42 patients with transformed lymphoma. For the diagnosis, Ki67 expression in lymphoma cells was detected in the bone marrow, pleural effusion, and ascites or lymph node samples. The present study was approved by the Ethical Committee of Tongji Hospital, Tongji Medical College, and Huazhong University of Science and Technology (permit number TJ-IRB20200716), and all procedures conducted followed the protocols of the Declaration of Helsinki.
Mao X., Li Y., Liu S., He C., Yi S., Kuang D., Xiao M., Zhu L, & Wang C. (2023). Multicolor flow cytometric assessment of Ki67 expression and its diagnostic value in mature B-cell neoplasms. Frontiers in Oncology, 13, 1108837.
Publication 2023
Ascites Aspiration Biopsy, Fine-Needle B-Cell Lymphomas Biopsy Bone Marrow Burkitt Lymphoma Cells Chronic Lymphocytic Leukemia Diagnosis Flow Cytometry Hairy Cell Leukemia Lymphoma Lymphoma, Follicular Mucosa-Associated Lymphoid Tissue Lymphoma Nodes, Lymph Patients Pleural Effusion Tissues Waldenstrom Macroglobulinemia
5
Transcriptional Profiling of CML and B-ALL Samples
The following publicly available GEO datasets were analyzed: GSE76312, GSE1922, GSE51083, GSE12211, GES7182 and GSE34861. GSE76312 is comprised of scRNA-seq data for CD34+ cells isolated from healthy donors, BCR-ABL+CD34+ cells isolated from CML different phases, and CML patients treated with TKIs. GSE1922 is microarray data of K562 cells treated with 1 μM Imatinib for 24 h. GSE51083 is a microarray data of K562 cells treated with 100 nM Dasatinib for 4, 8 and 12 h. GES7182 is microarray data of Ph+ B-ALL cell lines treated with 10 μM Imatinib for 16 h. GSE12211 is microarray data of CD34+ cells isolated from chronic phase CML patients receiving Imatinib therapy. GSE34861 is microarray data of adult B-lineage acute lymphoblastic leukemia (B-ALL) with Ph+ subtypes. All datasets were re-analyzed and the expression of TSPAN32 was determined using standard methods.
Qiu Q., Sun Y., Yang L., Li Q., Feng Y., Li M., Yin Y., Zheng L., Li N., Qiu H., Cui X., He W., Wang B., Pan C., Wang Z., Huang J., Sample K.M., Li Z, & Hu Y. (2023). TSPAN32 suppresses chronic myeloid leukemia pathogenesis and progression by stabilizing PTEN. Signal Transduction and Targeted Therapy, 8, 90.
Publication 2023
Adult Cells Chronic Lymphocytic Leukemia Dasatinib Donors Imatinib K562 Cells Leukemia, Myeloid, Chronic-Phase Microarray Analysis Patients Precursor Cell Lymphoblastic Leukemia Lymphoma Single-Cell RNA-Seq Therapeutics

Top products related to «Chronic Lymphocytic 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.
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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.
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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.
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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.

More about "Chronic Lymphocytic Leukemia"

Chronic lymphocytic leukemia (CLL) is a type of slow-growing blood cancer that primarily affects older adults.
It is also known as chronic lymphoid leukemia or small lymphocytic lymphoma (SLL).
CLL is characterized by the accumulation of mature-appearing lymphocytes in the blood, bone marrow, and lymphoid tissues.
These abnormal lymphocytes, often referred to as CLL cells, can crowt out healthy blood cells, leading to various complications.
CLL often progresses slowly, and some individuals may not require treatment for many years.
However, in some cases, the disease can progress more rapidly and require immediate treatment.
Effective management of CLL requires a careful balance between monitoring the disease and providing timely interventions when necessary.
Researchers and clinicians are continously working to improve the understanding and treatment of this complex hematologic malignancy.
CLL studies often utilize cell lines like MEC-1, which are derived from CLL patients, as well as culture media like RPMI 1640 supplemented with fetal bovine serum (FBS), L-glutamine, and penicillin/streptomycin antibiotics to support cell growth and survival.
By leveraging the power of artificial intelligence and data analysis, researchers can optimize chronic lymphocytic leukemia research protocols, locate relevant studies from literature, preprints, and patents, and compare them to identify the best options for their CLL research.
This approach can enhance the rigor and efficiency of CLL studies, ultimately leading to improved understanding and treatment of this disease.