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4 results on '"LSC, leukemic stem cell"'

1. Phenotyping and Target Expression Profiling of CD34+/CD38− and CD34+/CD38+ Stem- and Progenitor cells in Acute Lymphoblastic Leukemia

Author

Blatt, K, Menzl, I, Eisenwort, G, Cerny-Reiterer, S, Herrmann, H, Herndlhofer, S, Stefanzl, G, Sadovnik, I, Berger, D, Keller, A, Hauswirth, A, Hoermann, G, Willmann, M, Rülicke, T, Sill, H, Sperr, WR, Mannhalter, C, Melo, JV, Jäger, U, Sexl, V, Valent, P, and Imperial College Trust

Subjects
Original article, GO, gemtuzumab-ozogamicin, NSG, NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ, Antigens, CD34, PB, peripheral blood, TKI, tyrosine kinase inhibitor, lcsh:RC254-282, Cell Line, OS, overall survival, Mice, LSC, leukemic stem cell, CML, chronic myeloid leukemia, Mice, Inbred NOD, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, hemic and lymphatic diseases, Biomarkers, Tumor, Animals, Humans, Oncology & Carcinogenesis, Ph, Philadelphia chromosome, Gene Expression Regulation, Leukemic, Stem Cells, 1103 Clinical Sciences, MNC, mononuclear cell, ALL, acute lymphoblastic leukemia, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, ADP-ribosyl Cyclase 1, Leukemia, Myeloid, Acute, BM, bone marrow, Neoplastic Stem Cells, Female, SCT, stem cell transplantation
Abstract

Leukemic stem cells (LSCs) are an emerging target of curative anti-leukemia therapy. In acute lymphoblastic leukemia (ALL), LSCs frequently express CD34 and often lack CD38. However, little is known about markers and targets expressed in ALL LSCs. We have examined marker- and target expression profiles in CD34+/CD38- LSCs in patients with Ph+ ALL (n = 22) and Ph- ALL (n = 27) by multi-color flow cytometry and qPCR. ALL LSCs expressed CD19 (B4), CD44 (Pgp-1), CD123 (IL-3RA), and CD184 (CXCR4) in all patients tested. Moreover, in various subgroups of patients, LSCs also displayed CD20 (MS4A1) (10/41 = 24%), CD22 (12/20 = 60%), CD33 (Siglec-3) (20/48 = 42%), CD52 (CAMPATH-1) (17/40 = 43%), IL-1RAP (13/29 = 45%), and/or CD135 (FLT3) (4/20 = 20%). CD25 (IL-2RA) and CD26 (DPPIV) were expressed on LSCs in Ph+ ALL exhibiting BCR/ABL1p210, whereas in Ph+ ALL with BCR/ABL1p190, LSCs variably expressed CD25 but did not express CD26. In Ph- ALL, CD34+/CD38- LSCs expressed IL-1RAP in 6/18 patients (33%), but did not express CD25 or CD26. Normal stem cells stained negative for CD25, CD26 and IL-1RAP, and expressed only low amounts of CD52. In xenotransplantation experiments, CD34+/CD38- and CD34+/CD38+ cells engrafted NSG mice after 12-20 weeks, and targeting with antibodies against CD33 and CD52 resulted in reduced engraftment. Together, LSCs in Ph+ and Ph- ALL display unique marker- and target expression profiles. In Ph+ ALL with BCR/ABL1p210, the LSC-phenotype closely resembles the marker-profile of CD34+/CD38- LSCs in chronic myeloid leukemia, confirming the close biologic relationship of these neoplasms. Targeting of LSCs with specific antibodies or related immunotherapies may facilitate LSC eradication in ALL.

Published
2018

2. Cancer stem cell biology: from leukemia to solid tumors

Author

Jordan, Craig T

Subjects
*TUMORS, *STEM cells, *CANCER treatment, *HEMATOPOIETIC system, *ONCOLOGY, *MEDICAL genetics
Abstract

The biology of stem cells and their intrinsic properties are now recognized as integral to tumor pathogenesis in several types of cancer. This observation has broad ramifications in the cancer research field and is likely to impact our understanding of the basic mechanisms of tumor formation and the strategies we use to treat cancers. A role for stem cells has been demonstrated for cancers of the hematopoietic system, breast and brain. Going forward it is likely that stem cells will also be implicated in other malignancies. Hence, a detailed understanding of stem cells and how they mediate tumor pathogenesis will be critical in developing more effective cancer therapies. [Copyright &y& Elsevier]

Published
2004
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3. Molecular techniques for the personalised management of patients with chronic myeloid leukaemia

Author

Letizia Foroni, Jane F. Apperley, Mary Alikian, and Robert Peter Gale

Subjects
Oncology, Pathology, SCT, stem cell transplant, Review Article, Disease, Biochemistry, lcsh:Microbiology, CMR, complete molecular response/remission, ZMW, zero-mode wave-guided, 0302 clinical medicine, LSC, leukemic stem cell, EURO-SKI, European Stop Tyrosine Kinase Inhibitor Study, DESTINY, De-Escalation and Stopping Treatment of Imatinib, Nilotinib or sprYcel in Chronic Myeloid Leukaemia, NTC, No Template Control, PCR, Polymerase Chain Reaction, lcsh:QH301-705.5, ABL, RT, reverse transcription, CP, chronic phase, ALL, acute lymphoblastic leukaemia, CAP, College of American Pathology, KDa, Kilo Dalton, AP, accelerated phase, μg, microgram, RT-dPCR, reverse transcription-digital polymerase chain reaction, 030220 oncology & carcinogenesis, NGS, TKD, tyrosine kinase domain, ARQ, armored RNA Quant, IRIS, interferon and cytarabine versus STI571, medicine.medical_specialty, Cancer therapy, IS, International Scale, cDNA, coding or complimentary DNA, RT-qPCR, reverse transcription-quantitative polymerase chain reaction, Chronic myeloid leukaemia, 03 medical and health sciences, ELN, European Leukaemia Net, STIM, stop imatinib, Molecular Biology, CML, chronic myeloid leukaemia, LPC, leukemic progenitor cells, NGS, next generation sequencing, BMT, bone marrow transplantation, Q-PCR, quantitative polymerase chain reaction, respiratory tract diseases, IC, inhibotory concentration, MMR, major molecular response/remission, SMRT, single-molecule real-time sequencing, Mbp, mega base pair, dPCR, digital polymerase chain reaction, m-bcr, minor-breakpoint cluster region, dMIQE, Minimum Information for Publication of Quantitative Digital PCR Experiments, PFS, Progression Free Survival, lcsh:QR1-502, GUSB, glucuronidase beta gene, Kbp, Kilo Base Pairs, μ-bcr, micro-breakpoint cluster region, ABL1, Abelson murine leukaemia virus, MRD, minimal residual disease, TKI, tyrosine kinase inhibitor, DNA, deoxyribonucleic acid, Structural Biology, hemic and lymphatic diseases, CES, capillary electrophoresis sequencing, CML, μl, microliter, breakpoint cluster region, Myeloid leukemia, allo-SCT, Allogeneic Stem Cell Transplantation, LoQ, limit of quantification, mRNA, messenger RNA, medicine.anatomical_structure, MRD, emPCR, emulsion PCR, Molecular Medicine, Ph, Philadelpia, WHO, World Health Organisation, ATP, adenosine triphosphate, Bp, base pair, NCCN, National Comprehensive Cancer Network, QC, Quality Control, BC, blast crisis, LoD, limit of detection, PB, Peripheral Blood, gDNA, genomic deoxyribonucleic acid, Internal medicine, InDels, insertions and deletions, Molecular monitoring, medicine, EAC, Europe Against Cancer, nM, manomolar, business.industry, dPCR, MR, deep molecular response/remission, M-bcr, major-breakpoint cluster region, Gold standard (test), lcsh:Biology (General), NEQAS, National External Quality Assessement Service, BM, bone marrow, BCR, breakpoint cluster region, Bone marrow, business, 030215 immunology
Abstract

Chronic myeloid leukemia (CML) is the paradigm for targeted cancer therapy. RT-qPCR is the gold standard for monitoring response to tyrosine kinase-inhibitor (TKI) therapy based on the reduction of blood or bone marrow BCR-ABL1. Some patients with CML and very low or undetectable levels of BCR-ABL1 transcripts can stop TKI-therapy without CML recurrence. However, about 60 percent of patients discontinuing TKI-therapy have rapid leukaemia recurrence. This has increased the need for more sensitive and specific techniques to measure residual CML cells. The clinical challenge is to determine when it is safe to stop TKI-therapy. In this review we describe and critically evaluate the current state of CML clinical management, different technologies used to monitor measurable residual disease (MRD) focus on comparingRT-qPCR and new methods entering clinical practice. We discuss advantages and disadvantages of new methods.

Published
2017
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4. Molecular techniques for the personalised management of patients with chronic myeloid leukaemia.

Author

Alikian M, Gale RP, Apperley JF, and Foroni L

Abstract

Chronic myeloid leukemia (CML) is the paradigm for targeted cancer therapy. RT-qPCR is the gold standard for monitoring response to tyrosine kinase-inhibitor (TKI) therapy based on the reduction of blood or bone marrow BCR-ABL1 . Some patients with CML and very low or undetectable levels of BCR-ABL1 transcripts can stop TKI-therapy without CML recurrence. However, about 60 percent of patients discontinuing TKI-therapy have rapid leukaemia recurrence. This has increased the need for more sensitive and specific techniques to measure residual CML cells. The clinical challenge is to determine when it is safe to stop TKI-therapy. In this review we describe and critically evaluate the current state of CML clinical management, different technologies used to monitor measurable residual disease (MRD) focus on comparingRT-qPCR and new methods entering clinical practice. We discuss advantages and disadvantages of new methods.

Published
2017
Full Text
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