1. Cell cycle control in acute myeloid leukemia - PMC - NCBI
Classic therapeutic agents for leukemia, such as anthracyclines or cytarabine, prevent leukemia cells from cycling. This is achieved through induction of DNA ...
Acute myeloid leukemia (AML) is the result of a multistep transforming process of hematopoietic precursor cells (HPCs) which enables them to proceed through limitless numbers of cell cycles and to become resistant to cell death. Increased proliferation ...
2. [PDF] STAAR Biology May 2017 - Texas Education Agency
33 People who have leukemia, a cancer that affects white blood cells, are often given Cytarabine. This drug inhibits the synthesis of DNA. Which phase of ...
3. TEKS Biology High School - B.5.A: Cell Cycle | Quizalize
People who have leukemia, a cancer that affects white blood cells, are often given Cytarabine. ... Which phase of the cell cycle is most affected by Cytarabine?
Quiz your students on TEKS Biology High School - B.5.A: Cell Cycle practice problems using our fun classroom quiz game Quizalize and personalize your teaching.
4. 13 People who have leukemia, a cancer that affects white blood cells ...
May 15, 2022 · This drug inhibits the synthesis of DNA. Which phase of the cell cycle is most affected by Cytarabine? A Interphase B Cytokinesis C Prophase ...
VIDEO ANSWER: So during the occurrence of cancer, cancer is uncontrolled cell growth. So the cell growth in this case is uncontrolled. So I write it as U. N. C…
5. How Chemotherapy Drugs Work - American Cancer Society
Missing: synthesis | Show results with:synthesis
Chemotherapy drugs work on cancer cells at different parts of the cell cycle. Learn about the different types of chemotherapy and what cancers they often treat.
6. The Cell Cycle | CancerQuest
Missing: leukemia, white blood
Further information on the topics on this page can also be found in most introductory Biology textbooks, we recommend Campbell Biology, 11th edition.1
7. Antibody drug conjugate: the “biological missile” for targeted ...
Mar 22, 2022 · Antibody–drug conjugate (ADC) is typically composed of a monoclonal antibody (mAbs) covalently attached to a cytotoxic drug via a chemical ...
Antibody–drug conjugate (ADC) is typically composed of a monoclonal antibody (mAbs) covalently attached to a cytotoxic drug via a chemical linker. It combines both the advantages of highly specific targeting ability and highly potent killing effect to achieve accurate and efficient elimination of cancer cells, which has become one of the hotspots for the research and development of anticancer drugs. Since the first ADC, Mylotarg® (gemtuzumab ozogamicin), was approved in 2000 by the US Food and Drug Administration (FDA), there have been 14 ADCs received market approval so far worldwide. Moreover, over 100 ADC candidates have been investigated in clinical stages at present. This kind of new anti-cancer drugs, known as “biological missiles”, is leading a new era of targeted cancer therapy. Herein, we conducted a review of the history and general mechanism of action of ADCs, and then briefly discussed the molecular aspects of key components of ADCs and the mechanisms by which these key factors influence the activities of ADCs. Moreover, we also reviewed the approved ADCs and other promising candidates in phase-3 clinical trials and discuss the current challenges and future perspectives for the development of next generations, which provide insights for the research and development of novel cancer therapeutics using ADCs.
8. Response and Toxicity to Cytarabine Therapy in Leukemia and Lymphoma
This results in inhibition of DNA polymerase, chain termination and stalling DNA and RNA synthesis with the consequent blockage of the cell cycle from G1 to the ...
Cytarabine is a pyrimidine nucleoside analog, commonly used in multiagent chemotherapy regimens for the treatment of leukemia and lymphoma, as well as for neoplastic meningitis. Ara-C-based chemotherapy regimens can induce a suboptimal clinical outcome in a fraction of patients. Several studies suggest that the individual variability in clinical response to Leukemia & Lymphoma treatments among patients, underlying either Ara-C mechanism resistance or toxicity, appears to be associated with the intracellular accumulation and retention of Ara-CTP due to genetic variants related to metabolic enzymes. Herein, we reported (a) the latest Pharmacogenomics biomarkers associated with the response to cytarabine and (b) the new drug formulations with optimized pharmacokinetics. The purpose of this review is to provide readers with detailed and comprehensive information on the effects of Ara-C-based therapies, from biological to clinical practice, maintaining high the interest of both researcher and clinical hematologist. This review could help clinicians in predicting the response to cytarabine-based treatments.
9. [PDF] Chronic Myeloid Leukemia
With current drug therapies, most people diagnosed with chronic phase CML can expect to ... People with certain types of blood cancer often have low LAP levels.
10. Arabinosylguanine-induced Apoptosis of T-Lymphoblastic Cells
To test this hypothesis, we performed experiments in a T-lymphoblastic leukemia cell line (CCRF-CEM) after synchronization with a double aphidicolin block.
Abstract. 9-β-d-Arabinosylguanine (ara-G) is a recently introduced and effective treatment for T-cell acute lymphoblastic leukemia, but how ara-G and ara-G triphosphate (ara-GTP) kill cells is not known. We hypothesized that, in cycling T-lymphoblastoid cells, ara-G may act directly by incorporation into DNA, which may lead to apoptosis. Hence, blocking the incorporation of ara-G monophosphate (ara-GMP) into DNA may prevent apoptosis. To test this hypothesis, we performed experiments in a T-lymphoblastic leukemia cell line (CCRF-CEM) after synchronization with a double aphidicolin block. Intracellular accumulation of ara-GTP was neither cell cycle dependent nor affected by aphidicolin (53 ± 5 μm/h without aphidicolin, 50 ± 5 μm/h with aphidicolin). Cells at the G1-S boundary accumulated 75 ± 7 μm ara-GTP with minimal incorporation into DNA (5 ± 2 pmol ara-GMP/mg DNA) and had little biochemical or morphological evidence of apoptosis. In marked contrast, cells in S phase had significantly more ara-G incorporated into DNA (24 ± 4 pmol ara-GMP/mg DNA), although the cytosolic concentration of ara-GTP (85 ± 7 μm) was similar to that in the G1-enriched population. In the S-phase cells, there was a corresponding increase in apoptosis (measured as high molecular weight DNA fragmentation and morphological changes), and the incorporation of ara-GTP into DNA resulted in a >95% inhibition of DNA synthesis. There was a direct linear relationship between the number of cells in S phase and both the total number of ara-GMP molecules in DNA and the inhibition of DNA synthesis. Blocking of ara-GTP incorporation into S-phase DNA abolished biochemical and morphological features of apoptosis, even in the presence of cytotoxic level of intracellular ara-GTP. Taken together, these data demonstrate that the incorporation of ara-GTP into DNA is the critical event that mediates the induction of apoptosis in CCRF-CEM cells.
11. [PDF] A Phase 2 study of WEE1 Inhibition with AZD1775 alone or combined ...
1.21 Background on Cytarabine, DNA Damage Repair and Cell Cycle. Checkpoints ... Only to be done in those patients with circulating tumor cells in their blood ...
12. Radotinib enhances cytarabine (Ara-C)-induced acute myeloid ...
Dec 4, 2020 · Acute myeloid leukemia (AML) is a heterogeneous disease that frequently relapses after standard chemotherapy. Therefore, there is a need for ...
Acute myeloid leukemia (AML) is a heterogeneous disease that frequently relapses after standard chemotherapy. Therefore, there is a need for the development of novel chemotherapeutic agents that could treat AML effectively. Radotinib, an oral BCR-ABL tyrosine kinase inhibitor, was developed as a drug for the treatment of chronic myeloid leukemia. Previously, we reported that radotinib exerts increased cytotoxic effects towards AML cells. However, little is known about the effects of combining radotinib with Ara-C, a conventional chemotherapeutic agent for AML, with respect to cell death in AML cells. Therefore, we investigated combination effects of radotinib and Ara-C on AML in this study. Synergistic anti-cancer effects of radotinib and Ara-C in AML cells including HL60, HEL92.1.7, THP-1 and bone marrow cells from AML patients have been examined. Diverse cell biological assays such as cell viability assay, Annexin V-positive cells, caspase-3 activity, cell cycle distribution, and related signaling pathway have been performed. The combination of radotinib and Ara-C was found to induce AML cell apoptosis, which involved the mitochondrial pathway. In brief, combined radotinib and Ara-C significantly induced Annexin V-positive cells, cytosolic cytochrome C, and the pro-apoptotic protein Bax in AML cells including HL60, HEL92.1.7, and THP-1. In addition, mitochondrial membrane potential and Bcl-xl protein were markedly decreased by radotinib and Ara-C. Moreover, this combination induced caspase-3 activity. Cleaved caspase-3, 7, and 9 levels were also increased by combined radotinib and Ara-C. Additionally, radotinib and Ara-C co-treatment induced G0/G1 arrest via the induction of CDKIs such as p21 and p27 and the inhibition of CDK2 and cyclin E. Thus, radotinib/Ara-C induces mitochondrial-dependent apoptosis and G0/G1 arrest via the regulation of the CDKI–CDK–cyclin cascade in AML cells. In addition, our results showed that combined treatment with radotinib and Ara-C inhibits AML cell growth, including tumor volumes and weights in vivo. Also, the combination of radotinib and Ara-C can sensitize cells to chemotherapeutic agents such as daunorubicin or idarubicin in AML cells. Therefore, our results can be concluded that radotinib in combination with Ara-C possesses a strong anti-AML activity.
13. Chemotherapy-induced differential cell cycle arrest in ... - Haematologica
Mar 1, 2018 · Given that cancer cells proliferate rapidly, Ara-C can kill cancer cells by interfering with their DNA synthesis during the S phase of the cell ...
Chemotherapeutic agents, e.g., cytarabine and doxorubicin, cause DNA damage. However, it remains unknown whether such agents differentially regulate cell cycle arrest in distinct types of B-cell lymphomas, and whether this phenotype can be exploited for developing new therapies. We treated various types of B cells, including primary and B lymphoma cells, with cytarabine or doxorubicin, and determined DNA damage responses, cell cycle regulation and sensitivity to a Wee1 inhibitor. We found that cyclin A2/B1 upregulation appears to be an intrinsic programmed response to DNA damage; however, different types of B cells arrest in distinct phases of the cell cycle. The Wee1 inhibitor significantly enhanced the apoptosis of G2 phase-arrested B-cell lymphomas by inducing premature entry into mitosis and mitotic catastrophe, whereas it did not affect G1/S-phase-arrested lymphomas. Cytarabine-induced G1-arrest can be converted to G2-arrest by doxorubicin treatment in certain B-cell lymphomas, which correlates with newly acquired sensitivity to the Wee1 inhibitor. Consequently, the Wee1 inhibitor together with cytarabine or doxorubicin inhibited tumor growth in vitro and in vivo more effectively, providing a potential new therapy for treating B-cell lymphomas. We propose that the differential cell cycle arrest can be exploited to enhance the chemosensitivity of B-cell lymphomas.
14. [PDF] PEdiAtRic LEUkEMiAS - ACCP
Although recent advancements have been made in improving the survival rate of children with acute lymphoblastic leukemia (ALL) and acute myeloid leukemia. (AML) ...
15. [PDF] Acute Myeloid Leukemia (AML) - Alberta Health Services
Consider a screening lumbar puncture in cases of myelomonocytic or monocytic acute myeloid leukemia. (AML) or in those with a presenting white cell count of >40 ...
16. [PDF] The pterocarpanquinone LQB‑118 compound induces apoptosis of ...
After 24 h of cytarabine treatment, more cells in the G2/M phase were detected ... of HL‑60R cells, with little effect on cell cycle progression. The present ...
17. Diagnosis and management of acute myeloid leukemia in adults
AML-related prognostic factors includes white blood count (WBC), existence of prior MDS, previous cytotoxic therapy for another disorder (see section 9), and ...
Abstract. In 2003, an international working group last reported on recommendations for diagnosis, response assessment, and treatment outcomes in acute myeloid l
18. [PDF] DNMT3A Harboring Leukemia-Associated Mutations ...
We show that cells expressing. DNMT3Amut are more sensitive to cytarabine-induced replication stress, and that this effect is independent of the cell- and ...
19. Chemotherapy Primer: Why? What? and How? | OncoLink
Most chemotherapy agents kill cancer cells by affecting DNA synthesis or function, a process that occurs through the cell cycle. Each drug varies in the way ...
An introduction to chemotherapy, including history, various classes of chemo, how it works and how it is given.
20. [PDF] ETOPOSIDE 1. Exposure Data - IARC Publications
First, most cancer patients are treated with combined treatment modalities (chemotherapy and radiotherapy), and multiple antineoplastic drugs are usually ...