Relevant bibliographies by topics / Leukemia Chemotherapy

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Leukemia Chemotherapy'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Leukemia Chemotherapy.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Leukemia Chemotherapy"

1

Narayanan, Geetha, M. T. Sugeeth, and Lali V. Soman. "Mixed Phenotype Acute Leukemia Presenting as Leukemia Cutis." Case Reports in Medicine 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/1298375.

Full text
Abstract:
Leukemia cutis (LC) is defined as infiltration of the skin by leukemic cells resulting in clinically recognizable cutaneous lesions. It is common in congenital leukemia and acute myeloid leukemia. However, LC has rarely been reported with mixed phenotypic acute leukemia (MPAL). We report the case of a lady who presented with erythematous papular and nodular lesions all over the body. Skin biopsy showed leukemic infiltration and bone marrow aspiration showed MPAL of the T/myeloid with monocytic differentiation lineage. This is the first report of an adult patient with MPAL of the T/myeloid with monocytic differentiation type presenting with leukemia cutis. She was started on chemotherapy with Hyper-CVAD. There is complete resolution of the skin lesions and she has achieved bone marrow remission after the first cycle of chemotherapy.
APA, Harvard, Vancouver, ISO, and other styles
2

Dias, Sergio, Margaret Choy, Kari Alitalo, and Shahin Rafii. "Vascular endothelial growth factor (VEGF)–C signaling through FLT-4 (VEGFR-3) mediates leukemic cell proliferation, survival, and resistance to chemotherapy." Blood 99, no. 6 (March 15, 2002): 2179–84. http://dx.doi.org/10.1182/blood.v99.6.2179.

Full text
Abstract:
Abstract Similar to solid tumors, growth of leukemias may also be angiogenesis dependent. Furthermore, tyrosine kinase receptors specific to endothelial cells are expressed on certain subsets of leukemias. We have previously demonstrated the existence of a VEGF/VEGFR-2 autocrine loop on leukemic cells that supports their growth and migration. Here, we demonstrate that in response to leukemia-derived proangiogenic and proinflammatory cytokines such as basic fibroblast growth factor and IL-1, endothelial cells release increasing amounts of another vascular endothelial growth factor (VEGF) family member, VEGF-C. In turn, interaction of VEGF-C with its receptor VEGFR-3 (FLT-4) promotes leukemia survival and proliferation. We demonstrate in 2 cell lines and 5 FLT-4+ leukemias that VEGF-C and a mutant form of the molecule that lacks the KDR-binding motif induce receptor phosphorylation, leukemia proliferation, and increased survival, as determined by increased Bcl-2/Bax ratios. Moreover, VEGF-C protected leukemic cells from the apoptotic effects of 3 chemotherapeutic agents. Because most leukemic cells release proangiogenic as well as proinflammatory cytokines, our data suggest that the generation of a novel paracrine angiogenic loop involving VEGF-C and FLT-4 may promote the survival of a subset of leukemias and protect them from chemotherapy-induced apoptosis. These results identify the VEGF-C/FLT-4 pathway as a novel therapeutic target for the treatment of subsets of acute leukemia.
APA, Harvard, Vancouver, ISO, and other styles
3

Wu, K. H., H. P. Wu, H. J. Lin, C. H. Wang, H. Y. Chen, T. Weng, C. T. Peng, and Y. H. Chao. "Concurrent hypopituitarism and leukemic retinopathy in a child with B-precursor acute lymphoblastic leukemia and isolated central nervous system relapse." Current Oncology 23, no. 4 (August 8, 2016): 431. http://dx.doi.org/10.3747/co.23.3006.

Full text
Abstract:
Hypopituitarism in leukemia is very rare. In addition, central nervous system (cns) relapse and leukemic retinopathy in childhood acute lymphoblastic leukemia (all) have declined with the use of modern systemic chemotherapy that includes cns prophylaxis. Here, we report the case of a 4-year-old girl who received chemotherapy and intrathecal therapy without cns radiation after a diagnosis of B-precursor all without cns involvement. Three months after chemotherapy completion, she presented with lower-extremity weakness and was diagnosed with an isolated cns relapse. Concurrent hypopituitarism and leukemic retinopathy were also found. After receiving craniospinal radiotherapy and systemic chemotherapy, her retinopathy and vision improved. She is now in complete remission, and she is still on chemotherapy according to the guideline from the Pediatric Oncology Group. Although rare, hypopituitarism and leukemic retinopathy should be taken into consideration in patients with cns involvement by leukemia.
APA, Harvard, Vancouver, ISO, and other styles
4

Falqués, Ton, Mattias Pilheden, Qirui Zhang, Louise Ahlgren, Helena Sturesson, Lars Ronnstrand, Axel Hyrenius Wittsten, Julhash U. Kazi, and Anna Hagstroem-Andersson. "Treatment Shapes Clonal Evolution and Resistance Patterns in Murine KMT2A-Rearranged Leukemia with Subclonal FLT3 N676K." Blood 138, Supplement 1 (November 5, 2021): 3354. http://dx.doi.org/10.1182/blood-2021-144760.

Full text
Abstract:
Abstract Our understanding of how individual mutations, whether present in all or just a fraction of the leukemia cells, affect cellular responses to therapy is limited. Leukemia mouse models provide a unique possibility to explore how therapy affects the evolution of genetically distinct clones and identify mechanisms of resistance allowing transfer to human disease. Herein, we studied how different therapies influenced survival, clonal evolution, and resistance patterns in mouse KMT2A-MLLT3 leukemia with subclonal FLT3 N676K. Bone marrow (BM) from a leukemia expressing KMT2A-MLLT3-mCherry in all cells and a FLT3 N676K-GFP in 40% of cells, were re-transplanted to sublethally irradiated recipients (Hyrenius-Wittsten el al, Nat Commun, 2018). Upon engraftment, treatment was started with either chemotherapy (cytarabine for 5 days + doxorubicin for 3 days), the FLT3 inhibitor AC220, chemotherapy followed by AC220, or AC220+Trametinib, a MEK inhibitor. Targeted treatment was given for 28 days; controls received vehicle (Fig. 1a). Survival was estimated by Kaplan-Meier and the developing leukemias were analyzed by flow-cytometry, RNA-sequencing and targeted gene re-sequencing. Each treatment prolonged survival with a median latency of 30 days for chemotherapy , 37.5 days for AC220, 42 days for chemotheraphy+AC220, and 45 days for AC220+Trametenib, versus 25.5 days for the control (Fig. 1b). Most leukemia cells expressed GFP/mCherry and mice displayed splenomegaly and leukocytosis. Next, we investigate how treatment impacted evolution of the KMT2A-MLLT3+FLT3 N676K cells and while they constituted all cells in control and chemotherapy-treated mice, the other treatments impacted their evolution. Three distinct patterns were discerned with either >80% of KMT2A-MLLT3+FLT3 N676K cells, >80% of cells expressing KMT2A-MLLT3 alone, or dual similar sized clones of cells expressing KMT2A-MLLT3 alone or KMT2A-MLLT3+FLT3 N676K(Fig. 1c). Eradication of the FLT3-leukemia cells was rare, but most common in mice receiving AC220+Trametinib and the frequency of dual clones increased when mice received chemotherapy followed by AC220, in line with treatment selectively affecting evolution of genetically distinct cells (Fig. 1d). To find clues to treatment resistance, RNA-sequencing (N=44) revealed segregation into three major clusters: 1) leukemias expressing KMT2A-MLLT3 alone, 2) control and chemotherapy-treated leukemias and 3) AC220 treated leukemias. Notably, a set of AC220-treated mice clustered close to the control and chemotherapy-treated mice (Fig. 1e). Flow-cytometry data showed that similar to the control and chemotherapy-treated leukemias, the myeloid BM cells of those AC220 samples, aberrantly expressed B220 (Fig. 1f). Gene set enrichment analysis revealed enrichment of gene sets correlating with stem cells and oxidative phosphorylation in those AC220-treated leukemias, suggesting a switch in cellular phenotype and metabolic state upon treatment. By contrast, the other AC220 leukemias (cluster 3), instead showed enrichment of gene sets correlating with granulocyte/macrophage progenitors and immune regulatory pathways, indicating selective dependence of distinct cellular pathways upon resistance (Fig. 1g). Finally, acquisition of AC220 resistance mutations was rare with a FLT3 D835Y and a Ptpn11 G503V detected in two leukemias only. Taken together, these results show that the specific treatment given not only affected survival of the FLT3 N676K mutated KMT2A-MLLT3 leukemia, but also impacted how the genetically distinct cells evolved. The general lack of acquired mutations upon targeted treatment suggests that target-independent mechanisms that result in alternate activation of survival/proliferation explains acquired resistance in a majority of mice and provides novel insights into treatment resistance. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
APA, Harvard, Vancouver, ISO, and other styles
5

Moha, Rico. "Chemotherapy medication of Vincristine and Vinblastine." Cancer Research and Cellular Therapeutics 1, no. 1 (December 8, 2017): 01–02. http://dx.doi.org/10.31579/2640-1053/007.

Full text
Abstract:
Cancers treated with Vincristine and vinblastine include: acute leukemia, Hodgkin's and non- Hodgkin's lymphoma, neuroblastoma, rhabdomyosarcoma, Ewing's sarcoma, Wilms' tumor, multiple myeloma, chronic leukemias, thyroid cancer, brain tumors, non-small cell lung cancer, bladder cancer, melanoma, and testicular cancer andIt is also used to treat some blood disorders. It is given by injection into a vein. Vincristine and vinblastine exhibit differential activity against tumors and normal tissues. In this work, a number of cultured cell lines were assayed for their sensitivity to the antiproliferative and cytotoxic effects of the two drugs following short-term (4 hr) or during continuous exposures. Differential activity was not seen when cells were subjected to continuous exposures. The concentrations of Vincristine and vinblastine, respectively, that inhibited growth rates by 50% were: mouse leukemia L1210 cells, 4.4 and 4.0 nw; mouse lymphoma S49 cells, 5 and 3.5 nM; mouse neuroblastoma cells, 33 and 15 nw; HeLa cells, 1.4 and 2.6 nw; and human leukemia HL-60 cells, 4.1 and 5.3 nM. In contrast, differential toxicity was seen when cells were subjected to 4-hr exposures and transferred to drug-free medium: the 50% growth-inhibitory concentrations for Vincristine and vinblastine, respectively, for inhibition (a) of proliferation of L1210 cells were 100 and 380 nM and of HL-60 cells were 23 and 900 nM and (b) of colony formation of L1210 cells were 6 and >600 nM and of HeLa cells were 33 and 62 nM. Uptake and release of [3H]- vincristine and [3H]vinblastine were examined in L1210 cells under the conditions of growth experiments. Uptake of both drugs was dependent on the pH of culture media, and signifi cantly greater amounts of [3H]vinblastine than of [3H]vincristine were associated with cells after 4-hr exposures to equal concen trations of either drug. When cells were transferred to drug-free medium after 4-hr exposures, vinblastine was released much more rapidly from cells than was Vincristine, and by 0.5 hr after resuspension of cells, the amount of Vincristine associated with the cells was greater than the amount of vinblastine and remained so for up to at least 6 hr.
APA, Harvard, Vancouver, ISO, and other styles
6

Becker, Pamela S. "Dependence of Acute Myeloid Leukemia on Adhesion within the Bone Marrow Microenvironment." Scientific World Journal 2012 (2012): 1–4. http://dx.doi.org/10.1100/2012/856467.

Full text
Abstract:
Acute myeloid leukemia (AML) cells home to the endosteal region of the bone marrow. They interact with bone marrow stromal components including extracellular matrix proteins, glycosaminoglycans, and stromal cells, by which they derive proliferative and growth inhibitory signals. Furthermore, adhesion to marrow stroma confers chemotherapy drug resistance and thereby promotes leukemia survival. A subpopulation of the leukemic blasts, known as leukemia stem cells, that are capable of propagating the leukemia, remain sheltered in the bone marrow microenvironment, exhibit resistance to chemotherapy, and serve as the origin of relapse after a variable period of remission. Detachment of these cells from the bone marrow in combination with chemotherapy may improve the outcome of therapy for AML.
APA, Harvard, Vancouver, ISO, and other styles
7

Frankfurt, Olga, and Martin S. Tallman. "Growth Factors in Leukemia." Journal of the National Comprehensive Cancer Network 5, no. 2 (February 2007): 203–15. http://dx.doi.org/10.6004/jnccn.2007.0020.

Full text
Abstract:
The role of myeloid growth factors, such as granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor, in the management of acute myeloid and acute lymphoblastic leukemias has been evaluated extensively in multiple clinical trials. Growth factors have been given before, concurrently, or sequentially with chemotherapy with the goal of reducing the duration of neutropenia and consequently the incidence and severity of infections, and improving the rate of remissions and overall survival. They also have been studied as chemotherapy-sensitizing agents in an effort to recruit dormant myeloid stem cells into the sensitive phase of the cycle. Additionally, growth factors, shown to stimulate proliferation and differentiation of leukemia cells in vitro, were evaluated as monotherapy in patients with acute leukemia. Most studies show modest improvement in the duration of the neutropenia, which does not consistently correlate with the severity of infection, rate or duration of remissions, or disease-free and overall survival. Attempts to enhance the chemosensitivity of the leukemic cells and decrease drug resistance failed to improve the rate of remission and survival in several large series. However, more recent reports suggested an improved outcome in younger patients with acute myeloid leukemia with normal karyotype. Several anecdotal case reports have shown that growth factor monotherapy can induce a complete remission in patients with acute leukemia. Data from the published clinical trials do not seem to support emergence of drug-resistant leukemia, worsening toxicity, and bone marrow failure with growth factor administration.
APA, Harvard, Vancouver, ISO, and other styles
8

DeAngelo, Daniel J., Eytan M. Stein, and Farhad Ravandi. "Evolving Therapies in Acute Myeloid Leukemia: Progress at Last?" American Society of Clinical Oncology Educational Book, no. 36 (May 2016): e302-e312. http://dx.doi.org/10.1200/edbk_161258.

Full text
Abstract:
Acute myeloid leukemia (AML) is an acquired disease characterized by chromosomal translocations and somatic mutations that lead to leukemogenesis. Systemic combination chemotherapy with an anthracycline and cytarabine remains the standard induction regimen for “fit” adults. Patients who achieve complete remission generally receive postinduction therapy with cytarabine-based chemotherapy or an allogeneic bone marrow transplant. Those unfit for induction chemotherapy are treated with hypomethylating agents (HMAs), low-dose cytarabine, or they are offered supportive care alone with transfusions and prophylactic antimicrobials. The revolution in understanding the genetics of AML, facilitated by next-generation sequencing, has led to many new drugs against driver mutations. Better methods of identification of leukemic blasts have provided us with better means to detect the disease left behind after cytotoxic chemotherapy regimens. This measurable residual disease has been correlated with poorer relapse-free survival, demonstrating the need for novel strategies to eradicate it to improve the outcome of patients with acute leukemias. In this article, we discuss adapting and improving AML therapy by age and comorbidities, emerging targeted therapies in AML, and minimal residual disease (MRD) assessment in AML.
APA, Harvard, Vancouver, ISO, and other styles
9

Kumar, Bijender, Marvin Orellana, Jamison Brooks, Srideshikan Sargur Madabushi, Liliana E Parra, Darren Zuro, Qiong Wang, Ching-Cheng Chen, and Susanta Hui. "Leukemia Cells Remodel Adipocyte Niches and Their Progenitor Functions to Generate Leukemia Favoring Niche." Blood 132, Supplement 1 (November 29, 2018): 1294. http://dx.doi.org/10.1182/blood-2018-99-115689.

Full text
Abstract:
Abstract Increasing evidence suggests that the cancer cells take shelter in different osteoblastic and adipocytic niches, where they hide from chemotherapy and continue to survive. As yet, how leukemia cells alter the bone marrow (BM) adipocytic niches to facilitate their expansion and assist them in evading chemotherapy is unclear. We have previously shown that the acute myeloid leukemia (AML) cells directly or through their exosomes, reprogram BM osteoblastic niche which facilitates their expansion and suppress normal hematopoiesis(Kumar B et al, Leukemia 2018,32(3):575-587). In this study , we provide further evidences that AML and Acute lymphoid leukemia (ALL) transformed the BM adipocytic niche to facilitate their expansion and suppress normal hematopoiesis. Using MLL-AF9 (AML) knock-in mouse, MLL-AF9 or BCR-ABL(p190, ALL) HSC transduction transplantation leukemia mice models, we performed flow cytometry analysis to show that the leukemia cells stimulate expansion of BM derived CD45-Ter119-CD31-CD166-Sca1+CD140a+(PaS)MSCs population compared to normal mice (p=0.04, p=0.001 and p=0.002 respectively).Further, the BM osteoblasts specific Osteocalcin mRNA expression in sorted stroma cells and flow cytometry based osteoblasts population (CD45-Ter119-CD31- CD166+Sca1-) numbers were also significantly reduced in AML (p=0.04) and ALL (p=0.02) mice models suggesting bone loss with the leukemia development. Similar to osteoblasts loss, mature adipocytes (Perilipin, PPARg mRNA) were also significantly reduced in the ALL/AML mice compared to control. The triglyceride content and white adipose tissue(WAT) mass was diminished in leukemic mice , suggesting leukemia may have utilized adipocyte for survival. Adipocyte loss in the leukemia mice was accompanied by long term hematopoietic stem cells(LT-HSC ) and erythroid megakaryocyte progenitor (MEP) populations reduction in the leukemic mice (p=0.01 and p=0.02 respectively). To dissect the mechanism of adipocytes reduction is either due to adipocyte loss or adipocytes maturation defect in leukemic mice, we analyzed different stromal progenitors in normal and leukemic mice and identified that the leukemia cells stimulate the growth of BM derived adipocytic committed progenitors (CD45-Ter119-CD31-CD166-Sca1+CD140a+CD29+CD24-) and blocked the chondrocyte/osteoblastic/adipocytic multipotent progenitors (CD45-Ter119-CD31- CD166-Sca1+CD140a+CD29+CD24+) population (p=0.02,p=0.01 respectively).Despite the increase in number of MSCs and adipocytic progenitors, the in-vitro adipocytic differentiation potential of sorted adipocyte committed progenitors was severely compromised in ALL and AML compared to control. The WAT western blot analysis showed significantly increased expression of ATGL and pHSL(Ser-563) expression involved in triglyceride lipolysis in the leukemic mice .The ALL leukemic adipocytic stroma had increased expression of IL-1β and IL-6 cytokine levels compared to normal stroma and provided more survival advantage to leukemia cells in in-vitro co-culture experiments in nutrient deprived conditions and during chemo-radiotherapy treatment. Further, the ATGL and HSL pharmacological inhibitors rescued leukemia induced lipolysis, reduced leukemia proliferation and increased chemotherapy induced apoptosis in leukemia cells. Overall, this data strongly suggests the notion of progressive decline in functional LT-HSCs & normal hematopoiesis, adipocytes and osteoblasts numbers with leukemia progression due to activation of lipolytic enzymes resulting in increased availability of fatty acids for leukemia expansion and is a common feature in both lymphoid and myeloid leukemias. Disclosures No relevant conflicts of interest to declare.
APA, Harvard, Vancouver, ISO, and other styles
10

Hapsari, Happy Indri. "INCREASING KNOWLEDGE OF PARENTS IN CARE OF THE SIDE EFFECTS OF CHEMOTHERAPY IN LEUKEMIA CHILDREN THROUGH BOOKLET IN DR. MOEWARDI GENERAL HOSPITAL SURAKARTA." Jurnal Ilmiah Kesehatan Media Husada 8, no. 2 (October 24, 2019): 39–47. http://dx.doi.org/10.33475/jikmh.v8i2.196.

Full text
Abstract:
Leukemia is the number one cancer that attacks children aged 0 to 18 years. Parents who have children with leukemia will experience a heavy burden in caring for children. Health education is one way for nurses to ease the burden of parents in finding information about leukemia. The use of booklets has long been known as a medium in health education, where effectiveness is very significant in increasing parental knowledge. The purpose of the study: to determine the effect of health education with booklets on the level of knowledge of parents in caring for leukemic children who are on chemotherapy. Method: quasi experiment and using Wilcoxon data analysis. Results: p-value 0.00, where the p - value <0.005 so that there is an effect of booklets in increasing parental knowledge about the treatment of side effects of chemotherapy in children with leukemia. Conclusion: booklet administration increases parental knowledge about the treatment of chemotherapy side effects in leukemic children.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Leukemia Chemotherapy"

1

Palle, Josefine. "Optimizing Chemotherapy in Childhood Acute Myeloid Leukemia." Doctoral thesis, Uppsala University, Department of Women's and Children's Health, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9189.

Full text
Abstract:

Despite major advances in our understanding of the biology of childhood acute myeloid leukemia (AML) and the development of new cytotoxic drugs, the prognosis of long-term survival is still only 60-65 %.

In the present research, we studied the pharmacokinetics of drugs used in the induction therapy of childhood AML and performed in vitro drug sensitivity testing of leukemic cells from children with AML.

The aims of the studies were to correlate the results of the analysis to biological and clinical parameters and to identify subgroups of AML with specific drug sensitivity profiles in order to better understand why treatment fails in some patients and how therapy may be improved.

Blood samples were analysed to study the pharmacokinetics of doxorubicin (n=41), etoposide (n=45) and 6-thioguanine (n=50). Doxorubicin plasma concentration and total body clearance were correlated to the effect of induction therapy, and doxorubicin plasma concentration was an independent factor for complete remission, both in univariate and multivariate analysis including sex, age, and white blood cell count at diagnosis. For etoposide and 6-thioguanine no correlation was found between pharmacokinetics and clinical effect. Children with Down syndrome (DS) tended to reach higher blood concentrations of etoposide and thioguanine nucleotides, indicating that dose reduction may be reasonable to reach the same drug exposure as in children without DS.

Leukemic cells from 201 children with newly diagnosed AML, 15 of whom had DS, were successfully analysed for in vitro drug sensitivity by the fluorometric microculture cytotoxicity assay (FMCA). We found that samples from children with DS were highly sensitive to most drugs used in AML treatment. In non-DS children, the t(9;11) samples were significantly more sensitive to cytarabine (p=0.03) and doxorubicin (p=0.035) than other samples. The findings might explain the very favorable outcome reported in children with DS and t(9;11)-positive AML. A specific drug resistance profile was found for several other genetic subgroups as well. A detailed study of MLL-rearranged leukemia showed that cellular drug sensitivity is correlated both to partner genes and cell lineage, findings that support the strategy of contemporary protocols to include high-dose cytarabine in the treatment of patients with MLL-rearrangement, both in AML and acute lymphoblastic leukemia (ALL).

Our results indicate that drug resistance and pharmacokinetic studies may yield important information regarding drug response in different sub-groups of childhood AML, helping us to optimize future chemotherapy in childhood AML.

APA, Harvard, Vancouver, ISO, and other styles
2

Masquelier, Michèle. "Leukemia chemotherapy : experimental studies on pharmacological optimisation /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-046-X/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Kwok, Suet-kei Gladys. "The effectiveness of a chemotherapy educational programme (CEP) for Leukaemia and Lymphoma patients." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31972937.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

O'Connor, Brian 1961. "Studies towards the synthesis of the novel antileukemic agent CI-920 and the addition of cuprates to vinyltriphenylphosphonium bromide : a synthesis of 1,5-disubstituted 1Z,4Z-pentadienes." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75443.

Full text
Abstract:
A new method for the preparation of 1,5-disubstituted-1Z,4Z-pentadienes by the addition of alkenyl cuprates to vinyltriphenylphosphonium bromide followed by an aldehyde is described. This method is used for the syntheses of 6Z,9Z-heneicosadiene and 15,15-(diethyldithio)-13S-t-butyldiphenylsilyloxy-6Z,9Z,11E-pentadecatriene. Syntheses of $(-)$-(5R)-argentilactone and (+)-(5R)-goniothalamin are described. Model studies towards the synthesis of the novel antileukemic agent CI-920 were carried out.
APA, Harvard, Vancouver, ISO, and other styles
5

李富榮 and Foo-wing Lee. "Pharmacokinetics of homoharringtonine in Chinese leukemia patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1990. http://hub.hku.hk/bib/B31209233.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Fuentes, Gari Maria. "A mathematical model of cell cycle heterogeneity for personalizing leukemia chemotherapy." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/26301.

Full text
Abstract:
Acute myeloid leukemia is a type of blood cancer characterized by an excessive build-up of immature blood cells in the bone marrow and blood streams. As a result, healthy stem cells become space- and resource-limited, and do not produce enough functional cells for the body to operate normally. Treatment is required immediately, consisting of intensive chemotherapy. Chemotherapy dosage and schedule are derived from established protocols which do not account for patient-specific and disease-specific heterogeneity. Over- or under- dosage are thus common; a more rational and personalized approach to chemotherapy treatments is required. Specifically, incorporating the effect of chemotherapy in a cell cycle phase-specific manner would be highly beneficial. In this work, we developed a population balance model (PBM) of the cell cycle based on the underlying biology that captures the progress of cells within and between phases. It was validated with three leukemia cell lines separately for the duration of one cell cycle, and in variable mixtures where forward and backward kinetics as well as clonal identification were successfully performed. The model was compared against two other cell cycle models: an existing ODE model and a newly developed DDE model featuring phase durations as delays. The PBM outperformed the other two in recapitulating biological features, and displayed a higher sensitivity to treatment when coupled to an existing pharmacokinetic/pharmacodynamic model of chemotherapy treatment. The PBM was further used in the prediction of clonal evolution during chemotherapy, highlighting the important heterogeneity in treatment response between clones but also the competitive features among them that could be critical in the success of the treatment. Finally, the first steps towards implementing this technology at clinical level were taken by defining converted, measurable data sets. A prototype application, "ChemoApp", was developed at the user interface level for the introduction of this research into clinical practice.
APA, Harvard, Vancouver, ISO, and other styles
7

Kam, Kevin, and 甘季燐. "Therapeutic potential of demethylation agents and histone deaceytlase inhibitors in NK-cell lymphoma and leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011564.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Gregory, Bradley Barnes Battaglini Claudio L. "In-hospital individualized prescriptive exercise intervention for acute leukemia patients undergoing chemotherapy." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,678.

Full text
Abstract:
Thesis (M.A.)--University of North Carolina at Chapel Hill, 2006.
Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment for the degree of Master of Arts in the Department of Exercise and Sport Science (Exercise Physiology)." Discipline: Exercise and Sports Science; Department/School: Exercise and Sport Science.
APA, Harvard, Vancouver, ISO, and other styles
9

Frost, Britt-Marie. "Chemotherapy in Childhood Acute Lymphoblastic Leukemia : In vitro cellular drug resistance and pharmacokinetics." Doctoral thesis, Uppsala University, Department of Women's and Children's Health, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2664.

Full text
Abstract:

The aims of the studies described in this thesis were to investigate the pharmacokinetics of and cellular resistance to chemotherapy as causes of treatment failure in childhood acute lymphoblastic leukemia (ALL).

Leukemic cells from 370 children with newly diagnosed ALL were tested by the Fluorometric Microculture Cytotoxicity Assay to measure their resistance to each of ten standard cytotoxic drugs. In the high-risk group, increased in vitro resistance to each of the drugs dexamethasone, etoposide and doxorubicin was associated with a worse clinical outcome. Combining the results for these drugs yielded a drug resistance score, showing a relative risk of relapse in the most resistant group that was 9.8 times higher than in the most sensitive group. In the standard-risk and intermediate-risk groups, final evaluation must await longer follow-up.

The new cytotoxic agent CHS 828 was equally active in vitro in samples from children with acute myeloblastic leukemia (AML) and ALL, with 50% cell kill at concentrations achievable in vivo. In AML samples CHS 828 also displayed high frequencies of synergistic interactions with four standard drugs. The well-known differences in clinical outcome between Down´s syndrome (DS) and non-DS children with acute leukemia may partly be explained by our finding of differences in drug resistance at the cellular level.

Pharmacokinetic studies were performed at the start of induction treatment of ALL. Doxorubicin was assayed by reversed-phase liquid chromatography with fluorometric detection, and vincristine by high performance liquid chromatography with electrochemical detection. Plasma doxorubicin concentrations were measured in 107 children after 23 h of a 24-h infusion. The median steady-state concentration in children 4-6 years old, a group known to have a favorable outcome of treatment, was about 50% higher than in those 1-2 and >6 years old Vincristine pharmacokinetics was evaluated in 98 children. There was no correlation between age and total body clearance or any other pharmacokinetic parameters.

In vitro testing of cellular drug resistance might be useful in predicting the outcome in high-risk ALL. The further exploration of CHS 828 in childhood leukemia seems warranted. There is no pharmacokinetic rationale for the common practice of administering relatively lower doses of vincristine to adolescents than to younger children.

APA, Harvard, Vancouver, ISO, and other styles
10

Landier, Wendy. "Predictors of Non-Adherence to Oral Chemotherapy in Children with Acute Lymphoblastic Leukemia." Diss., University of Hawaii at Manoa, 2010. http://hdl.handle.net/10125/22058.

Full text
Abstract:
Overall survival for pediatric patients with acute lymphoblastic leukemia (A.L.L.) treated with contemporary therapy now exceeds 85%; however, approximately 20% will experience relapse. Since A.L.L. is the most common malignancy in children, relapsed patients comprise a large proportion of the total number of children with cancer. The prognosis for long-term survival following relapse is generally poor; thus, relapsed A.L.L. is a significant contributor to cancer-related mortality in children. Poor adherence to oral medication is a substantial problem in contemporary health care and may contribute to unexplained relapses in children with A.L.L. Therapy for pediatric A.L.L. includes a prolonged “maintenance” phase that requires daily 6- mercaptopurine (6MP), a self- or parent/caregiver-administered oral chemotherapy agent given for approximately two years. 6MP has been shown to be a critical component of the curative regimen for A.L.L.; thus, children with A.L.L. who fail to adhere to oral 6MP chemotherapy as prescribed may be at increased risk of leukemia relapse. This study used extant questionnaire data from a cohort of children with A.L.L enrolled on a Children’s Oncology Group study (AALL03N1) to determine the prevalence of self/parent-reported non-adherence to oral 6MP during the maintenance phase of A.L.L. therapy, and to identify sociodemographic and behavioral predictors of non-adherence to oral 6MP. Twenty-two percent of children in the cohort were non-adherent to oral chemotherapy, defined as missing more than one dose of 6MP for non-medical reasons over the 112-day observation period. The risk of non-adherence was significantly increased for those who failed to perceive the severity of the child’s illness (Odds ratio [OR] 1.89, 95% Confidence Interval [CI] 1.00-3.55, P=0.049) or the benefits of treatment with oral 6MP (OR 1.78, 95%CI 1.07-2.94, P=0.025). Vulnerable subgroups included Hispanic ethnicity (OR 2.25, 95%CI 1.30-3.90, P=0.004) and older age (OR 1.07 per year, 95%CI 1.02-1.12, P=0.005). Study findings suggest that even occasional reports of missed 6MP doses may herald a significant adherence problem; that patients and their parents may need ongoing reminders regarding the subclinical and asymptomatic nature of leukemia in remission; and that frequent review with families regarding the purpose, function, and proper administration of oral 6MP is imperative.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Leukemia Chemotherapy"

1

Ueda, Takanori, ed. Chemotherapy for Leukemia. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Schmidt, Carolina Witchmichen Penteado, and Kaléu Mormino Otoni, eds. Chemotherapy and Pharmacology for Leukemia in Pregnancy. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-54058-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Heinemann, Volker. Supportive therapy in leukemia patients: Clinical handbook with checklist. Stuttgart ; New York: G. Thieme Verlag ; New York : Thieme Medical Publishers, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Rebirth: A leukemia survivor's journal of healing during chemotherapy, bone marrow transplant and recovery. [Place of publication not identified]: Xlibris Corp., 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

1946-, Cheson Bruce D., Keating Michael J. 1943-, and Plunkett William 1943-, eds. Nucleoside analogs in cancer therapy. New York: M. Dekker, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

1951-, Pui Ching-Hon, ed. Treatment of acute leukemias: New directions for clinical research. Totowa, N.J: Humana Press, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Hancock, Sarah. Fludarabine as first line therapy for chronic lymphocytic leukaemia. Birmingham: University of Birmingham, Department of Public Health and Epidemiology, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Kaspers, G. J. L., 1963-, Pieters R, and International Symposium on Drug Resistance in Leukemia and Lymphoma (3rd : 1998 : Amsterdam, Netherlands), eds. Drug resistance in leukemia and lymphoma III. New York: Kluwer Academic/Plenum Press, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Heim, Marcel U. The leukemia patient as a partner in therapy: A guidebook for patients, relatives, nurses, and physicians. Stuttgart: GTV Stuttgart, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Kaspers, G. J. L., 1963-, ed. Drug resistance in leukemia and lymphoma: The clinical value of laboratory studies. Chur, Switzerland: Harwood Academic Publishers, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Leukemia Chemotherapy"

1

Ueda, Takanori. "An Overview." In Chemotherapy for Leukemia, 1–7. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kiyoi, Hitoshi. "FLT3 Inhibitors." In Chemotherapy for Leukemia, 167–79. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Asou, Norio. "Retinoic Acid, All-trans Retinoic Acid (ATRA), and Tamibarotene." In Chemotherapy for Leukemia, 183–211. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Kizaki, Masahiro. "The Molecular Basis of Arsenic Trioxide Treatment for Acute Promyelocytic Leukemia (APL)." In Chemotherapy for Leukemia, 213–20. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Emi, Nobuhiko. "Arsenic Trioxide: Clinical Pharmacology and Therapeutic Results." In Chemotherapy for Leukemia, 221–38. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Yamauchi, Takahiro, and Takanori Ueda. "Nelarabine." In Chemotherapy for Leukemia, 241–50. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Yamauchi, Takahiro, and Takanori Ueda. "Forodesine." In Chemotherapy for Leukemia, 251–60. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Parker, William B., and Varsha Gandhi. "Clofarabine: Structure, Mechanism of Action, and Clinical Pharmacology." In Chemotherapy for Leukemia, 261–86. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

McCloskey, James, Jamie Koprivnikar, Stefan Faderl, Dirk Reinhardt, and Nobuko Hijiya. "Clinical Use of Clofarabine for Adults and Children with Leukemia." In Chemotherapy for Leukemia, 287–309. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Sarkisjan, Dzjemma, Renske D. M. Steenbergen, Jacqueline Cloos, and Godefridus J. Peters. "Re-emerging Antimetabolites with Novel Mechanism of Action with Respect to Epigenetic Regulation: Basic Aspects." In Chemotherapy for Leukemia, 311–26. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3332-2_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Leukemia Chemotherapy"

1

Sadakata, H., H. Iri, T. Uchiyama, K. Andoh, H. Tanaka, N. Kobayashi, and T. Maekawa. "PROSPECTIVE STUDY ON DOSE SCHEDULE OF HEPARIN THERAPY FOR DIC COMPLICATION IN LEUKEMIA PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644195.

Full text
Abstract:
From the retrospective analysis of correlation between the activity of tissue factor (TFA) of leukemia cells (LC) and DIC complication in patients with acute leukemia, we have already reported an adequate dose schedule of heparin treatment for DIC can be calculated in accordance with the TFA of LC To evaluate this dose schedule, the prospective analysis was designed. Prior to the remission induction chemotherapy, TFA of LC obtained from 67 patients with leukemia (ANLL: M1;5, M2;22, M;34, M4;8, M5;4, M6;3, CML-BC: 11) was measured by Nemerson's two-stage method reported previously. Regardless of DIC complication, continuous heaprin therapy with 0, 15,000 or 9,700X + 9,000 units/day (X: logarithm value of TFA) was started with chemotherapy in patinet with 0, 0.8−4.1 U or >4.1 U of TFA, respectively. The complete remission and significant decrease of LC were achieved in 16 patients with ANLL and 5 patients with CML-BC, respectively. In 20 patients whose LC had 0.8 U of TFA or more (group A), 15 and 1 patients were complicated by DIC before and after start of the chmotherapy, respectively. DIC was improved in all of these patients. Other 4 patients were not complicated by DIC. There was no major bleeding due to heparin administration. In 47 patients whose LC had less than 0.8 U of TFA (group B), 40 patients were not complicated by DIC throughout the observation period. Remaining 4 and 3 patients were complicated by DIC before and after start of the chemotherapy, respectively. Among these patients, only one, whose DIC was due primarily to endotoxinemia, failed in control of the DIC. Consequently, in 67 patients subjected to this study, only one patient died of complicated DIC, although 17 patients (group A:4, group B:13) died of various causes other than DIC during the observation periods. These results suggest that our dose schedule of heparin is appropriate for both prevention and treatment of DIC complication in leukemia patients.
APA, Harvard, Vancouver, ISO, and other styles
2

De Hoyos Reyes, Alicia. "Simulation of a Novel Intrathecal Device for CSF Sampling and Delivery of Chemotherapy in Leukemia Patients." In 2019 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/dmd2019-3246.

Full text
Abstract:
Current chemotherapy delivery methods and CSF sampling in leukemia pediatric patients represents a challenge with multiple associated risks creating the need for a more efficient technique. The proposed design of a novel intrathecal device was submitted to computer simulation analysis finding promising results regarding the fluid behavior inside the port and the structural performance of the components.
APA, Harvard, Vancouver, ISO, and other styles
3

Hamsaeed, Payman, and Amera Muhammad. "Staphylococcus Spp Bacteremia Complications in Acute leukemia patient after chemotherapy." In 4th International Scientific Conference of Cihan University-Erbil on Biological Sciences. Cihan University-Erbil, 2017. http://dx.doi.org/10.24086/bios17.20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Long, Xin, and Michele Redell. "Abstract 543: Stroma-mediated chemotherapy resistance in acute myeloid leukemia cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-543.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Zhang, Cathy C., Zhengming Yan, Bernadette Pascual, Stephen Huang, Qing Zong, Mark Elliot, and Patrick Lappin. "Abstract LB-277: Induction chemotherapy induces enrichment of leukemic stem cells in PDX models of acute myeloid leukemia." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-277.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Mordechai, Shaul, J. Mordehai, Jagannathan Ramesh, C. Levi, Mahmud Huleihal, Vitaly Erukhimovitch, A. Moser, and J. Kapelushnik. "Application of FTIR microspectroscopy for the follow-up of childhood leukemia chemotherapy." In International Symposium on Optical Science and Technology, edited by Cam Nguyen. SPIE, 2001. http://dx.doi.org/10.1117/12.450167.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Bhatia, Smita. "Abstract IA07: Adherence to oral chemotherapy in children with Acute Lymphoblastic Leukemia." In Abstracts: Ninth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; September 25-28, 2016; Fort Lauderdale, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7755.disp16-ia07.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Silveira, Vanessa, Augusto Andrade, Gustavo Cruzeiro, Rosane Queiroz, Luiz Gonzaga Tone, and Carlos Alberto Scrideli. "Abstract C158: Shoc2 gene induces chemotherapy sensitivity in acute lymphoblastic leukemia cell line." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c158.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

McNeer, Nicole, John Philip, Heather Geiger, Rhonda E. Ries, Vincent-Philippe Lavallee, Michael Walsh, Minita Shah, et al. "Abstract 2870: Genetic mechanisms of primary chemotherapy resistance in pediatric acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2870.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

McNeer, Nicole, John Philip, Heather Geiger, Rhonda E. Ries, Vincent-Philippe Lavallee, Michael Walsh, Minita Shah, et al. "Abstract 2870: Genetic mechanisms of primary chemotherapy resistance in pediatric acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2870.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Leukemia Chemotherapy"

1

Getz, Kelly D., Julia E. Szymczak, Farah Contractor, Brian T. Fisher, and Richard Aplenc. Comparing Chemotherapy Recovery at Home versus in the Hospital for Children with Acute Myeloid Leukemia. Patient-Centered Outcomes Research Institute (PCORI), January 2021. http://dx.doi.org/10.25302/01.2021.cer.140922827.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Yin, Xuewei, Yi Ding, Liming Yu, Chenchen Guo, Yanyan Cui, Xixi Zhai, Yan wang, et al. Efficacy and safety of chemotherapy combined with different doses of IL-2 maintenance therapies for acute myeloid leukemia: A protocol for a Bayesian network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0106.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Leukemia Chemotherapy' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography