Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy

Patrick Olanrewaju Osho; Okunnuga Ndidi; Ojo Matilda; Odunlade Olufunke

doi:doi:10.11648/j.crj.20210902.15

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Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy

Patrick Olanrewaju Osho, Okunnuga Ndidi, Ojo Matilda, Odunlade Olufunke

Published in Cancer Research Journal (Volume 9, Issue 2)

Received: 21 April 2021 Accepted: 17 May 2021 Published: 25 June 2021

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Abstract

Chronic myeloid leukemia (CML) is a triphasic clonal myeloproliferative disorder characterized by the presence of Philadelphi a chromosome (Ph) in over 95% of cases alongside excessive accumulation of clonal myeloid cells in hematopoietic tissues. This occurs as a result of reciprocal translocation between the long arms of chromosome 9 and 22 t (9;22) (q34; q11) creating the fusion oncogene BCR–ABL1 which exhibits constitutive tyrosine kinase activity. It is one of the commonest haematological malignancies in low economies around the world including Nigeria. The clinical features of CML are often described in 3 phases namely the chronic phase (CP), accelerated phase (AP), and blastic phase (BP) while CP is the most common stage with progression to AP and BP occurring later. Despite that, prognosis of CML is dependent on phase of disease, age, and response to therapy, the only curative approach in use currently is hematopoietic stem cell transplantation with other drugs being used for cytogenetic responses. This study focuses on the aetiopathophysiology, cytogenetics, molecular biology, clinical/laboratory features and treatment options of CML. Rigorous review of literature on the study was retrieved from relevant oncology journals and textbooks abstracted and indexed in PubMed, Google Scholar, ProQuest, CINAHL, and Science Direct. The study discovered that, resistance of CML to imatinib has been reported with research having reached the advanced stage on the use of alternative drugs (e.g., Nilotinib and Desatinib). There are also potentials for these new drugs to become the treatment choice and first line drugs for the treatment of CML.

Published in	Cancer Research Journal (Volume 9, Issue 2)
DOI	10.11648/j.crj.20210902.15
Page(s)	111-121
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2021. Published by Science Publishing Group

Keywords

Chronic Myeloid Leukemia, Oncogene, Imatinib, Tyrosine Kinase, Scoring System

References

[1]	Durosinmi M. A. Haemato-Oncology Chemotherapy. pp 15-17.
[2]	J. V. Melo, T. P. Hughes, and J. F. Apperley, “Chronic myeloid leukemia, The American Society of Hematology, pp. 132–152, 2003. Faderl S, Kantarjian HM, Talpaz M. Chronic myelogenous leukemia: update on biology and treatment. Oncology. 1999; 13: 169–184.
[3]	Oyekunle A. A., Durosinmi, M. A., Bolarinwa R. A. and Owojuyigbe T. Chronic Myeloid Leukemia in Nigerian Patients: Anemia is an Independent Predictor of Overall Survival. Clinical Medicine Insights: Blood Disorders 2016: 9 9.
[4]	Lateef Salawu and Norah O. Akinola Lihteh Wu, Joaquin Martinez, Andrew W. Opthalmologic Manifestations of Leukemias. Medscape. 2020.
[5]	Caroline E. O and Olatunji E. Trends in Pattern of Leukaemia incidence in a Tertiary Hospital in Nigeria: 1990-2004. Journal of Medicine and Biomedicine research 2006. (5): 44-49.
[6]	Boma PO, Durosinmi MA, Adediran lA, Akinola NO, Salawu I. Clinical and prognostic features of Nigerians with Chronic Myeloid Leukemia. Niger PostgradMedJ. 2006; 13: 47-52.
[7]	Oyekunle AA, Zander AR, Binder M, et al. Outcome of allogeneic SCT in patients with chronic myeloid leukemia in the era of tyrosine kinase inhibitor therapy. Ann Hematol. 2012; 92 (4): 487–496.
[8]	Michael W. D. Chronic Myeloid Leukemia: An Historical Perspective. Haematol Educ Prog. 2008: (1): 418.
[9]	Nwagu M. U., Awodu O. A. Chronic Myelogenous Leukemia - A Review of Pathophysiology, Clinico-Laboratory Features and Emerging Treatment Options. Nig Hosp Pract. (6), 2010, 93-96.
[10]	Victor Hoffbrand, Douglas Higgs, David Keeling, Atul B Mehta Postgraduate Haematology. pp 419-437.
[11]	Maren Rohrbacher and Joerg Hasford. Etiology and Epidemiology of Chronic Myeloid Leukemia. Neoplastic Diseases of the Blood, 2013 (2): 11-17.
[12]	Goldman J. M., Melo J. V. Chronic myeloid leukemia – Advances in biology and new approaches to treatment. N Eng J Med. 2003; 349: 1451-1464.
[13]	Talpaz M., Shah N. P., Kantarijan (2006). Dasatinib in imatinib-resistant Philadephia chromosome-positive leukemias. N. Engl. J. Med. 354, 2531-41.
[14]	Ishikura H, Yufu Y, Yamashita S, Abe Y, Okamura T, Motomura S, Nishimura J, Nawata H (1997). Biphenotypic blast crisis of chronic myelogenous leukemia: abnormalities of p53 and retinoblastoma genes. Leuk Lymphoma 25: 573–578.
[15]	Goldman J. M. Monitoring minimal residual disease in BCR-ABL positive chronic myeloid leukemia in imatinib era. Current Opinion in Haematology.
[16]	Bain B. (2003). Cytogenetic and molecular genetic aspects if eosinophilic leuekemias. British Journal of Haematology. 122: 173-9.
[17]	Skorski T (2002) BCR/ABL regulates response to DNA damage: the role in resistance to genotoxic treatment and in genomic instability. Oncogene 21: 8591–8604.
[18]	Janowska-Wieczorek A, Majka M, Marquez-Curtis L, Wertheim JA, Turner AR, Ratajczak MZ (2002) Bcr-abl positive cells secrete angiogenic factors including matrix metalloproteinases and stimulate angiogenesis in vivo in Matrigel implants. Leukemia 16: 1160–1166.
[19]	Sillaber C., Mayerhofer M., Agis H., Sagaster V., Mannhalter V., Sperr W. R., Geissler K., and Valent P. Chronic myeloid leukemia: Pathophysiology, diagnostic parameters, and current treatment concepts. Wien Klin Wochenschr (2003) 115/13–14: 485–504.
[20]	Vardiman JW, Pierre R, Thiele J, Imbert M, Brunning RD, Flandrin G (2001) Chronic myelogenous leukaemia. In: Jaffe ES, Harris NL, Stein H, Vardiman JW (eds) Tumours of haematopoietic and lympoid tissues. IARC Press, Lyon, pp 20–26.
[21]	Tefferi A, Thiele J, Orazi A et al. Proposals and rationale for revision of the world health organization diagnostic criteria for polycythemia vera, essential thrombocythemia and primary myelofibrosis: recommendation from an ad hoc international expert panel. Blood 2007; 110: 1092-1097.
[22]	Tefferi A. Classification, diagnosis and management of myeloproliferative disorders in the JAK2V617Fera. Hematology Am Soc Hematol Educ Program 2006; 240-245.
[23]	Shirish M. K. Essentials of Haematology. 2^nd edition 2013. pp 284-287.
[24]	Baccarani M, Deininger MW, Rosti G et al. (2013) European Leukemia Net recommendations for the management of chronic myeloid leukemia: 2013. Blood 122: 872–84.
[25]	Kyrsiak K., Christopher M., Skidmore Z., Demeter R., Magrini V., Kunisaki J., Laughlin M., Duncavage E., Miller C., Ozenberger B., Griffith M., Wartman L. A genomic analysis of Philadelphia chromosome-negative AML arising in patients with CML (2016). Blood Cancer Journal. 6; 413.
[26]	Solary E., Itzykson R. How I treat chronic myelomonocytic leukemia. Blood. (2017). 130 (2): 126-136.
[27]	Szuber N., Tefferi A. Chronic neutrophilic leukemia: new science and new diagnostic criteria (2018). Blood Cancer Journal. 8: 19.
[28]	Thakral Beenu, Wang A. Haematology and Coagulation. A comprehensive review for board preparation, certification, and clinical practice. 2015, pages 93-115.
[29]	Andolina J. R., Neudorf S. M., Corey S. J. (2012) How I treat childhood CML. Blood 119: 1821-30.
[30]	Apperley J (2009) CML in pregnancy and childhood. Best Practice in Research and Clinical Haematology 22: 455–74.
[31]	Faber E. (2015) Prognostic Scoring Systems in CML – Improvement Impossible? Journal of Leukemia, S1: 001.
[32]	Verstovsek S, Kantarjian H, Manshouri T, Cortes J, Giles FJ, Rogers A, Albitar M (2002) Prognostic significance of cellular vascular endothelial growth factor expression in chronic phase chronic myeloid leukemia. Blood 99: 2265–2267.
[33]	Sokal JE, Cox EB, Baccarani M, Tura S, Gomez GA, et al. (1984) Prognostic discrimination in “good-risk” chronic granulocytic leukemia. Blood 63: 789-799.
[34]	Hasford J, Pfirrmann M, Hehlmann R, Baccarani M, Guilhot F, Mahon FX, Kluin-Nelemans HC, Ohnishi K, ThaleeJ, Steegmann JL (2003) Prognosis and prognostic factors for patients with chronic myeloid leukemia: nontransplant therapy. Semin Hematol 40: 4-12.
[35]	Hasford J, Ansari H, Pfirrmann M, Hehlmann R (1996) Analysis and validation of prognostic factors for CML. German CML Study Group. Bone Marrow Transplant 17 Suppl 3: S49-54.
[36]	Hasford J, Baccarani M, Hoffmann V, Guilhot J, Saussele S, et al. (2011) Predicting complete cytogenetic response and subsequent progression-free survival in 2060 patients with CML on imatinib treatment: the EUTOS score. Blood 118: 686-692.
[37]	Marin D, Ibrahim AR, Goldman JM (2011) European Treatment and Outcome Study (EUTOS) score for chronic myeloid leukemia still requires more confirmation. J Clin Oncol 29: 3944-3945.
[38]	Jabbour E, Cortes J, Nazha A, O’Brien S, Quintas-Cardama A, et al. (2012). EUTOS score is not predictive for survival and outcome in patients with early chronic phase chronic myeloid leukemia treated with tyrosine kinase inhibitors: a single institution experience. Blood 119: 4524-4526.
[39]	Hoffmann VS, Baccarani M, Lindoerfer D, Castagnetti F, Turkina A, et al. (2013) The EUTOS prognostic score: review and validation in 1288 patients with CML treated frontline with imatinib. Leukemia 27: 2016-2022.
[40]	Druker BJ, Guilhot F, O'Brien SG et al. Five-year follow-up of patients receiving Imatinib for Chronic Myeloid Leukaemia. New England Journal of Medicine. 2006; 355 (20): 2408–2417.
[41]	Goldman J. M., Druker B. Chromic myeloid leukemia: current treatment options. Blood. 98: 2039-42.
[42]	Hasford J, Pfirrmann M and Hocchaus A. How long will chronic myeloid leukemia patients treated with imatinib mesylate live? Leukemia 2005; 19: 497-499.
[43]	Christian S., Matthias M., Hermine A., Verena S., Christine M., Wolfgang R., Klaus G., and Peter V. Chronic myeloid leukemia: Pathophysiology, diagnostic parameters, and current treatment concepts. (2003) 115/13–14: 485–504.
[44]	Deininger, M. W. N., Druker, B. J., 2003. Specific targeted therapy of chronic myelogenous leukemia with imatinib. Pharmacological Reviews, 55 (3), 401–423.
[45]	Rubin, B. P., Schuetze, S. M., Eary, J. F., Norwood, T. H., Mirza, S., Conrad, E. U., Bruckner, J. D., 2002. Molecular targeting of platelet-derived growth factor B by imatinib mesylate in a patient with metastatic dermatofibrosarcoma protuberans. J. Clin. Oncology, 20 (17), 3586–3591.
[46]	Durosinmi et al. The use of imatinib mesylate in Nigerians with chronic myelogenous leukemia. Cellular Therapy and Transplantation (CTT) 2008; vol 1 No. 2.
[47]	Guido Marcucci, Danilo Perrotti, and Michael A. Caligiuri. Understanding the Molecular Basis of Imatinib Mesylate Therapy in Chronic Myelogenous Leukemia and the Related Mechanisms of Resistance. 9, 1248–1252, April 2003.
[48]	Adeagbo B. A, Bolaji O. O., Olugbade T. O, Durosinmi M. A., Bolarinwa R. A., Masimirembwa C.
[49]	Gambacorti-Passerini, C. B., Gunby, R. H., Piazza, R., Galietta, A., Rostagno, R., and Scapozza, L. Molecular mechanisms of resistance to imatinib in Philadelphia-chromosome-positive leukaemias. Lancet Oncol., 4: 75–85, 2003.
[50]	Branford S, Melo JV and Hughes TP (2009) Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR-ABL mutation status really matter? Blood 114: 5426–35.
[51]	Gotlib J, Maxson JE, George TI and Tyner JW (2013) The new genetics of chronic neutrophilic leukemia and atypical CML: implications for diagnosis and treatment. Blood 122: 1707–11.
[52]	Hagop M. Kantarjian et al. Long-term outcomes with frontline nilotinib versus imatinib in newly diagnosed chronic myeloid leukemia in chronic phase: ENESTnd 10-year analysis. Leukemia (2021) 35: 440–453.
[53]	Simona S., Andreas H., Franck E., Franz G., Thoralf L., Giuseppe S., Fabrizio P., Martin C., Thomas E., Rosti G., Porkka K., Baccarani M., Nicholas C. P. and Giovanni Martinelli. BCR-ABL kinase domain mutation analysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors: recommendations from an expert panel on behalf of European LeukemiaNet. Blood, 2011 volume 118, number 5.
[54]	Oyekunle A. A. Haematopoietic Stem Cell transplantation: Prospects and Challenges in Nigeria. Annals of Ibadan Post graduate medicine. Vol. 4. No 1 June 2006.
[55]	Oyekunle A. A. Recent Advances in Stem Cell Biology: Implications for Tropical Haematology Practice. Annals of Tropical Pathology Vol. 2 No 1 June, 2011.
[56]	Körbling M, Freireich EJ. Twenty-five years of peripheral blood stem cell transplantation. Blood 2011; 117: 6411-6.
[57]	Vamvakas EC, Blajchman MA. Transfusion-related mortality: the ongoing risks of allogeneic blood transfusion and the available strategies for their prevention. Blood 2009; 113: 3406-17.

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APA Style

Patrick Olanrewaju Osho, Okunnuga Ndidi, Ojo Matilda, Odunlade Olufunke. (2021). Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy. Cancer Research Journal, 9(2), 111-121. https://doi.org/10.11648/j.crj.20210902.15

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ACS Style

Patrick Olanrewaju Osho; Okunnuga Ndidi; Ojo Matilda; Odunlade Olufunke. Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy. Cancer Res. J. 2021, 9(2), 111-121. doi: 10.11648/j.crj.20210902.15

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AMA Style

Patrick Olanrewaju Osho, Okunnuga Ndidi, Ojo Matilda, Odunlade Olufunke. Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy. Cancer Res J. 2021;9(2):111-121. doi: 10.11648/j.crj.20210902.15

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@article{10.11648/j.crj.20210902.15,
  author = {Patrick Olanrewaju Osho and Okunnuga Ndidi and Ojo Matilda and Odunlade Olufunke},
  title = {Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy},
  journal = {Cancer Research Journal},
  volume = {9},
  number = {2},
  pages = {111-121},
  doi = {10.11648/j.crj.20210902.15},
  url = {https://doi.org/10.11648/j.crj.20210902.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.crj.20210902.15},
  abstract = {Chronic myeloid leukemia (CML) is a triphasic clonal myeloproliferative disorder characterized by the presence of Philadelphi a chromosome (Ph) in over 95% of cases alongside excessive accumulation of clonal myeloid cells in hematopoietic tissues. This occurs as a result of reciprocal translocation between the long arms of chromosome 9 and 22 t (9;22) (q34; q11) creating the fusion oncogene BCR–ABL1 which exhibits constitutive tyrosine kinase activity. It is one of the commonest haematological malignancies in low economies around the world including Nigeria. The clinical features of CML are often described in 3 phases namely the chronic phase (CP), accelerated phase (AP), and blastic phase (BP) while CP is the most common stage with progression to AP and BP occurring later. Despite that, prognosis of CML is dependent on phase of disease, age, and response to therapy, the only curative approach in use currently is hematopoietic stem cell transplantation with other drugs being used for cytogenetic responses. This study focuses on the aetiopathophysiology, cytogenetics, molecular biology, clinical/laboratory features and treatment options of CML. Rigorous review of literature on the study was retrieved from relevant oncology journals and textbooks abstracted and indexed in PubMed, Google Scholar, ProQuest, CINAHL, and Science Direct. The study discovered that, resistance of CML to imatinib has been reported with research having reached the advanced stage on the use of alternative drugs (e.g., Nilotinib and Desatinib). There are also potentials for these new drugs to become the treatment choice and first line drugs for the treatment of CML.},
 year = {2021}
}

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TY  - JOUR
T1  - Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy
AU  - Patrick Olanrewaju Osho
AU  - Okunnuga Ndidi
AU  - Ojo Matilda
AU  - Odunlade Olufunke
Y1  - 2021/06/25
PY  - 2021
N1  - https://doi.org/10.11648/j.crj.20210902.15
DO  - 10.11648/j.crj.20210902.15
T2  - Cancer Research Journal
JF  - Cancer Research Journal
JO  - Cancer Research Journal
SP  - 111
EP  - 121
PB  - Science Publishing Group
SN  - 2330-8214
UR  - https://doi.org/10.11648/j.crj.20210902.15
AB  - Chronic myeloid leukemia (CML) is a triphasic clonal myeloproliferative disorder characterized by the presence of Philadelphi a chromosome (Ph) in over 95% of cases alongside excessive accumulation of clonal myeloid cells in hematopoietic tissues. This occurs as a result of reciprocal translocation between the long arms of chromosome 9 and 22 t (9;22) (q34; q11) creating the fusion oncogene BCR–ABL1 which exhibits constitutive tyrosine kinase activity. It is one of the commonest haematological malignancies in low economies around the world including Nigeria. The clinical features of CML are often described in 3 phases namely the chronic phase (CP), accelerated phase (AP), and blastic phase (BP) while CP is the most common stage with progression to AP and BP occurring later. Despite that, prognosis of CML is dependent on phase of disease, age, and response to therapy, the only curative approach in use currently is hematopoietic stem cell transplantation with other drugs being used for cytogenetic responses. This study focuses on the aetiopathophysiology, cytogenetics, molecular biology, clinical/laboratory features and treatment options of CML. Rigorous review of literature on the study was retrieved from relevant oncology journals and textbooks abstracted and indexed in PubMed, Google Scholar, ProQuest, CINAHL, and Science Direct. The study discovered that, resistance of CML to imatinib has been reported with research having reached the advanced stage on the use of alternative drugs (e.g., Nilotinib and Desatinib). There are also potentials for these new drugs to become the treatment choice and first line drugs for the treatment of CML.
VL  - 9
IS  - 2
ER  -

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Author Information

Patrick Olanrewaju Osho

Department of Hematology and Immunology, University of Medical Sciences, Akure, Nigeria
Okunnuga Ndidi

Departments of Surgery (Oncology), University of Medical Sciences, Akure, Nigeria
Ojo Matilda

Department of Hematology and Immunology, University of Medical Sciences, Akure, Nigeria
Odunlade Olufunke

Department of Paediatrics, University of Medical Sciences, Akure, Nigeria

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Patrick Olanrewaju Osho, Okunnuga Ndidi, Ojo Matilda, Odunlade Olufunke. (2021). Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy. Cancer Research Journal, 9(2), 111-121. https://doi.org/10.11648/j.crj.20210902.15

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ACS Style

Patrick Olanrewaju Osho; Okunnuga Ndidi; Ojo Matilda; Odunlade Olufunke. Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy. Cancer Res. J. 2021, 9(2), 111-121. doi: 10.11648/j.crj.20210902.15

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AMA Style

Patrick Olanrewaju Osho, Okunnuga Ndidi, Ojo Matilda, Odunlade Olufunke. Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy. Cancer Res J. 2021;9(2):111-121. doi: 10.11648/j.crj.20210902.15

Copy | Download

@article{10.11648/j.crj.20210902.15,
  author = {Patrick Olanrewaju Osho and Okunnuga Ndidi and Ojo Matilda and Odunlade Olufunke},
  title = {Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy},
  journal = {Cancer Research Journal},
  volume = {9},
  number = {2},
  pages = {111-121},
  doi = {10.11648/j.crj.20210902.15},
  url = {https://doi.org/10.11648/j.crj.20210902.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.crj.20210902.15},
  abstract = {Chronic myeloid leukemia (CML) is a triphasic clonal myeloproliferative disorder characterized by the presence of Philadelphi a chromosome (Ph) in over 95% of cases alongside excessive accumulation of clonal myeloid cells in hematopoietic tissues. This occurs as a result of reciprocal translocation between the long arms of chromosome 9 and 22 t (9;22) (q34; q11) creating the fusion oncogene BCR–ABL1 which exhibits constitutive tyrosine kinase activity. It is one of the commonest haematological malignancies in low economies around the world including Nigeria. The clinical features of CML are often described in 3 phases namely the chronic phase (CP), accelerated phase (AP), and blastic phase (BP) while CP is the most common stage with progression to AP and BP occurring later. Despite that, prognosis of CML is dependent on phase of disease, age, and response to therapy, the only curative approach in use currently is hematopoietic stem cell transplantation with other drugs being used for cytogenetic responses. This study focuses on the aetiopathophysiology, cytogenetics, molecular biology, clinical/laboratory features and treatment options of CML. Rigorous review of literature on the study was retrieved from relevant oncology journals and textbooks abstracted and indexed in PubMed, Google Scholar, ProQuest, CINAHL, and Science Direct. The study discovered that, resistance of CML to imatinib has been reported with research having reached the advanced stage on the use of alternative drugs (e.g., Nilotinib and Desatinib). There are also potentials for these new drugs to become the treatment choice and first line drugs for the treatment of CML.},
 year = {2021}
}

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TY  - JOUR
T1  - Pathosphysiology of Chronic Myeloid Leukemia, Prognistic Factors and Emerging Treatment Options in a Low Resource Economy
AU  - Patrick Olanrewaju Osho
AU  - Okunnuga Ndidi
AU  - Ojo Matilda
AU  - Odunlade Olufunke
Y1  - 2021/06/25
PY  - 2021
N1  - https://doi.org/10.11648/j.crj.20210902.15
DO  - 10.11648/j.crj.20210902.15
T2  - Cancer Research Journal
JF  - Cancer Research Journal
JO  - Cancer Research Journal
SP  - 111
EP  - 121
PB  - Science Publishing Group
SN  - 2330-8214
UR  - https://doi.org/10.11648/j.crj.20210902.15
AB  - Chronic myeloid leukemia (CML) is a triphasic clonal myeloproliferative disorder characterized by the presence of Philadelphi a chromosome (Ph) in over 95% of cases alongside excessive accumulation of clonal myeloid cells in hematopoietic tissues. This occurs as a result of reciprocal translocation between the long arms of chromosome 9 and 22 t (9;22) (q34; q11) creating the fusion oncogene BCR–ABL1 which exhibits constitutive tyrosine kinase activity. It is one of the commonest haematological malignancies in low economies around the world including Nigeria. The clinical features of CML are often described in 3 phases namely the chronic phase (CP), accelerated phase (AP), and blastic phase (BP) while CP is the most common stage with progression to AP and BP occurring later. Despite that, prognosis of CML is dependent on phase of disease, age, and response to therapy, the only curative approach in use currently is hematopoietic stem cell transplantation with other drugs being used for cytogenetic responses. This study focuses on the aetiopathophysiology, cytogenetics, molecular biology, clinical/laboratory features and treatment options of CML. Rigorous review of literature on the study was retrieved from relevant oncology journals and textbooks abstracted and indexed in PubMed, Google Scholar, ProQuest, CINAHL, and Science Direct. The study discovered that, resistance of CML to imatinib has been reported with research having reached the advanced stage on the use of alternative drugs (e.g., Nilotinib and Desatinib). There are also potentials for these new drugs to become the treatment choice and first line drugs for the treatment of CML.
VL  - 9
IS  - 2
ER  -

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