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Research & Reviews: Journal of Medical and Health

Sciences

Acute Lymphocytic Leukaemia Diagnosis and Treatment - A Review

Rishu Bala*, Deepika Sharma, Amandeep Kaur
Department of Medical Biotechnology, Dolphin Life Science, Punjabi University, Chandigarh, India

Review Article

Received date: 10/08/2016 ABSTRACT

Accepted date: 12/08/2016
Intense lymphoblastic leukemia (ALL) is a sort of blood growth. Otherwise
Published date: 19/08/2016
called intense lymphocytic leukemia or intense lymphoid leukemia, it is
the slightest basic sort of leukaemia in adults. ALL is portrayed by an over
*For Correspondence
production of juvenile white platelets, called lymphoblast or leukemic impacts.
These cells swarm the bone marrow, keeping it from making ordinary platelets.
Rishu Bala, Department of Medical They can likewise spill out into the circulatory system and course around the
Biotechnology, Dolphin PG College of Life body. Because of their adolescence, these cells can't work appropriately to
Sciences, Chandigarh, Tel: 7032524881.
forestall or battle disease. Insufficient quantities of red cells and platelets being
made by the marrow cause frailty, and simple draining and bruising. Each year
E-mail: [email protected] in Australia more than 300 individuals are determined to have ALL. In general,
ALL is an uncommon malady, representing 0.3% of all growths analysed.
Keywords: Lymphoblasts, Platelets,
Juvenile.

INTRODUCTION
Intense lymphocytic leukemia (ALL), additionally called intense lymphoblastic leukemia, is a malignancy that begins from
the early form of white platelets called lymphocytes in the bone marrow [1-5]. The expression "intense" implies that the leukemia
can advance rapidly and if not treated would most likely be lethal inside a couple of months. Lymphocytic means it creates from
right on time (juvenile) types of lymphocytes, a kind of white platelet [6-10]. This is not quite the same as intense myeloid leukemia
(AML), which creates in other platelet sorts found in the bone marrow.
The bone marrow is the delicate internal part of the bones [1], where fresh recruit cells are made. It more often than not grows
rapidly over days or weeks. It is the most well-known kind of leukemia to influence youngsters however can likewise influence
adults [11-16]. Childhood leukemia speaks to 12% of all leukemia; 60% of all intense lymphoblastic leukemia.
Different sorts of growth that begin in lymphocytes are known as lymphomas (Non-Hodgkin lymphoma or Hodgkin lymphoma)
[17-25].
The principle contrast between these sorts of malignancies is that leukemia like ALL principally influences the bone marrow
and the blood, and may spread to different spots, while lymphomas primarily influence the lymph hubs or different organs however
may include the bone marrow. Here and there destructive lymphocytes are found in both the bone marrow [26-30] and lymph hubs
when the tumor is initially analyzed, which can make it difficult to discern whether the malignancy is leukemia or lymphoma. In the
event that more than 25% of the bone marrow is supplanted by harmful lymphocytes, the illness is typically considered leukemia
[31-38].
The extent of lymph hubs is additionally imperative. The greater they are, the more probable the infection will be viewed as
a lymphoma.

CAUSES OF ACUTE LYMPHOCYTIC LEUKEMIA

• Idiopathic (most)
• Underlying hematologic disorders
• Chemicals, drugs
• Ionizing radiation

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• Viruses (HTLV I)
• Hereditary/genetic conditions

TYPES OF ACUTE LYMPHOCYTIC LEUKEMIA

There are three unique sorts of intense lymphocytic leukemia
• Pre (forerunner) B cell ALL is the most widely recognized sort in grown-ups
• Mature B cell ALL – this write is distinguished by specific hereditary [39,40] changes
• Pre (forerunner) T cell ALL will probably influence youthful grown-ups and is more regular in men.
Developed B cell ALL is some of the time called Burkitt sort ALL since it is like another malignancy called Burkitt lymphoma.
A more established framework that specialists utilize less regularly is the FAB framework (French American British order
framework). The FAB arrangement additionally partitions ALL into three sorts: L1 to L3. In L1 the lymphocytes look very like full
grown lymphocytes [41-45]. In L3 the lymphocytes are exceptionally juvenile and look irregular. L2 is some place in the middle of and
is the most widely recognized sort in grown-ups [46-55].

DIAGNOSING OF INTENSE LYMPHOBLASTIC LEUKEMIA

Philadelphia chromosome
A few people with ALL have an adjustment in the leukemia cells called the Philadelphia chromosome [56-60]. This is called
Philadelphia positive ALL. The Philadelphia chromosome is the point at which a quality called the ABL quality on chromosome 9
severs and adheres to a quality called the BCR quality on chromosome 22. This creates another quality called BCR-ABL [61-75]. This
causes the phone to make a lot of a protein called tyrosine kinase. This protein urges leukemic cells to develop and increase.
FISH (fluorescence in situ hybridization)
FISH is a test that searches for quality changes in cells. It can help the authority to work out which treatment given to the
patients [76-78].
Lumbar cut
A lumbar cut appears if there are leukemia cells in the liquid around your cerebrum and spine [79-85]. The liquid is called
cerebrospinal lumbar cut or CSF. The specialist will put a needle into patient spine and gather a little measure of liquid that
channels out.
Mid-section X-beam
Patients may have X-beams to check general wellbeing. In intense lymphoblastic leukemia, now and then have a "knot"
of leukemic cells developing in the focal point of the mid-section, in the zone around the heart. This region is known as the
mediastinum and the knot is known as a mediastina mass [42].
CT examine
A CT sweep is a kind of modernized X-beam. CT output to check for specific indications of leukemia, for example, the
mediastinal mass or to check tolerant general wellbeing [86-90].

TREATMENT OF ACUTE LYMPHOBLASTIC LEUKEMIA

Patients have a few distinctive chemotherapy drugs in cycles of treatment.
Disposing of ALL (abatement instigation)
The treatment toward the starting plans to get leukemia into abatement [91-94]. Abatement implies there are no leukemia cells
in your blood or bone marrow. This period of treatment is called instigation treatment or abatement impelling. Patients have a few
distinctive chemotherapy drugs and a steroid [95-98].
Treatment to stop ALL coming back (consolidation)
The second period of treatment is called combination treatment. Patients have this when leukemia has gone into abatement.
There are distinctive sorts of union treatment. May have high measurements of one of the chemotherapy sedates that patients
had as a major aspect of their incitement treatment.
Halting ALL spreading into the cerebrum or spinal liquid (CNS prophylaxis)
Prophylaxis just means prevention. Leukemia cells can go into the mind and spinal line. Chemotherapy into a vein can't
break through to execute them. In this way, chemotherapy infused into the liquid that flows around the mind and the spinal rope
(the cerebrospinal liquid, CSF). The chemotherapy medication is generally methotrexate

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Keeping ALL away, long haul (support)
This is known as upkeep treatment. It is more chemotherapy, however in lower dosages than patient have in alternate pe-
riods of treatment. Patient will have the capacity to have this as an outpatient. Counting support treatment, the entire ALL treat-
ment course goes on for around 2 years.

SIDE EFFECTS OF CHEMOTHERAPY FOR ALL

Drugs influence individuals in various ways. Not everybody has the same reactions with the same medication. The regular
reactions are prone to have with treatment for intense lymphoblastic leukemia are:
• A drop in your platelet checks
• Feeling and being wiped out
• Complete male pattern baldness
• A sore mouth and mouth ulcers
• Diarrhea
• Tiredness
Every one of the medications used to treat ALL will make platelet tallies fall. This incorporates red platelets, platelets and
white platelets. The danger of disease persists for a couple of weeks after the treatment. Amid ALL treatment the vast majority
need anti-toxins into a vein sooner or later, to treat disease.

CONTROL THE IMPACTS OF ALL TREATMENT

Chemotherapy medications can bring about a few impacts that should be controlled .To control others impact of chemotherapy,
may take solutions, for example, allopurinol tablets. These tablets help the body to prepare the waste materials from the dead
leukemia cells [99,100]. In the event that white platelet levels are high, or if T cells ALL, take a solution called rasburicase by dribble,
rather than allopurinol tablets.

CONCLUSION
In conclusion, Leukemia can be fatal, but with early diagnosis, proper treatments, and a lot of luck, it can be put into
remission. With treatment options improving constantly, there may one day be a sure cure. Leukemia is a very dominant disease
and very hard to treat. The key may be in the causes.

REFERENCES
1. Liu J, et al. Evaluation of vitamin D level and fatigue in acute leukemia patients undergoing chemotherapy. J Leuk.
2015;3:194.
2. Sharma RK, et al. Applicability of a single 5 color cytoplasmic markers tube as primary panel in routine immunophenotyping
of acute leukemia. J Blood Disord Transfus. 2015;6:309.
3. Tanyildiz HG, et al. Vitamin b12 deficiency mimicking acute leukemia in a child. J Clin Case Rep. 2014;4:430.
4. Brahimi M, et al. The use of cd45/ ssc dot plots in the classification of acute leukemias. J Hematol Thromb Dis. 2014;2:e107.
5. Wong GC, et al. Invasive mould disease – predictive risk factors in acute leukemia patients receiving intensive chemo-
therapy and its impact on survival. J Blood Disord Transfus. 2013;4:156.
6. Dogan S, et al. Comparison of mll fusion genes expression among the cytogenetics abnormalities of acute myeloid leuke-
mia and their clinical effects. J Biom Biostat. 2016;7:312.
7. Blanc K, et al. Acute respiratory failure in a patient presenting t-cell pro-lymphocytic leukemia: specific leukemic lung in-
volvement? J Clin Respir Dis Care. 2016;2:116.
8. Haggag R, et al. Study of plasma endostatin level in patients with acute myeloid leukemia. Adv Oncol Res Treat. 2016;1:107.
9. Zhu HH, et al. CD34-Negative is highly associated with T (15;17), T (V; 11q23) and the NPM1-mutation subtypes in 343
newly diagnosed patients with acute myeloid leukemia . Chemo Open Access. 2016;5:200.
10. Elbedewy TA and Elashtokhy HE. The utility and applicability of chronic myeloid leukemia scoring systems for predicting the
prognosis of Egyptian patients on imatinib: Retrospective Study. J Leuk. 2016;4:210.
11. Tulara NK. Adult t cell leukemia/lymphoma in a 56 years old Indian male with history of miliary Koch’s on anti-tubercular
therapy. Oncol Cancer Case Rep. 2016;2:110.

RRJMHS| Volume 5 | Issue 3 | September, 2016 3

 e-ISSN:2319-9865
p-ISSN:2322-0104
12. Chang F, et al. Clinical and hematological profile of acute myeloid leukemia (aml) patients of Sindh. J Hematol Thrombo
Dis. 2016;4:239.
13. Barik S. Combination therapy for chronic lymphoid leukemia. J Cancer Sci Ther. 2016;8:078-079.
14. Cheng H, et al. A new mutation identified in an imatinib and nilotinib resistant chronic myeloid leukemia patient. Chemo
Open Access. 2016;5:193.
15. Kodidela S, et al. Genotype distribution of dihydrofolatereductase variants and their role in disease susceptibility to acute
lymphoblastic leukemia in Indian population: An Experimental and Computational Analysis. J Leuk. 2016;4:209.
16. Hummel HD, et al. Adverse events in adults with relapsed or refractory acute lymphoblastic leukemia (all): a literature re-
view of recent clinical trials. J Leuk. 2016;4:208.
17. Frezzato F, et al. Targeting bruton’s tyrosine kinase in chronic lymphocytic leukemia at the crossroad between intrinsic and
extrinsic pro-survival signals. J Leuk. 2016;4:207.
18. Olaya N, et al. Bovine leukemia: zoonosis associated with breast cancer in humans?. J Med Surg Pathol. 2016;1:110.
19. Xu M, et al. Aggressive natural killer cell leukemia secondary to hodgkin lymphoma: a case report and review of the litera-
ture. Chemo Open Access. 2016;5:182.
20. Yi-Zhi J, et al. Life-threatening capillary leak syndrome in an adult with refractory acute myeloid leukemia during allogeneic
transplantation: a case report and review of literature. Transplant Rep . 2015;1:101.
21. Essa N, et al. autoimmune hemolytic anemia in a patient with acute myelomonocytic leukemia. J Blood Disord Transfus.
2016;7:336.
22. Babi MA, et al. Bilateral borderzone infarcts in hypereosinophilic leukemia without proximal vessel stenosis. J Neurol Neu-
rophysiol. 2016;7:349.
23. Dhar PK, et al. Analytical model for the assessment of efficiency of stem cell transplantation with suicidal gene construct
for the treatment of leukemia. Oncol Trans Res. 2015;1:103.
24. Harif M. Hairy cell leukemia associated with bone marrow tuberculosis. J Cytol Histol. 2016;7:382.
25. Ngaeje M, et al. A case of a child with chronic myeloid leukemia presenting with vision and hearing loss. J Blood Disord
Transfus. 2016;7:333.
26. Bhinder MTM, et al. Pharmacogenetic testing for methotrexate treatment in leukemia patients. J Biomol Res Ther.
2016;4:134.
27. Agius LM. A dual origin for bcr-abl gene translocation/fusion as dynamics of synergism of the hematopoietic stem cell and
hemangioblast in chronic myeloid leukemia. J Leuk. 2015;3:203.
28. Cuttler JM and Welsh JS. Leukemia and ionizing radiation revisited. J Leuk. 2015;3:202.
29. Zakharova and Stolyarevich ES. Clinical presentation and pathology spectrum of kidney damage in non-Hodgkin lympho-
ma/leukemia and lymphoplasmacytic lymphomas. J Leuk. 2015;3:201.
30. Oliveira PN, et al. Congenital acute lymphoblastic leukemia with placental involvement: Case report x. J Preg Child Health.
2015;2:204.
31. Tamai H, et al. Effective management of acute promyelocytic leukemia with high risk of fatal intracranial hemorrhage. Biol
Med (Aligarh). 2015;8:262.
32. Belhadj M, et al. Hemophagocytic lymphohistiocytosis due to acute myeloid leukemia relapse: A very unusual association.
J Leuk. 2015;3:198.
33. Huang C, et al. The association between mRNA expression levels of ephx1 and prognosis of acute myeloid leukemia. J
Integr Oncol. 2015;4:154.
34. Polzer H, et al. Individualized treatment strategy with small-molecular inhibitors in acute myeloid leukemia with concurrent
flt3-itd and flt3-tkd mutation. J Clin Case Rep. 2015;5:622.
35. Omran A, et al. Cd44 and cd44 variant 6 in children with acute lymphoblastic leukemia. J Cancer Sci.2015.
36. Yongabi KA, et al. Spectrum of systemic yeast infections in leukemia patients in Cameroon and sensitivity of isolates to
griseofulvin, ketoconazole and organic extracts of four medicinal plants . J Leuk. 2015;3:195.
37. Sparkes AH, et al. A comparative study of the efficacy of a canarypox based recombinant leukemia vaccine against a natu-
ral contact felv challenge in cats. J Vaccines Vaccin. 2016;6:300.
38. Berbis G, et al. Implications of basic research in clinical practice: Toward a personalized medicine in T-cell acute lympho-
blastic leukemia (t-all). Mol Biol. 2013;4:142.
39. Gargantilla P, et al. Primary plasma cell leukemia presenting with chest pain. J Hematol Thrombo Dis 3:225.

RRJMHS| Volume 5 | Issue 3 | September, 2016 4

 e-ISSN:2319-9865
p-ISSN:2322-0104
40. Hassanein M. Prognostic value of hematogones in patients with acute myeloid leukemia in first complete remission. J
Blood Disord Transfus. 2015;6:319.
41. Bahoush GR, et al. Identification of children with acute lymphoblastic leukemia at low risk for tumor lysis syndrome. J Blood
Disord Transfus. 2016;6:318.
42. Kumar H, et al. Systemic review on chronic myeloid leukemia: Therapeutic targets, pathways and inhibitors. J Nucl Med
Radiat Ther. 2015;6:257.
43. Elsawi R, et al. Using a simple, non-expensive in vitro model for studying chronic myeloid leukemia in research laboratories.
Clon Transgen. 2016;4:145.
44. Zhang Q, et al. Regulatory roles of klf3 in hematopoiesis of k562 leukemia cells. J Stem Cell Res Ther. 2014;5:310.
45. Liu J, et al. Evaluation of vitamin d level and fatigue in acute leukemia patients undergoing chemotherapy. J Leuk.
2016;3:194.
46. Elhadary AMA. Assessment of cytogenetic instability and gene transcription of chronic myelogenous leukemia cells ex-
posed to non-thermal plasma. J Cytol Histol. 2016;6:371.
47. Somasundaram V, et al. Unusual hairy projections in a case of t-acute lymphoblastic leukemia, a cause for diagnostic di-
lemma: a case report. J Hematol Thrombo Dis. 2015;3:223.
48. Gargantilla P, et al. leukemia and origami crane. J Hematol Thrombo Dis. 2015;3:217.
49. Elbossaty WE, et al. Prognostic relevance of ww-oxidoreductase gene expression in patients with acute lymphoblastic leu-
kemia. J Cancer Sci Ther. 2015;7:302-307.
50. Gadhia P, Three ways Philadelphia variant in chronic myeloid leukemia. J Leuk. 2015;3:191.
51. Atfy M, CD200 suppresses the natural killer cells and decreased its activity in acute myeloid leukemia patients. J Leuk.
2015;3:190.
52. Reure J, et al. Posterior reversible encephalopathy syndrome during induction treatment of Philadelphia positive acute
lymphoblastic leukemia in an adult patient: First case report and literature review. J Blood Lymph. 2015;5:141.
53. Neanaa H, et al. Comparative study between valproic acid combined with conventional chemotherapy versus conventional
chemotherapy alone in Egyptian acute myeloid leukemia patients. J Blood Lymph. 2015;5:140.
54. Sharma RK, et al. Applicability of a single 5 color cytoplasmic markers tube as primary panel in routine immunophenotyping
of acute leukemia. J Blood Disord Transfus. 2015;6:309.
55. Ribers JM. Blinatumomab: A promising new drug in the therapeutic armamentarium for acute lymphoblastic leukemia.
Chemo Open Access. 2014;4:164.
56. Leite LAC, et al. Acute abdominal pain revealing primary plasma cell leukemia: A rare and aggressive case of plasma cell
dyscrasia. J Cytol Histol. 2016;6:364.
57. Bülbül,et al. Spontaneous remission in congenital leukemia aml-m1 with pericardial effusion. J Neonatal Biol. 2014;4:196.
58. Hela BJ, et al. Recurrent ischemic cerebrovascular accidents with recurrent acute ischemia of the left upper limb revealing
acute myeloid leukemia. J Vasc Med Surg. 2015;3:209.
59. Mansour SA. E-cadherin immunohistochemistry stain and acute erythroid leukemia, the emerging story. J Cytol Histol.
2015;6:352.
60. Pennisi A, et al. Acute lymphoblastic leukemia evolving from atypical chronic myelogenous leukemia: case report and re-
view of the literature. J Leuk S. 2016;1:007.
61. Chi J, et al. The evolution of genetics techniques for leukemia diagnosis. Adv Tech Biol Med. 2016; 3:e111.
62. Hamid GA. Treatment development of chronic myeloid leukemia. J Develop Drugs. 2015;4:e144.
63. Robak T. Bcl-2 inhibitors for chronic lymphocytic leukemia. J Leuk. 2016;3:e114.
64. Yokus and Gedik H. Severe neurological signs due to hyponatremia in patient with acute myeloid leukemia; ethiological
factors and therapeutic approach. J Blood Disord Transfus. 2015;5:001.
65. Okuno N, et al. A case of t-cell prolymphocytic leukemia/lymphoma suggested thyroid origin. Thyroid Disorders Ther.
2016;4:190
66. Azad NA, Phytohemagglutinin-induced peripheral blood cytogenetics: A valid means for diagnosis and imatinib therapy
monitoring of chronic phase chronic myeloid leukemia patients. J Cancer Sci Ther. 2015;7:242-248.
67. Pathak P. The changing therapeutic landscape of chronic lymphocytic leukemia. J Blood Lymph. 2015 5:e120.
68. Yahia S, et al. Cognitive function and quality of life in Egyptian children with acute lymphoblastic leukemia. J Blood Disord
Transfus. 2015;6:291.
RRJMHS| Volume 5 | Issue 3 | September, 2016 5
 e-ISSN:2319-9865
p-ISSN:2322-0104
69. Balci Y, et al. Mature B cell acute lymphoblastic leukemia presenting with hypercalcemia. J Leuk. 2015;S1:002.
70. Kaleem B. Plasma cell leukemia-behind a disguise. J Clin Case Rep. 2015;5:533.
71. Alsara, et al. Advances in the treatment of hairy cell leukemia. J Hematol Thrombo. Dis.2016; 3:210.
72. Takemoto S, et al. Serum soluble CD30 levels to detect activation and aggression status of adult T-cell leukemia/lym-
phoma cells. J Hematol Thrombo Dis. 2015;3:205.
73. Kallus SJ and George NB. A case of hypergranular acute promyelocytic leukemia (French-American-British Classification
M3) Neil Batta, MS3. J Clin Case Rep. 2015;5:i105.
74. Reksodiputro AH, et al. Epidemiology study and mutation profile of patients with chronic myeloid leukemia (CML) in Indo-
nesia. J Blood Disord Transfus. 2015;6:271.
75. Druhan L, et al. Acute heart failure in a patient with acute myeloid leukemia following daunorubicin treatment: A case re-
port. J Leuk. 2015;3:185.
76. Knauf W. Chronic lymphocytic leukemia: Raising expectations in the treatment of elderly patients. J Leuk. 2015;3:181.
77. Massimo B, et al. Early molecular response in chronic myeloid leukemia and halving time: Latest evidences. 2015;48:20-25.
78. Alves APNR, et al. Reversine triggers mitotic catastrophe and apoptosis in K562 cells. 2015;48:26-31.
79. Bellosillo B, et al. Characterization of CD34+ hematopoietic progenitor cells in JAK2V617F and CALR-mutated myeloprolif-
erative neoplasms. 2015;48:11-15.
80. Al Dallal S, et al. Zfp521 promotes B-cell viability and cyclin D1 gene expression in a B cell culture system. 2016;46:10-17.
81. Wang Q, et al. Sam68 affects cell proliferation and apoptosis of human adult T-acute lymphoblastic leukemia cells via AKT/
mTOR signal pathway. 2015;46:1-19.
82. Hernández-Sánchez M and Rodríguez-Vicente AE. miRNA expression profile of chronic lymphocytic leukemia patients with
13q deletion. 2015;46:30-36.
83. Zhang H, et al. Identification of tbk1 and ikkε, the non-canonical iκb kinases, as crucial pro-survival factors in htlv-1-trans-
formed t lymphocytes. 2015;46:37-44.
84. Yousaf M, et al.The miR-17∼92 cluster contributes to MLL leukemia through the repression of MEIS1 competitor PKNOX.
2015;146:51-60.
85. Cao XX, et al. The clinical spectrum of IgM monoclonal gammopathy: A single center retrospective study of 377 patients.
2015;46:85-88.
86. Manzoni D, et al. The ibrutinib B-cell proliferation inhibition is potentiated in vitro by dexamethasone: Application to chronic
lymphocytic. Leukemia Research. 2015;47:1-7.
87. Yamaguchi T, et al. Acute megakaryoblastic leukemia, unlike acute erythroid leukemia, predicts an unfavorable outcome
after allogeneic HSCT. Leukemia Research. 2015;47:47-53.
88. Jing XM, et al. oxaliplatin with sandwiched radiotherapy in the treatment of newly-diagnosed extranodal nature killer (NK)/T
cell lymphoma. 2015;47:26-31.
89. Niemöller C, et al. Single cell genotyping of exome sequencing-identified mutations to characterize the clonal composition
and evolution of inv(16) aml in a cbl mutated clonal hematopoiesis leukemia research. 2015; 47:41-46.
90. Tang FF. Allogeneic hematopoietic cell transplantation for adult patients with treatment-related acute myeloid leukemia
during first remission: Comparable to de novo acute myeloid leukemia. 2015;4 :8-15.
91. Xiaohong XU, et al. Cell adhesion induces overexpression of chromodomain helicase/ATPase DNA binding protein 1-like
gene (CHD1L) and contributes to cell adhesion-mediated drug resistance (CAM-DR) in multiple myeloma cells. Leukemia
Research. 2015;47:54-62.
92. Heinz T. Dysplastic erythroid precursors in the myelodysplastic syndromes and the acute myeloid leukemias: Is there bio-
logic significance? (How should blasts be counted?). Leukemia research. 2015;47:63-69.
93. Heim D, et al. Increase of endothelial progenitor cells in acute graft-versus-host disease after allogeneic haematopoietic
stem cell transplantation for acute myeloid leukemia. Leukemia Research. 2015;47:22-25.
94. Wang J. The sensitivity of chronic myeloid leukemia CD34 cells to Bcr-Abl tyrosine kinase inhibitors is modulated by ce-
ramide levels. Lukemia Research. 2015;47:32-40.
95. Eidukaite, et al. Defining the significance of IGF2BP1 overexpression in t(12;21)(p13;q22)- positive leukemia REH cells.
Leukemia Research. 2016;47: 16-21.
96. Miyashita M, et al. Evaluation of care for leukemia and lymphoma patients during their last hospitalization from the per-
spective of the bereaved family. Leukemia Research. 2015;47:93-99.

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97. Curry V and Choladda. Are micromegakaryocytes specific for refractory cytopenia of childhood (RCC)? A study of 38 pediat-
ric patients with thrombocytopenia unrelated to RCC. Leukemia Research. 2015; 47: 84–87.
98. Yin J, et al. BCL11A expression in acute phase chronic myeloid leukemia. Leukemia Research. 2015 47:88-92.
99. Ritam C, et al. Alteration of classical and hematopoiesis specific p53 pathway in the bone marrow hematopoietic stem/
progenitor compartment facilitates leukemia progression in experimental mice .leukemia research. 2015;47:70-77.
100. Wang, et al. Clinical significance of acquired loss of the X chromosome in bone marrow. Lukemia Research. 2015;47:109-

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