p-ISSN 0854-4263

Vol. 24, No. 1, November 2017 e-ISSN 2477-4685

INDONESIAN JOURNAL OF

CLINICAL PATHOLOGY AND

MEDICAL LABORATORY
Majalah Patologi Klinik Indonesia dan Laboratorium Medik

EDITORIAL TEAM

Editor-in-chief:
Puspa Wardhani

Editor-in-chief Emeritus:
Prihatini
Krisnowati

Editorial Boards:
Jusak Nugraha, Ida Parwati, Adi Koesoema Aman, Edi Widjajanto, Rahayuningsih Dharma, Aryati,
Kusworini Handono, Mansyur Arif, Budi Mulyono, Rismawati Yaswir, Yuyun Widaningsih, Purwanto AP,
Osman Sianipar, Umi Solekhah Intansari, Banundari Rachmawati, Andaru Dahasihdewi, Agnes Rengga Indrati,
Nyoman Suci Widyastuti, Hani Susianti, Efrida, Rikarni, Tenri Esa, Uleng Bahrun, July Kumalawati,
Liong Boy Kurniawan, Ninik Sukartini, Maimun Zulhidah Arthamin, Tahono, Rachmawati Muhidin

Editorial Assistant:
Dian Wahyu Utami

Language Editors:
Yolanda Probohoesodo, Nurul Fitri Hapsari

Layout Editor:
Dian wahyu Utami

Editorial Adress:
d/a Laboratorium Patologi Klinik RSUD Dr. Soetomo, Gedung Diagnostik Center Lt. IV
Jl. Mayjend. Prof. Dr Moestopo 6–8 Surabaya, Indonesia
Telp/Fax. (031) 5042113, 085-733220600 E-mail: majalah.ijcp@yahoo.com, jurnal.ijcp@gmail.com
Website: http://www.indonesianjournalofclinicalpathology.or.id

Accredited No. 36a/E/KPT/2016, Tanggal 23 Mei 2016

 p-ISSN 0854-4263
Vol. 24, No. 1, November 2017 e-ISSN 2477-4685

INDONESIAN JOURNAL OF

CLINICAL PATHOLOGY AND

MEDICAL LABORATORY
Majalah Patologi Klinik Indonesia dan Laboratorium Medik

CONTENTS

RESEARCH
Serum Zinc and C-Reactive Protein Levels as Risk Factors for Mortality in Systemic Inflammatory
Response Syndrome
(Kadar Zinc dan C-Reactive Protein Serum Sebagai Faktor Kebahayaan Kematian di Pasien Systemic
Inflammatory Response Syndrome)
Dwi Retnoningrum, Banundari Rachmawati, Dian Widyaningrum ......................................................... 1–5
Correlations between Mean Platelet Volume and Immature Platelet Fraction to Hemoglobin A1c in
Patients with Type 2 Diabetes Mellitus
(Kenasaban antara Mean Platelet Volume dan Immature Platelet Fraction terhadap Hemoglobin A1c di
Pasien Diabetes Melitus Tipe 2)
Dian W Astuti, Sony Wibisono, Arifoel Hajat, Sidarti Soehita .................................................................. 6–11
Methicillin-Resistant Staphylococcus Aureus Colonization and Screening Method Effectiveness for
Patients Admitted to the Intensive Care
(Kejadian dan Ketepatgunaan Penapisan Kolonisasi Methicillin-Resistant Staphylococcus aureus di
Pasien Perawatan Intensif)
Andaru Dahesihdewi, Budi Mulyono, Iwan Dwiprahasto, Supra Wimbarti ................................................... 12–18
Correlation between Visceral Adipose Tissue-Derived Serpin with Fasting Blood Glucose Level in
Obesity
(Hubungan Kadar Visceral Adipose Tissue-Derived Serpin Dengan Kadar Glukosa Darah Puasa Pada
Kegemukan)
Novi Khila Firani, Agustin Iskandar, Anik Widijanti, Nonong Eriani ....................................................... 19–23
Serum Glial Fibrillary Acidic Protein Levels Profile in Patients with Severe Traumatic Brain Injury
(Profil Kadar Glial Fibrillary Acidic Protein Serum di Pasien Cedera Otak Berat)
Arief S. Hariyanto, Endang Retnowati, Agus Turchan .............................................................................. 24–28
Phylogenetic Profile of Escherichia coli Causing Bloodstream Infection and Its Clinical Aspect
(Profil Filogenetik Escherichia coli Penyebab Infeksi Aliran Darah dan Aspek Klinisnya)
Osman Sianipar, Widya Asmara, Iwan Dwiprahasto, Budi Mulyono................................................................. 29–35
Comparison of Glycemic State in Patients with and without Hyperuricemia
(Perbedaan Status Glikemia pada Pasien dengan dan tanpa Hiperurisemia)
Corrie Abednego, Banundari Rachmawati, Muji Rahayu ......................................................................... 36–41
Analysis of Laboratory Parameters as Sepsis Markers in Neonatals with Hyperbilirubinemia
(Analisis Tolok Ukur Laboratorium Sebagai Petanda Sepsis di Neonatus dengan Hiperbilirubinemia)
Bachtiar Syamsir, Rachmawati Muhiddin, Uleng Bahrun......................................................................... 42–46
Correlation Percentage of S and G2/M with Percentage of Lymphoblasts in Pediatric Acute
Lymphoblastic Leukemia
(Kenasaban Persentase S dan G2/M dengan Persentase Limfoblas di Pasien Leukemia Limfoblastik Akut
Anak)
Erawati Armayani, Yetti Hernaningsih, Endang Retnowati, Suprapto Ma´at, I Dewa Gede Ugrasena . 47–52

Printed by Airlangga University Press. (OC 252/08.17/AUP-A1E). E-mail: aup.unair@gmail.com

Kesalahan penulisan (isi) di luar tanggung jawab AUP
 Correlation of Blast Percentage to CD34 of Bone Marrow in All Pediatric Patients
(Kenasaban Persentase Blas Dengan CD34 di Sumsum Tulang pada Pasien LLA Anak)
Rahmi Rusanti, Yetti Hernaningsih, Endang Retnowati, Mia Ratwita Andarsini, Andy Cahyadi ........... 53–58
Analysis of Decreased Glucose Level in Stored Samples Correlated to Serum Separation and
Temperature Storage
(Analisis Penurunan Glukosa Dari Sampel Yang Disimpan Dalam Kaitannya Dengan Pemisahan Serum
dan Suhu Penyimpanan)
Gustamin, Liong Boy Kurniawan, Ruland DN Pakasi ............................................................................... 59–63
Diagnostic Concordance between Next Generation and High Sensitive Troponin-I in Angina Pectoris
Patients
(Kesesuaian Diagnostik Troponin-I Next generation dan High sensitive di Pasien Angina Pectoris)
Erna R Tobing, Jusak Nugraha, Muhammad Amminuddin ..................................................................... 64–69
Elevated Serum S100B Protein Level as a Parameter for Bad Outcome in Severe Traumatic Brain
Injury Patients
(Peningkatan Kadar Serum Protein S100B Sebagai Tolok Ukur Keluaran Buruk di Pasien Cedera Kepala
Berat)
Ridha Dharmajaya, Dina Keumala Sari, Ratna Akbari Ganie .................................................................. 70–75
Analysis of Mean Platelet Volume As A Marker For Myocardial Infarction and Non-Myocardial
Infarction in Acute Coronary Syndrome
(Analisis Mean Platelet Volume sebagai Pembeda Infark Miokard dan Non-Infark Miokard di Sindrom
Koroner Akut)
Wandani Syahrir, Liong Boy Kurniawan, Darmawaty Rauf ...................................................................... 76–80
Anti-Dengue IgG/IgM Ratio for Secondary Adult Dengue Infection in Surabaya
(Rasio IgG/IgM Anti Dengue untuk Infeksi Dengue Sekunder Dewasa di Surabaya)
Aryati, Puspa Wardhani, Ade Rochaeni, Jeine Stela Akualing, Usman Hadi ........................................... 81–85
Analysis of Blood Urea Nitrogen/Creatinin Ratio to Predict the Gastrointestinal Bleeding Tract Site
(Analisis Rasio Blood Urea Nirogen/Kreatinin Untuk Meramalkan Lokasi Perdarahan pada Saluran
Cerna)
Arfandhy Sanda, Mutmainnah, Ibrahim Abdul Samad ............................................................................ 86–90
The Differences of Sodium, Potassium and Chloride Levels in STEMI and NSTEMI Patients
(Perbedaan Kadar Natrium, Kalium dan Klorida di Pasien STEMI dan NSTEMI)
Freddy Ciptono, Muji Rahayu ................................................................................................................... 91–94

LITERATURE REVIEW
Macrophage Autophagy in Immune Response
(Otofagi Makrofag dalam Respons Imun)
Jusak Nugraha ........................................................................................................................................... 95–101

CASE REPORT
Very Severe Hypertriglyceridemia in Suspected Familial Chylomicronemia Infant
(Hipertrigliseridemia Sangat Berat di Bayi Terduga Kausa Familial Chylomicronemia)
Fitry Hamka, Liong Boy Kurniawan, Suci Aprianti .................................................................................. 102–107

Thanks to editors in duty of IJCP & ML Vol 24 No. 1 November 2017

Rismawati Yaswir, Purwanto AP, Sidarti Soehita, July Kumalawati, Aryati,
Rahayuningsih Dharma, Adi Koesoema Aman, Yolanda Probohoesodo, Puspa Wardhani
 2017 November; 24(1): 47–52
p-ISSN 0854-4263 | e-ISSN 2477-4685
Available at www.indonesianjournalofclinicalpathology.or.id

RESEARCH

CORRELATION PERCENTAGE OF S AND G2/M WITH PERCENTAGE

OF LYMPHOBLASTS IN PEDIATRIC ACUTE LYMPHOBLASTIC
LEUKEMIA
(Kenasaban Persentase S dan G2/M dengan Persentase Limfoblas di Pasien
Leukemia Limfoblastik Akut Anak)

Erawati Armayani1, Yetti Hernaningsih1, Endang Retnowati1, Suprapto Ma,at1, I Dewa Gede Ugrasena2

ABSTRAK
Leukemia Limfoblastik Akut (ALL) merupakan keganasan klonal di sumsum tulang/Bone Marrow (BM). Angka bertahan hidup
5 tahun saat ini >85%, tetapi 15-20% relaps sehingga perjalanan penyakit jelek. Perjalan penyakit jelek jika setelah tahap induksi
limfoblas menetap di Darah Tepi (DT) dan BM >5% serta tahap S BM >6%. Tahap G2/M merupakan petunjuk prognosis ALL anak,
selain itu sebagai target pengobatan. Tujuan penelitian menganalisis kenasaban persentase tahap S dan G2/M dengan persentase
limfoblas DT pasien ALL anak sebelum dan sesudah kemoterapi induksi. Jenis penelitian analitik observasional longitudinal (kohor)
di ALL anak kasus baru diperiksa sebelum dan sesudah induksi. Persentase limfoblas secara mikroskopis. Persentase fase S dan G2/M
flowcytometryBD Facs Callibur. Kenasaban bermakna hanya persentase tahap S dan limfoblas sebelum induksi (r=0,449; p=0,007).
Kelainan gen ALL pada ekspresi cyclins dan CDK sehingga hilang kendali checkpoint siklus sel, merangsang transisi tahap G1 menjadi
tahap S. Persentase tahap S tidak berbeda pada remisi dan meninggal (p=0,138). Persentase tahap G2/M berbeda antara remisi dan
meninggal (p=0,006) dan bernasab dengan luaran kemoterapi induksi (koefisien Eta= 0,744), G2/M ≥1,26% meramalkan remisi.
Terdapat kenasaban antara persentase siklus sel tahap S dengan persentase limfobas sebelum kemoterapi induksi. Persentase siklus sel
tahap S memberikan gambaran siklus sel pada sel limfoblas. Terdapat kenasaban antara persentase siklus sel tahap G2/M dengan luaran
kemoterapi induksi tahap G2/M menjadi faktor peramal luaran kemoterapi induksi ALL. Perlu penelitian lanjutan dengan sampel BM,
subtipe dan pengamatan semua tahap kemoterapi.

Kata kunci: Limfoblas, siklus sel, tahap S, tahap G2/M, ALL

ABSTRACT
Acute Lymphoblastic Leukemia (ALL) is a Bone Marrow (BM) clonal malignancy. At the moment, the five year survival rate is
>85%, 15-20% relapse showing a bad prognosis. Persistant Peripheral Blood (PB) lymphoblasts, BM >5%, S phase BM >6% after
induction give a poor prognosis. G2/M phase is an indicator for the prognosis and treatment target in ALL. The research aimed
to analyze the correlation percentage of S phase and G2/M with the percentage of PB lymphoblasts in pediatric ALL patients
before and after chemotherapy induction. This was an analytical observational longitudinal (cohort) research in new pediatric ALL
cases, examined before and after induction. Percentage of lymphoblasts was examined microscopically, percentage of S phase and
G2/M by flowcytometry BD FacsCallibur. A significant correlation was only found in the percentage of S phase and lymphoblasts
before induction(r=0.449; p=0.007). ALL gene abnormalities were in the expression of cyclins and CDKs causing loss of control
checkpoint, stimulating G1 phase transition into S phase. Percentage of S phase did not differ between remission and who died
(p=0.138). Percentage of G2/M phase differed between remission and who died (p=0.006) and correlated with outcomes (coefficient
Eta=0.744). G2/M ≥1.26% predicting an increased remission. There was a correlation between the percentage of cell cycle S phase
and percentage of lymphoblasts before chemotherapy induction. The percentage of S phase gave an overview of lymphoblasts cell
cycle. There was a correlation between G2/M phase percentages with chemotherapy induction outcomes. G2/M was a predictive
factor for ALL chemotherapy induction outcomes. A further research is needed with BM samples, subtypes and observation of all
phases of chemotherapy.

Key words: Lymphoblasts, cell cycle, phase S, phase G2/M, ALL

1 Department of Clinical Pathology, Faculty of Medicine, Airlangga University/Dr. Soetomo Hospital, Surabaya, Indonesia.
E-mail: armamavi@gmail.com
2 Department of Pediatrics, Faculty of Medicine, Airlangga University/Dr. Soetomo Hospital, Surabaya, Indonesia

47
INTRUDUCTION checkpoint and results in uncontrolled proliferation.10
Lekemic cells have a high proliferation compared to
Acute Lymphoblastic Leukemia (ALL) is a malignant normal cells.11
(clonal) disease of the bone marrow in which early The purpose of this study was to analyze the
lymphoid precursors proliferate and replace the correlation between the percentage of cell cycle phases
normal hematopoietic cells of the marrow.1 Acute S and G2/M with the percentage of lymphoblasts
lymphoblastic leukemia is a common malignancy in in the peripheral blood before and after induction
the United States, the most common age is 1–4 years chemotherapy and the clinical benefit was to use
and occurance in males (45–55%) is more common the percentage of S and G2/M for stratification and
than females.2 A previous research in the Dr. Soetomo predicting induction chemotherapy outcomes in
Hospital reported that there were 82 pediatric ALL new pediatric ALL patients.
cases with outcomes after induction phase as remission
48.5%, no remission 14.7% and died 36.8%.3 The five
year survival rate for the last decade was 90.4% but METHODS
about 15-20% relapsed.4
Prognosis in ALL is inf luenced by several This research was an observational analytical
parameters such as age, number of leucocytes, cell design with longitudinal (cohort), from March to June
morphology immunophenotype and genotype. Blast 2016. Sampling in the Outpatient Clinic and patient
clearence speed in the peripheral blood during wards of the Department of Pediatrics Hemato-
therapy is a prognostic factor in the outcome of Oncology and sampling examination was performed
pediatric ALL.5 A research by Posadzy et al6 found in the Clinical Pathology Laboratory, Dr. Soetomo
out that lymphoblast Peripheral Blood (PB) which Hospital.
settled after one week and bone marrow >5% after Inclusion criteria samples were ALL patients
induction chemotherapy gave a poor prognosis.6 Early aged 1 month–16 years old who underwent regular
clearance of peripheral blood blasts after induction chemotherapy, received the approval of the parents/
chemotherapy predicts early marrow blast clearance, guardians. Exclusion criteria were ALL patients
complete remission, Relapse-Free Survival (RFS) and with congenital abnormalities complex, multi-organ
Overall Survival (OS).7 S phase of the cell cycle can be abnormalities, withdrawal from study participation.
a prognostic value in acute leukemia. Kumar8 stated Examination of the percentage of cell cycle was
that it was low, S phase <2.6% before chemotherapy by using flowcytometry BD FACS Callibur with
and > 6% after chemotherapy induction phase gave a Propidium Iodine (PI) dyes. Microscopic examination
poor response to induction chemotherapy and required of lymphoblast percentage with Wright staining.
intensive chemotherapy.8 Cell cycle G2/M phase was Statistical analysis for the difference in the percentage
related to the outcome of chemotherapy induction. A of cell cycle phases S and G2/ M with a percentage
high fraction was corelated with poor outcomes in ALL of lymphoblasts was done by t-test 2 samples and
patients. G2/M phase was the target of chemotherapy Wilcoxon Signed Rank, correlation of the percentage
drugs so it could stimulate an apoptotic signal and of cell cycle phases S and G2/M with a percentage of
induce apoptosis of cancer cells.9 lymphoblasts with Pearson and Spearman correlation
Currently, there is no research on the correlation of test, the difference between phase S and G2/M in
the S phase percentage of the cell cycle and G2/M with induction chemotherapy outcomes used the Mann-
the percentage of lymphoblast cells in peripheral blood Whitney U Test and correlation of cell cycle phase with
in pediatric ALL in the Dr Soetomo Hospital. induction chemotherapy outcomes with correlation Eta
The cell cycle is the sequence of events of cell test.
growth and division into two cells. Cell cycle is divided
into four stages, G1-S-G2-M. Cell cycle begins with
the activation of cyclin D-CDK4/6 is and controlled by RESULTS AND DISCUSSION
CDK inhibitor to activate the checkpoint signals so that
Total samples were 35 new pediatric ALL patients
cells stop proliferating. The DNA damage also activates
before chemotherapy then followed until completion
signals checkpoint so the cell has time to repair DNA
induction phase of chemotherapy. The final subjects
damage. Cell cycle abnormalities in ALL is on p 53
were 20 patients. Characteristics of the samples
expression causing malfunction of CDK inhibitors and
consisted of gender and age (can be seen in Table 1).
the cell can not stop proliferation if there is a stimulus

48 Indonesian Journal of Clinical Pathology and Medical Laboratory, 2017 November; 24(1): 47–52
Table 1. Characteristics of research subjects This research obtained 8 (22.86%) with leukocytes
> 100 x10³/μL and 4 (11.43%) < 3x10³/μL. Acute
Characteristics of research
f (%) lymphoblastic leukemia represented a group of
subjects
Gender B/T-precursor-stage lymphoid cell malignancies
Male 18 (51.4%) arising from genetic alterations that block lymphoid
Female 17(48%) differentiation and drive aberrant cell proliferation
Age
and survival. When this happens, white blood cell
Mean ± SD 5.75 ± 3.73
< 2 years 4 (11.43%) production becomes abnormal and increases the
2-5 years 16 (45.71%) number of white blood cell.15
6 – 9 years 8 (22.86%) The mean platelet count before induction
>10 years 7 (20 %)
chemotherapy was 84.26 x10³/μL. Low platelets are
an indication for lymphoblast cell infiltration in the
Research subjects were mostly males 18 (51.4%). bone marrow progenitor and causing suppression of
This result was the same with Sandeep et al12, 55 % megakaryocytes.5
males and 45% females. The high male incidence was Average lymphoblast PB was 18.37% in pre-
correlated with the Single Nucleotide Polymorphism induction chemotherapy, different from the research of
(SNP) that activated enhancers or activated promoter Rashmi et al5, with the average percentage of 87.3%.
regions and had regulatory effects on gene expression The difference was due to lymphoblast percentage
levels, this gene may counteract the suppressor effect variation in this study.5 Percentage of lymphoblast after
of estrogen-regulated in males.12 induction chemotherapy was 0%. This was similar to
Most of these research subjects were 2-5 years Rashmi5 reporting, the percentage of lymphoblast after
(45.71%). These results were the same with Ugrasena induction chemotherapy as 0.7%. Total lymphoblast PB
et al3, who also found that the age was 2-5 years in would disappear in <10 days and would give a better
pediatric ALL patients. The age had a twice lower risk prognosis. Pheripheral blood blast was negative in 6
of death compared with below 2 years. This age was days and predicted a reduction in BM blast occuring on
more common in type B ALL.2,12 day 14, which predicted complete remission.7
Examination results of hemoglobin, leukocytes, The mean and median percentage of S phase before
platelets, the percentage of cell cycle and the induction chemotherapy were 6.26% and 4.45, this
percentage of lymphoblasts, can be seen in Table 2. result was different from Kumar8, who found that in
The mean Hb before induction chemotherapy was type B ALL, the mean and median were 2.6% and
8.73 g/dL. The cause of anemia can be caused due to 2.3%. The difference in the results of this study with a
the effects of a chronic disease, specific nutritional previous research was due to differences in sampling
deficits, chronic bleeding, neoplastic infiltration of time, age and type of ALL which in this study did not
the BM, intercurrent, infections and autoimmune distinguish the type. Patients with B type ALL had a
hemolytic processes. A new research found that more lower S phase cell cycle.8
reduced erythropoiesis was the other cause of anemia Induction of chemotherapy outcomes in this study
because of molecular changes in the regulation of cell were mostly in remission 21 (60%) Table 3.
growth in the bone marrow micro-environment.13,14

Table 2. Results of examination on hemoglobin, total leukocytes, platelets, S phase, G1 phase, phase G2/M and S phase ALL
children patients before and after induction therapy

Pre induction (n=35) Post induction (n=20)

Parameter p
⎯x ± SD Min-Max ⎯x ± SD Min-Max
Hb (g/dL) 8.73±2.77 4.00–14.40 10.37±1.68 7.00–13.20 0.358
Leukocytes
89.40±166.76 1.85–67.00 6.64±1.97 3.60–10.00 0.244
(10³ /μL)
Platelets
84.26±71.81 11.00–312.00 131.91± 65.28 70.00–254.00 0.002
(10³ /μL)
Lymphoblasts (%) 18.37±21.87 0.00–80.00 0.00±0.00 0.00–0.00 0.000
G1(%) 92.60±5.47 70.56–98.55 94.34±6.21 72.78–99.33 0.063
G2/M (%) 1.14±1.82 0.00–7.19 0.86±1.64 0.00–7.36 0.113
S (%) 6.26±5.71 1.42–29.02 4.80±5.54 0.45–25.88 0.092

Correlations Percentage of S and G2M - Armayani, et al. 49

Table 3. Induction chemotherapy outcomes results transition into phase S. The proportion of cell cycle
phases in leukemic cells was mostly in the S phase. The
Outcomes Frequency %
Dead 14 40.0 S phase could represent leukemic cell proliferation.17
Remission 21 60.0 There was no significant correlation between
the percentage of G2/M phase and the percentage
of lymphoblasts (r=-0.306; p=0.074) before
This research result was different with Ugrasena et
chemotherapy (figure 2). The percentage of phase
al in 2010, who reported that the remission was 40.9%
S and G2/M with percentage of lymphoblasts after
and 48.5%. Remission rates improved more as time
induction chemotherapy could not be analysed because
goes because protocols had been developed and the
the percentage of lymfoblasts after chemotherapy was
latest regimen was used in ALL chemotherapy.3
0%.
There was a significant correlation between
Statistical analysis found no difference in outcomes
the percentage of S phase and the percentage of
according to the S phase after induction chemotherapy
lymphoblast before induction chemotherapy (r= 0.449;
(p=0.138), Table 4. This result showed that the S phase
p=0.007) Figure 1.
could not be used to predict induction chemotherapy
Detection of a damage that were activated in
outcomes. This result differed with Kumar 2015, where
normal hemotopoesis cells, the Ataxia-Telangiectasia
S phase could be used to predict relapse. Percentages
Mutated (ATM) played a central role in the activation
of S phase > 4% patient tended to relapse, relapse of
of the G1/S cell cycle checkpoint, preventing cells with
patients was usually because of an increasing activity
damaged DNA from starting the S phase.16 There was
of proliferation in bone marrow that made the cell
an abnormality in activity of ALL checkpoint. The
turnover and cell leukemic production increase.
gene abnormality that caused expression of cyclins
Increasing proliferation can be caused in effective
and Cyclin-Dependent Kinases (CDKs) disrupted so it
chemotherapy and drug resistance.8 The difference
could make a loss of cell cycle checkpoint control. The
was because this research was performed only
gene abnormalities stimulated the G1 phase cell cycle
until induction phase, the first phase of sequences

Figure 1. Graphic correlation percentages of G2/M phase and percentage lymphoblasts in peripheral blood before chemotherapy induction
of pediatric acute lymphoblastic leukemia

Figure 2. Graphic correlation percentages of G2/M phase and percentages of lymphoblasts before induction chemotherapy

50 Indonesian Journal of Clinical Pathology and Medical Laboratory, 2017 November; 24(1): 47–52
Table 4. Statistical analysis result in differences percentages of S phase cell cycle between induction chemotherapy outcomes in
all pediatric patients

Persentages S phase
Outcomes n p
⎯x SD Minimum Maximum
Remission 21 5.50 5.98 1.42 29.02
0.138
Dead 14 7.39 5.29 1.86 23.22

Table 5. Statistical analysis in percentages of G2/M phase between induction chemotherapy outcomes in all pediatric patients

Persentages G2/M phase

Outcomes n p
⎯x SD Minimum Maximum
Remission 21 1.74 2.13 0.00 7.19
0.006
Dead 14 0.23 0.47 0.00 1.26

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