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Skills development is imperative to sustaining traditional growth and development in a country like India which is experiencing a demographic dividend. It is a huge challenge not only for the government, but also for the private sector and educational institutions to rise up and specialize to make the country’s youth employable and ensure that there is no mismatch between demand and the offer. This study examines the role of Deen Dayal Upadhyay Grameen Kaushalya Vikas Yojana (DDU-GKY) in the development of rural youth in the Haryana State. Secondary data (2015-2021) were used for the study. The results show that the interest of the population towards DDU-GKY and the interns recruited has greatly diminished, which is a matter of concern. Key Words: Demographic Dividend, Inclusive Growth, Smart Cities, Skill India

Background: Circulating cell-free tumor DNA (ctDNA) analysis for minimal residual disease (MRD) detection is transforming cancer care. However, the sensitivity of these approaches remains subpar and there is significant risk of false negative results. We analyzed the most proximal biofluid (urine) in localized muscle-invasive bladder cancer (MIBC) patients, and performed two orthogonal ctDNA analytical techniques, one focusing on driver mutation detection, and another focusing on genome-wide copy number alterations. The primary objective of this combinatorial approach was to sensitively detect ctDNA MRD, predict pathologic complete response (pCR), and improve patient risk-stratification. Methods: Urine samples from 74 localized bladder cancer patients were collected preoperatively on the day of curative-intent radical cystectomy (RC) to assess urine tumor DNA (utDNA). We performed ultra-low pass whole genome sequencing (ULP-WGS) of urine cfDNA from all 74 patients as well as 15 healthy adults. Tumor fraction (TFx) level based on genome-wide copy number alterations was estimated using ichorCNA. Variant allele frequency (VAF) based on single-nucleotide variants (SNVs) was estimated by uCAPP-Seq. We also noninvasively inferred tumor mutation burden (iTMB). pCR was determined by surgical pathology. A random forest (RF) model with leave-one-out cross-validation (LOOCV) was utilized to predict disease status. Kaplan-Meier (KM) and Cox proportional hazards model survival analyses were performed to assess overall survival (OS) and progression-free survival (PFS). Results: Our study cohort consisted of 74 patients, of which 58 (78%) harbored localized MIBC, and 16 (22%) harbored treatment-refractory high-risk localized NMIBC. Among MIBC patients, 64% (37/58) received neo-adjuvant chemotherapy. VAF, iTMB and TFx levels significantly predicted pCR status. Our RF model incorporating these three utDNA parameters achieved a sensitivity of 87%, a negative predictive value of 77%, and a positive predictive value of 65% for predicting residual disease. AUC for the model was 0.80 (p Conclusions: Integration of ULP-WGS with uCAPP-Seq enabled robust detection of residual urine tumor DNA with high sensitivity and predicted survival in localized bladder cancer patients. In the future, this type of multimodal urine-based genomic analysis may lead to more precise risk stratification and nonoperative clinical decision-making for bladder cancer patients. Citation Format: Pradeep Singh Chauhan, Alexander L. Shiang, Irfan Alahi, R. Taylor Sundby, Wenjia Feng, Bilge Gungoren, Cayce Nawaf, Kevin Chen, Ramandeep K. Babbra, Peter K. Harris, Faridi Qaium, Casey Hatscher, Anna Antiporda, Lindsey Brunt, Lindsey R. Mayer, Jack F. Shern, Brian C. Baumann, Eric H. Kim, Melissa A. Reimers, Zachary L. Smith, Aadel A. Chaudhuri. Urine cell-free DNA multi-omics to detect molecular residual disease and predict survival in bladder cancer patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2219.

BREXIT provides opportunities and also poses challenges to India. India–UK relations are both wide ranging and robust, encompassing a broad vision for the future supported by a concrete and comprehensive road map for bilateral and global engagement. High-level visits on both sides in recent times have provided an opportunity to further cement the partnership.

Background: Electronic equipment manufacturing units are among the most common industries all over the world. It involves a large amount of employees required for processing, manufacturing, building and setting up electronic equipments. Workers are usually sedentary and involve very less physical movement. Chronic illnesses are common among these sedentary workers of which most important are cardiovascular diseases, hypertension, obesity and diabetes. Considering the importance of the subject and the lack of published evidence on health status of electronic manufacturing workers, our study was done with an aim of assessing selected morbidities among electronic equipment manufacturing units in Goa.Methods: Our retrospective record based cross-sectional study was conducted over a period of one month in March 2019. The study was done in electronic equipment manufacturing workers. Data included sociodemographic details of the workers and details of periodic medical check-up. The data analysis was done using and analyzed using SPSS version 22. Chi square test was used to assess association between qualitative variables.Results: Among the 109 electronic manufacturing workers, it was observed that 10.1% (11) had obesity with a BMI >30, 24.8% (27) had hypertension (>140/90) and 31.2% (34) had diabetes mellitus with HbA1c >6.5. In addition, 24.8% (27) had far vision defect and 39.4% (43) had near vision defect. 42.2% (46) had abnormal lung function tests, 0.9% (1) had hearing disability and 4.6% (5) had abnormal ECG findings. Among male workers 0.9% (1) had elevated PSA levels, whereas all PAPs smear reports were normal among female workers.Conclusions: This study highlights the need of periodic medical check-up of the electronic manufacturing workers for timely detection and early management of their health problems.

High incidence of nasopharyngeal carcinoma (NPC) has been reported from China, Southeast Asia and Northeast (NE) region of India. Populations at geographic regions having higher incidence of NPC display human leukocyte antigen (HLA) distribution patterns different from areas having low incidence. The current study has investigated the contribution of environmental risk factors and ethnic variation of microsatellite markers in HLA region for the high incidence of NPC in NE India. Genotyping of HLA region using 33 microsatellite markers by fragment length analysis was done in 220 study subjects (120 NPC patients and 100 healthy controls). Association analysis showed two adjacent microsatellite markers HL003 (allele 121) and D6S2704 (allele 218) in the HLA class I region having association with high risk of NPC while allele 127 of HL003 and allele 255 of D6S2678 conferred a protective effect. The environmental factors mainly use of firewood (odds ratio (OR) = 3.797385, confidence interval (CI) = 1.97-7.30, P

Despite the significance of data mining techniques to Heart Disease Data (HDD), there be a short of comprehensive literature review and a classification for it. This is the particular academic literature review of the application of data mining techniques to HDD (Heart Disease Data). It provides an academic database of literature amid the periods of 20062016 and proposes a classification scheme to classify the Mining techniques. The analysis and classification process was autonomously verified. Findings of this paper indicate that the research area of Heart Disease received most research attention. Classification and Association models are the two most commonly used models for data mining in Heart Disease Data. Our study provides a path to provide future research ideas and make easy creation about the application of data mining techniques in HDD.

clustering is a process in which we group the data by finding similarities between data based on their characteristics. These groups are called cluster. In clustering, there is a division of data into groups of similar objects. These groups are the clusters, consists of objects that are similar between themselves and dissimilar compared to objects of other groups. Clustering is unsupervised learning technique, based on the concept of maximize intra-clustering and minimize inter- clustering. Nowadays, clustering of biological dataset is the widely researched topic among computer science. Bio- informatics has become area that receive most of the attention of data mining techniques. Generally, bio- informatics targets to solve complicated problems like gene categorization and its functionality, gene expression analysis of data obtained from micro- array experiments etc. These clustering techniques are addressed with R. Clustering techniques are used to analyze the structure of biological data. There are many different methods but we study k- means, Hierarchical and Density- based clustering algorithm for Biological Data using R programming tool.

Our ability to assemble genome-wide expression data has far exceeded the ability of our diminutive human brains to analyses the raw data. We can refine the data down to a more understandable level by grouping the genes into a smaller number of categorization and then analyzing those. Clustering is one of the most popular techniques in gene expression. Many clustering algorithms have been initiated to analyze gene expression data, but less supervision is available to help choose among them. The evaluation of feasible and applicable clustering algorithms is becoming an important issue in today’s bioinformatics research. It is a method of grouping data into different clusters, in which each cluster must have data of great similarity and high dissimilarity with other cluster data. The basic clustering algorithms are K-mean and K-medoids. This paper presents a literature survey on the clustering application in gene expression. An attempt is made to provide a guide for the researchers who are working in the area of gene expression and data clustering.

In acute lymphoblastic leukemia (ALL), limited data are available on mTOR gene expression in clinical samples and its role in predicting response to induction chemotherapy. mRNA expression of mTOR gene was determined quantitatively by real-time PCR in 50 ALL patients (30 B-ALL and 20 T-ALL) and correlated with clinical outcome after induction chemotherapy. Expression level of mTOR was upregulated in more than 50% of cases of ALL. In T-ALL, high expression of mTOR was commonly seen, more in adults than children (82 vs. 55% cases), while in B-ALL it was same (~ 63% cases) in both adults and children. Mean fold change of mTOR expression was significantly higher in non-responders compared to responders of both adult B-ALL (7.4 vs. 2.7, p = 0.05) and T-ALL (13.9 vs. 2.4, p = 0.001). Similar results were seen in pediatric non-responders when compared to responders of both B-ALL (14.5 vs. 2.5, p = 0.006) and T-ALL (24.2 vs. 1.7, p = 0.002). Interestingly, we have observed that mTOR expression was two times higher in non-responders of children compared to adults in both B-ALL (14.5 vs. 7.4, p = 0.05) and T-ALL (24.2 vs. 13.9, p = 0.01). Multivariate analysis with other known prognostic factors revealed that mTOR expression independently predicts clinical response to induction chemotherapy in ALL. This study demonstrates that high mTOR expression is associated with poor clinical outcome in ALL and can serve as a potential target for novel therapeutic strategies.

Targeting breast cancer stem cells (BCSCs) offers a promising strategy for breast cancer treatment. We examined the plant alkaloid ellipticine for its efficacy to inhibit the expression of aldehyde dehydrogenase 1 class A1 (ALDH1A1)-positive BCSCs by in vitro and in silico methods. At 3 mM concentration, ellipticine decreased the expression of ALDH1A1-positive BCSCs by 62 % (p = 0.073) in the MCF7 cell line and by 53 % (p = 0.024) in the SUM159 cell line compared to vehicle-treated cultures. Ellipticine significantly reduced the formation of mammospheres, whereas paclitaxel enhanced mammosphere formation in both the treated cell lines. Interestingly, when treated with a combination of ellipticine and paclitaxel, the percentage of ALDH1A1-positive BCSCs dropped by several fold in vitro. A homology model of Homo sapiens ALDH1A1 was built using the crystal structure of NAD-bound sheep liver class I aldehyde dehydrogenase [PDB ID: 1BXS] as a template. Molecular simulation and docking studies revealed that the amino acids Asn-117 and Asn-121, Glu-249, Cys-302, and Gln-350, present in the active site of human ALDH1A1, played a vital role in interacting with the drug. The present study suggests that ellipticine reduces the proliferation and self-renewal ability of ALDH1A1-positive BCSCs and can be used in combination with a cytotoxic drug like paclitaxel for potential targeting of BCSCs.

Background.Mutations in NPM1 and FLT3 genes represent the most frequent genetic alterations and important diagnostic and prognostic indicators in patients with acute myeloid leukemia (AML).Objective.We investigated the prevalence and clinical characteristics of NPM1 and FLT3 mutations in 161 patients of de novo AML including adults and children.Results.NPM1 mutation was found in 21% and FLT3 mutation in 25% of the AML patients. Thirteen (8%) samples were positive for both NPM1 and FLT3/ITD mutations. Adult patients had significantly higher frequency of NPM1 mutation than children (25.8% versus 8.8%;P=0.02). Further, NPM1 mutation was found to be more frequent in patients above 45 years of age (P=0.02). NPM1 mutation was significantly associated with higher platelet count (P=0.05) and absence of hepatosplenomegaly (P=0.01), while FLT3/ITD mutation was associated with higher white blood count (P=0.01). Immunophenotypically, NPM1 mutation was associated with the lack of CD34 (P<0.001) and HLD-DR expression (P<0.001), while FLT3/ITD mutation was positively associated with the expression of CD7 (P=0.04). No correlation was found between NPM1 mutation and fusion gene. Interestingly, FLT3/ITD mutation was found to be inversely associated with AML/ETO fusion gene (P=0.04).Conclusions.The results suggest that distinct clinical and immunophenotypic characteristics of NPM1 and FLT3/ITD mutations present further insight into the molecular mechanism of leukemogenesis.

Polymorphisms in xenobiotic metabolizing genes are associated with altered metabolism of carcinogens in acute leukemia (AL). This study applied two data mining approaches to explore potential interactions among P53 and xenobiotic metabolizing genes in 230 AL patients [131 acute myeloid leukemia (AML) and 99 acute lymphoblastic leukemia (ALL)] and 199 controls. Individually, none of the genotypes showed significant associations with AML risk. However, in ALL the CYP1A12A TC genotype was associated with increased risk (OR = 2.02; 95% CI = 1.14-3.58; P = 0.01), whereas the GSTM1 null genotype imparted reduced risk (OR = 0.55; 95% CI = 0.31-0.96; P = 0.03). In classification and regression tree analysis, combinations of GSTM1 present, CYP1A12C AA or GG, EPHX1 exon3 TC, and EPHX1 exon4 AA or GG genotype strongly enhanced the risk of AML (OR = 5.89; 95% CI = 1.40-26.62; P = 0.01). In ALL, combinations of CYP1A12A TT, P53 GG or CC and GSTP1 AG genotypes conferred the highest risk (OR = 4.19; 95% CI = 1.45-12.25; P = 0.004). In multifactor dimensionality reduction analysis, a four locus model (GSTP1, P53, EPHX1 exon3, and CYP1A12A) was the best predictor model for ALL risk. The association between this model and ALL risk remained true even at low prior probabilities of 0.01% (false positive report probability = 0.05). Interaction entropy interpretations of the best model of ALL revealed that two-way interactions were mostly synergistic. These results suggest that high order gene-gene interactions play an important role in AL risk. Environ. Mol. Mutagen., 2012. © 2012 Wiley Periodicals, Inc.

Resistance to chemotherapy is a major impediment to the successful treatment of acute leukemia (AL). Expression of genes involved in drug resistance and apoptosis may be responsible for this. This study aimed to investigate the expression of drug resistance (MDR1, MRP1, LRP, BCRP, GSTP1, DHFR) and apoptotic genes (p53, BCL-2, Survivin) in adult acute leukemias and compare them with clinical and hematological findings and response to induction chemotherapy. Eighty-five patients with AL [45 with acute myeloid leukemia (AML) and 40 with acute lymphoblastic leukemia (ALL)] were used as a study group. Real-time PCR results showed that expression level of MDR1 was significantly higher in AML whereas expression of DHFR, BCRP and Survivin was significantly higher in ALL patients. In AML, significant correlation was observed between LRP and MRP1 (r(s)=0.44, p=0.016), LRP and DHFR (r(s)=0.41, p=0.02), MDR1 and BCL-2 (r(s)=0.38, p=0.03). Expression of GSTP1 and LRP correlated with high white blood count (p=0.03 and p=0.03) and BCL-2 with high peripheral blast count (p=0.009). MDR1 expression was significantly associated with the expression of immature stem cell marker CD34 (p=0.002). In ALL, significant association was found between LRP gene and female sex (p

Widespread use of tobacco and betel quid consumption and a high incidence of tobacco-associated aerodigestive tract cancers have been reported in different ethnic groups from several regions of Northeast (NE) India. This study was done to explore the possibility of phase II metabolic enzymes being responsible for the high prevalence of cancers in this region of India.Samples from 370 cases with oral, gastric, and lung cancers and 270 controls were analyzed for polymorphism of glutathione-S-transferase (GST) genes using polymerase chain reaction-restriction fragment length polymorphism-based methods.Tobacco smoking and betel quid chewing were found to be high risk factors for oral and lung cancers but not for gastric cancer, whereas tobacco chewing was found to be a risk factor for oral cancer but not for gastric or lung cancer. The variant genotypes of GSTP1 were not associated with any of the aerodigestive tract cancers. GSTT1 and GSTM1 null genotypes appeared to play a protective role for lung cancer (odds ratio [OR] = 0.47, 95% confidence interval [95% CI]: 0.24-0.93, p = 0.03) and (OR = 0.52, 95% CI: 0.28-0.96, p = 0.04), but they were not associated with oral and gastric cancers. However, when data was analyzed in different geographic regions the GSTT1 null genotype was found to be a significant risk factor for oral (OR = 2.58, 95% CI 1.01-6.61, p = 0.05) as well as gastric cancer (OR = 3.08, 95% CI 1.32-7.19, p = 0.009) in samples obtained from the Assam region of NE India. This is the first study on the association of GST polymorphisms and aerodigestive tract cancers in the high-risk region of NE India.

Detoxifying glutathione S-transferase (GST) gene polymorphisms show variation in different ethnic populations. GST detoxifies and metabolizes carcinogens, including oxygen free radicals. GST polymorphisms have been associated with susceptibility to different diseases. In the current study, allelic polymorphisms of GSTM1 and GSTT1 were analyzed in three ethnic groups of North East (NE) India where a high prevalence of various cancers and other diseases such as hypertension, tuberculosis, and asthma have been reported.We compared the prevalence of GSTT1 and GSTM1 deletion genotypes, which were determined by multiplex polymerase chain reaction, in 422 voluntary, healthy NE Indians with those of other populations. The data was statistically analyzed.The GSTT1-null genotype was found in 51%, 34.3%, and 15.7% of individuals (from Mizoram, Sikkim, and Assam regions of NE India, respectively), whereas the GSTM1-null genotype was found in 46.9%, 46%, and 35% of individuals from the same areas.The NE Indians differ from the rest of the Indian population with reference to genotypic distribution of GST polymorphisms but the frequency was found to be similar to that which has been reported from China. This may explain the hypothesis of the common ancestral origin of both the NE Indians and the Chinese and a higher frequency of cancers such as gastric, esophageal, and oral cancers, which has been reported from these regions. This study establishes baseline frequency data for GST polymorphisms for future case control studies on the role these polymorphisms play with regard to diseases. The results presented here provide the first report on GST polymorphisms in the NE Indian population.

Polymorphisms in DNA repair and cell cycle genes contribute to increased breast cancer (BC) risk. Their association and interaction in relation to betel quid and tobacco chewing habits need exhaustive multi-analytical investigation to explain BC predisposition due to DNA damage. Polymorphism in TP53-72Arg>Pro, RAD51-135G>C, BRCA2, and CCND1-G870A were examined in 204 BC cases and 217 controls from Northeast Indian population. Multifaceted analytic approaches were used to explore relationships between polymorphisms, tobacco history, and BC susceptibility. Betel quid chewing was identified as the predominant risk factor. CCND-AA and dominant model showed protection towards BC in betel quid chewer (BQC) [(0.28 (0.10–0.77), 0.01 and 0.32 (0.12–0.81), 0.01)] and non-betel quid chewers (NBQC) [(0.26 (0.09–0.78), 0.01 and 0.37 (0.16–0.87), 0.02)]. TP53-Pro/Pro genotype showed protection towards BC in NBQC (0.29 (0.10–0.81), p = 0.01) and (0.51 (0.32–0.80), p = 0.003, respectively). RAD51-C allele was associated with BC risk (2.03 (1.26–3.30) 0.002) in BQC. Two BQC cases had BRCA2 8415G>T:K2729N mutation in Exon18. MDR analysis showed best four locus model with TBA 0.6765 (0.005) and CVC of 10/10 in NBQC. Interaction diagram concurred the interactions between TP53 and RAD51 (1.32 %) with independent effect (1.89 %) of CCND1in NBQC. In CART analysis, BQC with CCND1 GG genotype were at risk (OR = 33.0; 95 % CI = 6.08–179.07), p

The IL-1β -511 C/T polymorphism is associated with increased IL-1 production and with increased risk of developing cancers. In this study, 251 patients (125 with gastric cancer [GC] and 126 with oral cancer [OC]) and 207 normal controls from northeast (NE) India were genotyped for the IL-1β -511 C/T polymorphism by PCR-restriction fragment length polymorphism (RFLP) and sequencing. Analysis of results showed betel-quid chewing to be a major risk factor (OR = 2.01, 95% CI = 1.05-3.87; P = 0.035) for OC. Inheritance of the IL-1β -511 CT or TT resulted in a 2.6- to 3.05-fold increase in the risk of developing OC relative to that of participants who possessed the reference genotype (OR = 2.57, 95% CI = 1.06-6.22; P = 0.036 and OR = 3.05, 95% CI = 1.22-7.63; P = 0.017), after adjusting for potential confounders. The dominant genetic model also confirmed the presence of the T allele as a significant risk factor for OC (OR = 2.72, 95% CI = 1.15-6.42; P = 0.02). In GC, interaction of the CT genotype with tobacco and betel-quid chewing habits conferred a significant 78% and 89% reduced risk of cancer, respectively. In conclusion, for the NE Indian population, the IL-1β -511 CC and CT genotypes were significantly associated with increased risk of OC. However, the interaction of the CT genotype with risk habits may play a preventive role for GC but not for OC.

Complex disease such as cancer results from interactions of multiple genetic and environmental factors. Studying these factors singularly cannot explain the underlying pathogenetic mechanism of the disease. Multi-analytical approach, including logistic regression (LR), classification and regression tree (CART) and multifactor dimensionality reduction (MDR), was applied in 188 lung cancer cases and 290 controls to explore high order interactions among xenobiotic metabolizing genes and environmental risk factors. Smoking was identified as the predominant risk factor by all three analytical approaches. Individually, CYP1A1*2A polymorphism was significantly associated with increased lung cancer risk (OR = 1.69;95%CI = 1.11–2.59,p = 0.01), whereas EPHX1 Tyr113His and SULT1A1 Arg213His conferred reduced risk (OR = 0.40;95%CI = 0.25–0.65,p

Polymorphisms in genes encoding detoxification enzymes have been suggested as susceptibility factors for many solid tumors. However, their association with hematological malignancies is controversial. A case-control study was done to determine the association between glutathione S-transferase M1 (GSTM1), GSTT1, GSTP1, EPHX1, and p53 codon 72 polymorphisms as risk factors in 120 adult acute myeloid leukemia (AML) cases and 202 healthy controls by polymerase chain reaction-restriction fragment length polymorphism techniques. Data were analyzed using χ(2) and conditional logistic regression model. None of the polymorphisms studied alone was associated with increased risk for AML. However, the frequency of GSTT1 null genotype was higher among controls (28.7%) than AML cases (21.6%), which showed a protective effect of the null genotype (odds ratio = 0.58, 95% confidence interval: 0.33-1.05, p = 0.07). In a combined analysis, both EPHX1 (His113His) and GSTP1 (Ile/Val) genes imparted a fourfold risk for adult AML but did not reach statistical significance (odds ratio = 4.22, 95% confidence interval: 0.992-17.99, p = 0.05). These findings suggest that the etiology of adult AML cannot be explained by polymorphism at a single locus, perhaps because of complexity involved in the metabolism of diverse xenobiotic compounds, and therefore, multiple gene-gene interactions should be investigated to predict the risk of AML.

Acute myeloid leukemia (AML) with normal karyotype represents a clinically and molecularly heterogeneous disease. Molecular markers with prognostic significance have been examined to improve risk profile characterization of this group. Activating mutations on FLT3 receptor are one of the most common genetic alterations reported. However, the prevalence and prognostic significance of FLT3 genetic alterations in AML patients with cytogenetically normal karyotype is still controversial. In this study, FLT3/ITD and FLT3/D835 mutations were analyzed in 133 patients with de novo AML with normal cytogenetics by genomic PCR assay. Of 133 patients with AML with normal cytogenetics, FLT3 internal tandem duplication (ITD) and FLT3/D835 mutations were detected in 27 (20%) and 4 (3%) samples, respectively. Although statistically insignificant, the frequency of FLT3/ITD was higher in >15 year age group when compared to

Occurrence of aberrant phenotypes in childhood and adult acute leukemia (AL) differs considerably in independent studies and their association with prognostic factors is still controversial. In the present study, 214 patients with AL (106 children and 108 adults) were evaluated for the aberrant expression of CD33 in ALL (B cell and T cell) and CD3, CD5, CD7, and CD19 in AML. In B-ALL, aberrant expression of CD33 was found in 39 and 23% cases of adult and children, respectively. In T-ALL, CD33 was seen in 33% cases of adults while in children CD33 was not observed. In AML, aberrant expression of CD19 was expressed in 52 and 32% while CD7 was expressed in 14 and 15% cases of childhood and adult AML, respectively. Among FAB subtypes, aberrant expression of CD19 and CD7 was more commonly seen in M5 subtype. One adult patient (AML-M5) showed expression of CD3, CD5, and CD19. In summary, aberrant phenotype was commonly seen in adults than childhood B-ALL while in AML, aberrant phenotype was more common in children than adults. CD19 was most commonly expressed antigen followed by CD7 in both childhood and adult AML. Interestingly, aberrant phenotype was not found in childhood T-ALL; however, it was seen in 33% cases of adults. We did not find any association of aberrant phenotype with adverse prognosis factors, CD34 marker, and clinical outcome except the absence of auer rod which was found to be significantly associated with aberrant phenotype of childhood AML (P = 0.01).