Hemo

Comprehensive Leukemia Panel

The comprehensive multigene panel provides the advantage of understanding the clonal drivers at the time of presentation and during the course of disease evolution, thus helping in more informed treatment decisions in most of the leukemias, primarily for risk stratification and targeted therapy.

Comprehensive Panel (133 genes SNVs, small INDELs, CNVs and 600 Fusions)

SNVs, Indels and CNVs in 133 genes

(ABL1, ASXL1, ATM, ATRX, BCOR, BRAF, CALR, CBL, CBLB, CBLC, CDKN2A, CEBPA, CREBBP, CSF3R, CUX1, DNMT3A, ETV6, EZH2, FLT3, GATA1, GATA2, GNAS, HRAS, IDH1, IDH2, IKZF1, JAK2, JAK3, KDM6A, KIT, KMT2A, KMT2D, KRAS, MPL, MYD88, NOTCH1, NPM1, NRAS, PDGFRA, PHF6, PTEN, PTPN11, RAD21, RUNX1, SETBP1, SF3B1, SMC1A, SMC3, STAG2, TET2, TP53, WT1, ZRSR2)

And 600+ Fusions are tested (Fusions/Gene list will be provided on request)

Bone Marrow morphology report, Complete blood count report and/or FISH report if available should accompany the sample.

Leukemia Fusion Genes Panel by NGS

ABL1, AFDN, ALK, BCL11B, BCL2, BCL3, BCL6, BCR, BIRC3, BRAF, CBFA2T3, CDK6, CHD1, CIITA, CREBBP, CRLF1, CRLF2, CSF1R, DUSP22, TYK2, ZBTB16, ZMYM2, DUX4, EGFR, EIF4A1, EPOR, ETV6, FGFR1, FGFR2, FUS, GATA1, GLIS2, HMGA2, HOXA1, HOXA10, HOXA11, HOXA13, HOXA2, HOXA3, HOXA4, HOXA5, HOXA6, HOXA7, HOXA9, IKZF1, IKZF2, IKZF3, IL2RB, IL3, JAK2, KAT6A, KLF2, KMT2A, LMO1, LMO2, MALT1, MECOM, MEF2D, MET, MLLT10, MLLT3, MRTFA, MYBL1, MYC, MYD88, NF1, NFKB2, NPM1, NUP214, NUP98, P2RY8, PAG1, PAX5, PCM1, PDCD1LG2, PDGFRA, PDGFRB, PICALM, PRDM16, PTK2B, RANBP2, RARA, RBM15, ROS1, RUNX1, SEMA6A, SETD2, SSBP2, STIL, TCL1A, TCL1B, TET1, TFE3, TFG, TLX1, TLX3, TP63, TRIM24, TCF3, FGFR3, LCK, DEK, CCND3, CCND1, LYL1, ABL2, AFF1, ATF7IP, BIN2, CBFB, CDK5RAP2, CHIC2, CNTRL, CPSF6, DDIT3, EBF1, ELL, TAL1, TNKS2, TOP1, TPM3, WDR48, ZCCHC7, ZMIZ1, ZNF384, PBX1, PML, PRKG2, RCSD1, RUNX1T1, SART3, SEC31A, SEPTIN9, SET, SNX2, STAT5B,

STRN, EML1, EP300, EPS15, ERC1, ERG, FOXO3, FOXO4, GIT2, GOLGA4, GTF2I, KANK1, KDM5A, KIF5B, MKL1, MLF1, MLLT1, MLLT11, MYH11, MYO18A, NDE1, NIN, NOTCH1, NSD1, NTRK3

AML

The response to treatment and overall survival of patients with AML is heterogeneous
Several prognostic factors related to patient and tumor characteristics have been described for AML
Mutations in specific genes are found in many cases of AML and can be identified using genetic tests
The results of the tests can be used for diagnosis and patient risk stratification
Treatment of AML is based on risk stratification, mainly patient age and tumor cytogenetics
In patients with cytogenetically normal AML, the identification of mutations in several genes, including FLT3, NPM1, and CEBPA, have been proposed to allow for further segregation in the management of this heterogeneous disease
The most common mutations found in AML include FLT3, NPM1, DNMT3A, NRAS, CEBPA, TET2, WT1, IDH2, IDH1, and KIT.
Molecular mutations have been analyzed to subdivide AML with normal cytogenetics into prognostic subsets.

ALL

Confirmatory diagnosis and identification of important prognostic and predictive biomarkers to tailor therapy
Mutations involved in various key pathways are found in different subtypes of B-ALL. Genes related to various pathways such as:
- Transcriptional regulators (IKZF1)
- Cell-cycle regulation and tumor suppression (TP53 and CDKN2A)
- Tyrosine kinase receptor signaling (ABL1, FLT3, JAK2)
- RAS signaling (NRAS, KRAS, and HRAS)
- Epigenetic modification (CREBBP)
Among them, specific genetic alterations are found to be associated with adverse clinical outcomes and increased risk for relapse
Analysis of these genetic lesions enables the clinician to accurately assess the patient, considering age for precision medicine, predict the outcomes, and the possibility of allogeneic stem cell transplantation (Allo-SCT).
The mutational analysis may further aid in the diagnosis, evaluating response to treatment using minimal residual disease (MRD) and risk assessment.

MDS

Some of the subtypes in MDS are associated with clinical biomarkers that aid in disease diagnosis and overall survival
ETV6, DNMT3A, EZH2, CUX1, RUNX1, U2AF, and STAG2 mutations independently predict poor prognosis in MDS patients
DNMT3A mutations were particularly found to be associated with RARS and lowest with RA subtype
]MDS patients with DNMT3A mutation displayed a higher risk of leukemia evolution and shorter overall survival
TET2 is seen at a frequency of 20% in MDS and is a marker of a favorable prognosisSF3B1 mutation was found to be highest in RARS and lowest in RA subtype and has a favorable prognosis in MDS
With a frequency of 5% to 15% in MDS, mutant RAS has a high likelihood of transformation to AML and shows an overall poor prognosis

CLL

For decades, ‘watchful waiting’ has been the standard of care for patients with early-stage CLL
This approach has focused on minimizing toxicity for the minority of patients whose disease may never evoke clinical symptoms
Considering the clinical heterogeneity of CLL, genetic markers have been established as routinely used prognostic factors in addition to the traditional staging systems
There is strong evidence that several of the predictive markers could influence treatment decisions for tailored therapy
The predictive potential of genetic factors associated with CLL outcome is determined by
- Accessibility of the marker for routine use
- Stability of the marker throughout the course of the disease
- Sensitivity and specificity of the marker

Chronic myeloid Leukemia -CML

Failure in treatment of CML is often associated with poor compliance due to BCR-ABL1 mutation (resulting in altered drug binding) and acquisition of other gene mutations eventually leading to TKIs resistance
Mutations in genes such as IKZF1 and CDKN2A are classical mutations implicated in >50% of BP-CML patients.
Therefore, analysis of the network of genes aids in improving the prognosis and therapeutic relevance by assessing for risk-associated therapy and prevention of progression
During treatment BCR-ABL1 transcript levels may go undetectable, which may discourage the patient to follow the therapy
Discontinuing TKIs was found being risky as rapid recurrence has been observed in 60% of CML patients. Therefore, molecular testing also enables detection of minimum residual disease (MRD) for clinical evaluation of therapy

Other Related Tests

Acute Myeloid Leukemia (AML)

FISH for PML-RARA t(15;17)(q24,q21)
FISH for RUNX1-RUNX1T1 t(8;21)(q22;q22)
FISH for inv(16)/t(16;16)(p13.1;q22)
FISH for AML Panels (3, 5, or all 8 markers: inv3, del5, del7, MLL, t(15;17), t(8;21), inv16, BCR-ABL)
AML Basic Panel (RT-PCR / NGS options: FLT3, NPM1, CEBPA, KIT)
AML Comprehensive Panels (RT-PCR + NGS + Karyotyping)
AML-ETO MRD

Acute Lymphoblastic Leukemia (ALL)

FISH for iAMP21
FISH for TCRA/D (14q11.2)
FISH for ETV6-RUNX1 t(12;21)
FISH for E2A (19p13.3) Translocation
FISH for C-MYC (8q24)
FISH for ALL Panels (4–6 markers or full panel including MLL, iAMP21, BCR-ABL, IGH, TCR, E2A)
Comprehensive ALL Panel (FISH, Karyotyping, MLPA, NGS, RT-PCR)

Chronic Lymphoid Leukemia (CLL)

FISH for IGH (14q32) Gene rearrangement
FISH for Trisomy 11, Trisomy 12, del6q, del13q, del17p
CLL Panels (4 or 5 markers, or full panel)
Comprehensive Molecular Work-up for CLL Prognostication (NGS, Sanger, FISH)
IGHV Gene Mutation Analysis

Chronic Myeloid Leukemia (CML)

FISH for iso17q
FISH for CML Panels (4 markers: BCR-ABL, iso17q, del7, trisomy 8)
FISH for BCR-ABL t(9;22)(q34;q11.2)

Myelodysplastic Syndromes (MDS)

FISH for del5q, del7q, del20q, trisomy 8, inv3
MDS Panels (3–8 markers, customized or full)
FISH for MLL amplification

Multiple Myeloma (MM)

FISH for IGH/CCND1 t(11;14), IGH/FGFR3 t(4;14), IGH/MAF t(14;16)
FISH for del13q, del17p, C-MYC
Myeloma Panels (4 or 5 markers, or full plasma-cell–enriched workup)

Myeloproliferative Neoplasms (MPN)

FISH for PDGFRA (4q12), PDGFRB (5q32-33)
FISH for MPN Panels (3–5 markers: BCR-ABL, PDGFRA, PDGFRB, JAK2, FGFR1)
FIP1L1-PDGFRA rearrangement

Comprehensive / Other Panels

Comprehensive Leukemia Panel (57-gene NGS + FISH + RT-PCR)
Comprehensive T-ALL & T-PALL Work-up (NGS, Karyotyping, FISH)
DPYD Gene Analysis (5-FU Sensitivity)
IDH1 & IDH2 Mutation Analysis
KIT, PDGFRA, STAT3, H3F3A Sequencing
Liquid Biopsy (ctDNA) Testing for Solid Tumors

HEMATOLOGICAL MALIGNANCIES PANELS, TESTS AND WORKUPS

Comprehensive Leukemia Panel

AML

ALL

MDS

CLL

B-Pro-lymphocytic leukemia (PLL)

Chronic myeloid Leukemia -CML

Other Related Tests

Acute Myeloid Leukemia (AML)

Acute Lymphoblastic Leukemia (ALL)

Chronic Lymphoid Leukemia (CLL)

Chronic Myeloid Leukemia (CML)

Myelodysplastic Syndromes (MDS)

Multiple Myeloma (MM)

Myeloproliferative Neoplasms (MPN)

Comprehensive / Other Panels

HEMATOLOGICAL MALIGNANCIES PANELS, TESTS AND WORKUPS

Comprehensive Leukemia Panel

AML

ALL

MDS

CLL

B-Pro-lymphocytic leukemia (PLL)

Chronic myeloid Leukemia -CML

Other Related Tests

Acute Myeloid Leukemia (AML)

Acute Lymphoblastic Leukemia (ALL)

Chronic Lymphoid Leukemia (CLL)

Chronic Myeloid Leukemia (CML)

Myelodysplastic Syndromes (MDS)

Multiple Myeloma (MM)

Myeloproliferative Neoplasms (MPN)

Comprehensive / Other Panels

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