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1. Genetics and management of inherited cancer predisposition 1
- Prof. Joshua Schiffman
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2. Genetics and management of inherited cancer predisposition 2
- Prof. Joshua Schiffman
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3. The cytogenetics of childhood acute leukemia
- Dr. Susana C. Raimondi
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4. Chromosome translocations and cancer
- Prof. Felix Mitelman
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5. Acute myeloid leukemia: genetics, prognosis and treatments
- Prof. Stephen Nimer
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6. Genetic abnormalities in acute lymphoblastic leukemia
- Prof. Ching Hon Pui
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7. Molecular genetics of non-Hodgkin lymphoma
- Prof. Jude Fitzgibbon
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8. Genetics of breast and ovarian cancer
- Prof. Jeffrey Weitzel
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9. The genetics and genomics of familial renal carcinoma
- Prof. Eamonn Maher
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10. Genomics of lung cancer
- Prof. Ramaswamy Govindan
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11. The genetics of glioblastoma
- Dr. Hai Yan
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12. Genetics of tumor metastasis 1
- Prof. Robert Weinberg
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13. Genetics of tumor metastasis 2
- Prof. Robert Weinberg
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14. CML: genetic paradigm of targeted therapy 1
- Prof. Michael W. Deininger
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15. CML: genetic paradigm of targeted therapy 2
- Prof. Michael W. Deininger
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16. The non-coding RNA revolution in the cancer society
- Prof. George Calin
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17. Role of molecular markers in guiding therapy in cancer
- Prof. Joe Duffy
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18. Functional cancer genomics
- Prof. Roderick Beijersbergen
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19. Pharmacogenomics in cancer therapy
- Prof. Sharon Marsh
Printable Handouts
Navigable Slide Index
- Introduction
- ALL: the most common childhood cancer
- Children's overall 5-year survival by treatment era
- Genetic classification of childhood ALL
- ALL: polygenic disease by genome-wide analyses
- EFS & genetic abnormalities in children
- EFS of t(4;11)[MLL-AFF1] ALL by age
- EFS of [MLL-ENL] ALL by immunophenotype & age
- Infant/non-infant ALL with mutant MLL profiles
- Genetic subtype frequency differs by age
- Chemotherapy + imatinib vs. transplant in Ph+ ALL
- Philadelphia chromosome (Ph)-like ALL
- Characteristics of Ph-like ALL
- GWAS: Ph-like ALL vs. Non-ALL controls
- GATA3 SNP genotype and ALL relapse
- GATA3 SNPs rs3824662 allele frequency
- Ph-like ALL associated with poor outcome
- Minimal residual leukemia level
- Total XV: risk classification schema
- St. Jude total therapy study XV: results
- St. Jude risk assignment status of Ph-like cases
- No difference in EFS Ph-like ALL - Other B-ALL
- Ph-like ALL/Other B-ALL no survival difference
- Ph-like ALL/Other B-ALL no relapse CR difference
- Ph-like ALL/B-ALL no EFS diff. by risk group
- Ph-like ALL according to age
- Spectrum of kinase alterations in Ph-like ALL
- ABL class rearrangements
- JAK2 and EPOR rearrangements
- Ph-like ALL: kinase rearrangements
- Treatment of Ph-like ALL patients
- ABL1-class kinase fusions identification
- Early T-cell Precursor (ETP) ALL
- Mutational spectrum of early T-cell precursor ALL
- Hypodiploid ALL
- Genomics of hypodiploid ALL
- Hypodiploid ALL mutations
- TP53 mutation in a low-hypodiploid ALL kndred
- Germline mutations and ALL risk
- Germline cancer predisposition mutations
- Clonal relationship of diagnosis & relapse samples
- Drug resistance associated mutations in relapse
- Two genomes influence every cancer patient
- Host pharmacogenetics affecting leukemogenesis
- ARID5B inherited polymorphisms frequencies
- ARID5B polymorphisms - ethnic differences
- BMI1-PIP4K2A SNPs - ethnic differences
- GATA3 risk variant 3*higher in Hispanics vs Whites
- GATA3 SNP genotype - ALL genetic subtypes
- Gene variants associated with childhood ALL
- ARID5B, IKZF1, CEBPE, & BMI1-PIP4K2A variants
- TPMT SNPs affect mercaptopurine therapy
- TPMT genotype:reduce toxicity by dose dependent
- Downward dose adjustment of mercaptopurine
- East Asians - poorer mercaptopurine tolerance
- TPMT A719C: mercaptopurine intolerance predictor
- Second genome-wide significant locus: NUDT16
- NUDT15 C416T & mercaptopurine intolerance
- NUDT15: ancestry-related differences
- NUDT15 inactivates mercaptopurine metabolites
- CEP72 SNP & vincristine-induced neuropathy
- VCR-induced neuropathy & CEP72 Genotype
- Conclusions
Topics Covered
- Somatic genetic abnormalities
- Genetic classification
- Leukemogenesis
- Heterogeneity due to age of presentation, differences in cooperative mutations and target cells undergoing malignant transformation
- Genome-wide analysis disclosed novel genetic subtypes, driver mutations and targetable genetic lesions
- Germline polymorphisms and mutations affecting cancer susceptibility, treatment response and toxicity
- Precision medicine based on somatic and germline genetics
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Pui, C.H. (2015, October 29). Genetic abnormalities in acute lymphoblastic leukemia [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 14, 2024, from https://doi.org/10.69645/EKFG1360.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Ching Hon Pui has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Haematology
Transcript
Please wait while the transcript is being prepared...
0:00
My name is Ching-Hon Pui.
I'm a pediatric oncologist at
Saint Jude Children's Research Hospital in Memphis, Tennessee, USA.
This talk is about Genetic Abnormalities in
Acute Lymphoblastic Leukemia, focusing mainly on childhood cases.
For the rest of the talk,
I will mention its abbreviation, ALL.
ALL as shown in a bone marrow smear on
0:22
the left, and as a white column of sediment on the right is the most common childhood cancer,
representing one fourth of all cancers in children.
0:36
The treatment of children with ALL is one of
the greatest success stories of modern medicine.
The five-year survival rate has increased from
20 percent in the early 1960s to over 90 percent today.
The main reason for this remarkable achievement included
an effective treatment administered in controlled clinical trials,
precise diagnosis and risk classification,
and improved support care.
Because of the ease to obtain leukemia samples,
laboratory studies of child ALL have reviewed many of
the principles underlying current knowledge of cancer cell biology,
further boosting the treatment results.
1:21
With standard chromosomal and FISH analyses,
specific genetic abnormalities can be found in 75-80 percent of child ALL cases.
With a recent event of genome-wide analysis,
virtually all cases can now be classified based on
the primary genetic abnormalities, as shown in this slide.