We noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Cancer and molecular diagnostics
- The cytogenetics of acute lymphoblastic leukemia
- Cytogenetics of pediatric ALL
- ALL - Genetic classification
- Cytogenetics/genomics of pediatric ALL
- t(12;21)(p13;q22) ETV6-RUNX1(TEL-AML1)
- TXV therapy for ETV6-RUNX1-positive patients
- Intrachromosomal amplification 21q region in ALL
- FISH using ETV6-RUNX1 may show clustering
- der(21)(RUNX1 amp)
- We need to be careful…
- ALL - Ploidy
- Hypodiploidy <44 chromosomes in ALL
- Mosaicism for a near haploid clone
- Hyperdiploid (51+) karyotype in ALL
- “Doubled” near haploid karyotype with tetrasomies
- aCGH and NGS
- Risk factors in B-lineage childhood ALL
- Event-free survival of ALL according to era
- How genetic type should be classified?
- The cytogenetics of acute myeloblastic leukemia
- Acute myeloblastic leukemia (AML)
- AML WHO 2008 genetic changes
- AML cytogenetic classification in children
- t(8;21)(q22;q22) AML with maturation
- Inv(16)(p13.1q22) and t(16;16)(p13.1;q22)
- t(15;17)(q22;q21) APL
- Study of childhood 11q23/MLL- rearranged AML
- Survival curves for patients with 11q23/MLL
- MLL complex rearrangements: 10p12 and 11q24
- 11q23 Insertion (10;11)
- Identification using FISH
- t(6;9)(p23;q23)/DEK-NUP215
- Additional molecular genetic studies
- Subtle/cryptic abnormalities
- Cryptic abnormality (CBFA)
- Cryptic abnormality (NUP98)
- Rare chromosomal aberrations
- Somatic mutations in childhood AML
- Pediatric AML: association with age
- Prevalence of somatic mutations
- SJCRH AML02 3-years survival
- SJCRH 02
- Overall survival by treatment era
- Most children with AML are cured with chemo
- Summary
Topics Covered
- Application of new diagnostic techniques in clinical medicine, mainly in molecular cytogenetics of neoplasia
- Relevant chromosomal abnormalities that impact the diagnosis and prognosis of patients with acute lymphoblastic leukemia and acute myeloblastic leukemia
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Raimondi, S.C. (2016, May 31). The cytogenetics of childhood acute leukemia [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 3, 2024, from https://doi.org/10.69645/QVTY6083.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Susana C. Raimondi has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Other Talks in the Series: Cancer Genetics
Transcript
Please wait while the transcript is being prepared...
0:00
My name is Susana Raimondi.
I work at St. Jude
Children's Research Hospital.
I'm the director of the
Cytogenetics Laboratory,
and the presentation today
will be about the cytogenetics
of childhood acute leukemias.
0:17
Regarding the topic today,
the molecular changes
occur at the chromosome level, at
the gene level, or DNA sequences.
A full range of
genetic abnormalities
is indicative of cancer, but many
of the chromosomal alterations
observed by conventional
cytogenetics
alone do not induce leukemia.
Sometimes, there are no obvious
chromosomal alterations.
And some microscopic
genetics alterations may be
of leukemogenic/actionable events.
0:54
Regarding the cytogenetics of
acute lymphoblastic leukemia,
1:00
when we consider the pediatric
population, about 15% of the cases
are T-lineage.
They do have recurring
chromosomal aberrations.
However, they do not have
impact on the clinical behavior
of these patients with
T-lymphoblastic leukemia.
There's others that
have B-lineage leukemia.
About 50% of the cases have either
hyperdiploid with greater than 50
chromosomes, or a translocation that
is cryptic that is called t 12;21.
The other subsets are smaller.
And some of them are
strongly associated
with very poor prognosis.