Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

6.4K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
6.4K
Lineage Commitment01:21

Lineage Commitment

4.6K
Commitment is the  process whereby stem cells:
4.6K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

9.2K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
9.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

LDB1-dependent enhancer connectivity defines T-cell leukemia identities and masks metabolic vulnerabilities.

bioRxiv : the preprint server for biology·2026
Same author

A genomic and epigenomic lens into the biology of acute lymphoblastic leukaemia.

Nature reviews. Cancer·2026
Same author

FATP2-mediated lipid metabolism enhances chimeric antigen receptor T-cell therapy resistance in B-cell acute lymphoblastic leukemia.

Leukemia·2026
Same author

Long-term Follow-up of a Pediatric Regimen for AYA with Ph-negative ALL: 10-year Survival of CALGB 10403 (Alliance).

Blood advances·2026
Same author

Characterization of Genetic Etiologic Factors for Pediatric Acute Lymphoblastic Leukemia in Large Childhood Cancer Survivorship Cohorts.

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology·2026
Same author

Toxicity from asparaginase during acute lymphoblastic leukemia induction: a report from the Children's Oncology Group.

Blood advances·2026

Related Experiment Video

Updated: Apr 12, 2026

Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up
09:01

Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up

Published on: March 26, 2018

14.9K

Redefining ALL classification: toward detecting high-risk ALL and implementing precision medicine.

Stephen P Hunger1, Charles G Mullighan2

  • 1Department of Pediatrics and the Center for Childhood Cancer Research, Children's Hospital of Philadelphia, Philadelphia, PA; and.

Blood
|May 23, 2015
PubMed
Summary

Genomic analysis reveals new subtypes of childhood acute lymphoblastic leukemia (ALL), identifying genetic targets for precision medicine and understanding relapse risks.

More Related Videos

Murine Model of Leukemia Relapse to Induction Chemotherapy for Acute Lymphoblastic Leukemia
08:31

Murine Model of Leukemia Relapse to Induction Chemotherapy for Acute Lymphoblastic Leukemia

Published on: October 17, 2025

859
Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia
09:57

Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia

Published on: March 5, 2018

31.1K

Related Experiment Videos

Last Updated: Apr 12, 2026

Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up
09:01

Flow Cytometry to Estimate Leukemia Stem Cells in Primary Acute Myeloid Leukemia and in Patient-derived-xenografts, at Diagnosis and Follow Up

Published on: March 26, 2018

14.9K
Murine Model of Leukemia Relapse to Induction Chemotherapy for Acute Lymphoblastic Leukemia
08:31

Murine Model of Leukemia Relapse to Induction Chemotherapy for Acute Lymphoblastic Leukemia

Published on: October 17, 2025

859
Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia
09:57

Comprehensive Protocol to Sample and Process Bone Marrow for Measuring Measurable Residual Disease and Leukemic Stem Cells in Acute Myeloid Leukemia

Published on: March 5, 2018

31.1K

Area of Science:

  • Genomics
  • Pediatric Oncology
  • Molecular Biology

Background:

  • Acute lymphoblastic leukemia (ALL) is a major childhood cancer with significant mortality.
  • Recent advances in microarray and sequencing technologies have deepened the understanding of ALL's genetic landscape.

Purpose of the Study:

  • To elucidate the genetic basis of ALL by analyzing large patient cohorts.
  • To identify novel ALL subtypes and their associated molecular pathways.
  • To explore the interplay between germline genetics, somatic alterations, and disease progression.

Main Methods:

  • Microarray and next-generation sequencing of large ALL cohorts.
  • Genomic profiling to identify structural and sequence alterations.
  • Analysis of sequential samples from diagnosis, remission, and relapse.

Main Results:

  • Discovery of new ALL subtypes linked to specific genetic alterations affecting key cellular pathways.
  • Identification of kinase-activating lesions and epigenetic alterations as potential therapeutic targets.
  • Elucidation of the relationship between inherited variants, somatic mutations, clonal heterogeneity, and relapse risk.

Conclusions:

  • Genomic insights are revolutionizing the understanding and classification of ALL.
  • Precision medicine approaches targeting identified genetic pathways show promise for improved therapies.
  • Understanding genetic factors influencing relapse is crucial for developing effective treatment strategies.