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Related Concept Videos

Meiosis I01:49

Meiosis I

Meiosis is a carefully orchestrated set of cell divisions, the goal of which—in humans—is to produce haploid sperm or eggs, each containing half the number of chromosomes present in somatic cells elsewhere in the body. Meiosis I is the first such division, and involves several key steps, among them: condensation of replicated chromosomes in diploid cells; the pairing of homologous chromosomes and their exchange of information; and finally, the separation of homologous chromosomes by a...
Comparing Copy Number Variations and SNPs02:26

Comparing Copy Number Variations and SNPs

Sequencing of the human genome has opened up several best-kept secrets of the genome. Scientists have identified thousands of genome variations that exist within a population. These variations can be a single nucleotide or a larger chromosomal variation.
Copy number variations or CNVs are the structural variations that cover more than 1kb of DNA sequence. The single nucleotide polymorphism (SNP), on the other hand, is a single nucleotide change or a point mutation that is found in more than 1%...
Genome Copying Errors02:46

Genome Copying Errors

DNA replication is a well-evolved process that copies millions of base pairs with high fidelity during each cell division. Occasionally a wrong base or a long stretch of wrong bases may get added to the daughter strands. If the errors are left unchecked, cells might accumulate several mutations that might endanger their  survival. Therefore, the copying errors are checked and repaired at three levels.
Nondisjunction01:29

Nondisjunction

During meiosis, chromosomes occasionally separate improperly. This occurs due to failure of homologous chromosome separation during meiosis I or failed sister chromatid separation during meiosis II. In some species, notably plants, nondisjunction can result in an organism with an entire additional set of chromosomes, which is called polyploidy. In humans, nondisjunction can occur during male or female gametogenesis and the resulting gametes possess one too many or one too few chromosomes.
Nondisjunction01:21

Nondisjunction

Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold sister...
Karyotyping01:17

Karyotyping

Describing the number and physical features of chromosomes can reveal abnormalities that underlie genetic diseases. This description is facilitated by special staining techniques that produce a particular banding pattern on each chromosome. State-of-the-art techniques make this approach even more powerful, enabling the detection of individual genes that cause disease.A Simple Chromosome Staining Technique Provides Valuable Scientific InsightSome genetic diseases can be detected by looking at...

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Updated: Jun 18, 2026

Array Comparative Genomic Hybridization (Array CGH) for Detection of Genomic Copy Number Variants
09:16

Array Comparative Genomic Hybridization (Array CGH) for Detection of Genomic Copy Number Variants

Published on: February 21, 2015

DNA copy-number abnormalities do not occur in infant ALL with t(4;11)/MLL-AF4.

M Bardini1, R Spinelli, S Bungaro

  • 1Centro Ricerca Tettamanti, Clinica Pediatrica Univ. Milano-Bicocca, Ospedale San Gerardo, Via Pergolesi, 33, 20052 Monza, Italy. abiondi.unimib@gmail.com

Leukemia
|November 13, 2009
PubMed
Summary

Infant acute lymphoblastic leukemia (ALL) with MLL rearrangement appears unique, with few cooperating mutations needed for onset. Additional genetic changes are acquired later, during disease relapse.

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Area of Science:

  • Oncology
  • Genetics
  • Pediatric Hematology

Background:

  • Infant acute lymphoblastic leukemia (ALL) pathogenesis remains unclear.
  • Mixed-Lineage Leukemia (MLL) gene rearrangements are common in infant ALL, suggesting their critical role.
  • Previous mouse models have not fully elucidated the necessity of cooperating mutations for MLL-AF4-positive ALL development.

Purpose of the Study:

  • To investigate cooperating genetic aberrations in infant ALL with t(4;11) using single-nucleotide polymorphism (SNP) array technology.
  • To gain novel insights into the pathogenesis of infant ALL.
  • To compare the genomic landscape of infant ALL with other age groups.

Main Methods:

  • Genomic profiling of 28 infant ALL cases with t(4;11) using SNP array technology.
  • Detection of copy-number abnormalities and small-segmental uniparental disomy traits.
  • Comparative analysis with pediatric, adolescent, and adult ALL cases.

Main Results:

  • Infant ALL with MLL rearrangement exhibits a significantly lower frequency of copy-number abnormalities compared to other age groups.
  • Small-segmental uniparental disomy traits were frequently detected and are largely constitutional.
  • Additional genetic aberrations are predominantly acquired during disease relapse.

Conclusions:

  • The MLL rearrangement is a primary driver in infant ALL, potentially sufficient for leukemia onset without cooperating mutations.
  • Infant ALL represents a distinct disease entity with a unique genomic profile.
  • The MLL rearrangement drives leukemia onset, with further genetic lesions accumulating at relapse.