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Related Concept Videos

Mutations01:35

Mutations

42.5K
Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
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Mutations01:39

Mutations

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Overview
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Mutations in Microorganisms01:18

Mutations in Microorganisms

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Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
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Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

1.9K
Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
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Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
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Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

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Driver mutations in acute myeloid leukemia.

Ashwin Kishtagari1,2, Ross L Levine3,4, Aaron D Viny3,4

  • 1Department of Translational Hematology and Oncology Research.

Current Opinion in Hematology
|January 24, 2020
PubMed
Summary

Genomic sequencing reveals that mutations in acute myeloid leukemia (AML) genes impact more than just cancer growth. Understanding these gene functions is key to developing better AML treatments.

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Area of Science:

  • Hematology
  • Genomics
  • Molecular Biology

Background:

  • The mutational landscape of acute myeloid leukemia (AML) has significantly evolved over the last decade.
  • Recurrently mutated AML genes possess functional consequences extending beyond typical oncogene-driven growth and tumor suppressor loss.

Purpose of the Study:

  • To review the revised diagnostic, prognostic, and therapeutic strategies in AML.
  • To explore the functional consequences of recurrently mutated AML genes.

Main Methods:

  • Large-scale genomic sequencing efforts have been employed to map the complexity of AML.
  • Clinical trials investigating mutation-based targeted therapy for AML.

Main Results:

  • Genomic sequencing has elucidated the intricate complexity of AML.
  • Targeted therapies based on specific mutations have led to FDA-approved drugs for mutant-specific AML.
  • Recurrent mutations in genes affecting DNA methylation, chromatin modification, and spliceosomal machinery are observed across a spectrum from clonal hematopoiesis to overt AML.

Conclusions:

  • Understanding the molecular and pathophysiologic functions of key leukemogenic genes is crucial.
  • Translating these molecular insights into improved treatments for AML is essential.