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Related Concept Videos

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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Tumor Progression02:07

Tumor Progression

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Mismatch Repair01:20

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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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Differentiation of Common Myeloid Progenitor Cells01:15

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Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
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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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Updated: Oct 11, 2025

Characterizing Mutational Load and Clonal Composition of Human Blood
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Branching clonal evolution patterns predominate mutational landscape in multiple myeloma.

Akanksha Farswan1, Lingaraja Jena2, Gurvinder Kaur2

  • 1SBILab, Department of Electronics and Communication Engineering, Indraprastha Institute of Information Technology-Delhi (IIIT-D) Delhi 110020, India.

American Journal of Cancer Research
|December 7, 2021
PubMed
Summary
This summary is machine-generated.

Understanding multiple myeloma progression requires analyzing evolving mutations. This study reveals dynamic subclonal changes, identifying potential therapeutic targets and informing personalized treatment strategies for better patient outcomes.

Keywords:
Multiple myelomaNGSclonal evolutiondriver genesexome sequencingmutationsprogressiontumor mutation burden

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Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis
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Area of Science:

  • Genomics
  • Cancer Biology
  • Translational Medicine

Background:

  • Multiple Myeloma (MM) is characterized by clonal plasma cells with diverse molecular anomalies.
  • Understanding subclonal mutation dynamics during MM progression is crucial for effective treatment.

Purpose of the Study:

  • To investigate the evolution of subclonal mutations in MM from diagnosis to progression.
  • To identify actionable therapeutic targets based on temporal mutation patterns.

Main Methods:

  • Whole-exome sequencing of 62 MM patients at two time points (diagnosis and progression).
  • Novel ensemble approach for somatic variant calling using four variant callers.
  • Identification of actionable/druggable gene targets.

Main Results:

  • Significant intraclonal heterogeneity and branching evolution observed in most patients.
  • Hypermutator MM patients showed decreased tumor mutational burden from diagnosis to progression.
  • Identified recurrently decreasing driver mutations (e.g., BRAF, KRAS, ATM) and increasing mutations (e.g., NRAS, KMT2C), suggesting therapeutic opportunities.

Conclusions:

  • Multi-time point analysis of subclonal mutational landscapes is clinically relevant for MM.
  • Findings support risk stratification and tailored combination therapies based on evolving genomic profiles.