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Related Concept Videos

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.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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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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Adaptive Mechanisms in Cancer Cells02:53

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
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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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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
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  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Evolutionary Biology Of High-risk Multiple Myeloma.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Evolutionary Biology Of High-risk Multiple Myeloma.

Related Experiment Video

Establishment of a Human Multiple Myeloma Xenograft Model in the Chicken to Study Tumor Growth, Invasion and Angiogenesis
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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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Evolutionary biology of high-risk multiple myeloma.

Charlotte Pawlyn1, Gareth J Morgan2

  • 1The Institute of Cancer Research, 15 Cotswold Road, Sutton SM2 5NG, UK.

Nature Reviews. Cancer
|August 25, 2017

View abstract on PubMed

Summary
This summary is machine-generated.

Understanding myeloma progression from early stages to high-risk disease is key to improving patient outcomes. Identifying genetic drivers and clonal evolution offers new therapeutic targets for resistant myeloma.

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Multimodal Bioluminescent and Positronic-emission Tomography/Computational Tomography Imaging of Multiple Myeloma Bone Marrow Xenografts in NOG Mice
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Author Spotlight: Analyzing Bone Marrow Microenvironment in Murine Hematological Malignancies
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Area of Science:

  • Hematology
  • Cancer Biology
  • Genetics

Background:

  • Multiple myeloma outcomes have improved, but high-risk patients remain underserved.
  • Understanding disease evolution is crucial for improving outcomes in refractory myeloma.
  • Identifying genetic mechanisms driving myeloma progression is essential.

Purpose of the Study:

  • To review the evolutionary trajectories of high-risk myeloma.
  • To discuss diagnostic approaches for advanced myeloma.
  • To explore therapeutic strategies for resistant myeloma.

Main Methods:

  • Review of current literature on myeloma genetics and evolution.
  • Analysis of clonal evolution and microenvironmental interactions.
  • Discussion of end-stage high-risk disease characteristics.

Main Results:

  • Myeloma progression involves clonal evolution and genetic sub-cloning.
  • High-risk disease is characterized by treatment resistance and independent growth.
  • Understanding evolutionary pathways aids in diagnosis and treatment.

Conclusions:

  • Targeting genetic drivers and clonal evolution is vital for treating high-risk myeloma.
  • New insights into evolutionary trajectories improve diagnostic and therapeutic strategies.
  • Addressing the biological behavior of resistant myeloma is critical for effective treatment.