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Related Concept Videos

Mutations01:39

Mutations

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Overview
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Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

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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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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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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Rous Sarcoma Virus (RSV) and Cancer01:03

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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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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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Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
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IDH Mutations in Chondrosarcoma: Case Closed or Not?

Sanne Venneker1, Judith V M G Bovée1

  • 1Department of Pathology, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.

Cancers
|July 29, 2023
PubMed
Summary

Isocitrate dehydrogenase (IDH) mutations are common in chondrosarcoma but their role in later stages is unclear. Further research is needed to identify distinct IDH-mutant and wildtype subgroups for targeted therapies.

Keywords:
D-2-hydroxyglutarateIDH1IDH2chondrosarcomaisocitrate dehydrogenase mutationsarcoma

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Chondrosarcomas are malignant cartilage tumors often harboring IDH mutations.
  • IDH mutations are implicated in early cartilage tumor development, but their role in later stages and therapeutic targeting remains ambiguous.
  • The prognostic significance of IDH mutations in chondrosarcoma is unclear, contrasting with their established role in other cancers.

Purpose of the Study:

  • To investigate the role and prognostic value of IDH mutations in chondrosarcoma.
  • To explore the discrepancies in preclinical findings regarding IDH-targeted therapies for chondrosarcoma.
  • To highlight the importance of the genetic landscape and identify potential subgroups within IDH wildtype and mutant chondrosarcoma.

Main Methods:

  • Review of existing literature on IDH mutations in chondrosarcoma.
  • Analysis of factors contributing to discrepancies in preclinical studies (e.g., tumor type, D-2-hydroxyglutarate levels, in vitro models).
  • Consideration of the epigenetic landscape's influence on IDH mutation function and therapeutic strategies.

Main Results:

  • The prognostic value of IDH mutations in chondrosarcoma is not well-defined.
  • Preclinical studies have not yielded effective treatments targeting IDH mutations in chondrosarcoma.
  • Differences in tumor biology, metabolite levels, and experimental models may explain the varied findings.

Conclusions:

  • The simple dichotomy of IDH wildtype versus mutant chondrosarcoma is insufficient; distinct biological subgroups likely exist.
  • Future research should focus on characterizing these subgroups within both IDH wildtype and mutant chondrosarcoma.
  • Tailoring therapeutic strategies to these specific biological subgroups is crucial for improving patient outcomes.