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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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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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Actionable mutations in canine hemangiosarcoma.

Guannan Wang1, Ming Wu2, Martha A Maloneyhuss3

  • 1Department of Pathology and Laboratory Medicine, Raymond and Ruth Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States of America.

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|December 1, 2017
PubMed
Summary
This summary is machine-generated.

Comparative exome sequencing of canine hemangiosarcoma identified key mutations in PIK3CA, TP53, PTEN, and PLCG1. These findings offer potential therapeutic targets for both canine hemangiosarcoma and human angiosarcoma.

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Area of Science:

  • Comparative genomics
  • Oncology
  • Canine and human cancer research

Background:

  • Angiosarcomas (AS) are rare, deadly soft tissue sarcomas in humans, posing challenges for genomic discovery due to limited high-quality DNA from archival samples.
  • Visceral AS is particularly difficult to study due to case rarity and poor DNA quality from formalin-fixed, paraffin-embedded tissues.
  • Canine hemangiosarcoma (HSA), a histologically similar tumor, occurs frequently, offering a model for comparative genomic studies.

Purpose of the Study:

  • To investigate canine hemangiosarcoma (HSA) through exome sequencing to identify potential oncogenic drivers and therapeutic targets relevant to human angiosarcoma (AS).
  • To leverage the higher incidence of HSA in dogs as a model for understanding genetic alterations in AS.

Main Methods:

  • Whole exome sequencing of archived, matched tumor and normal tissue samples from dogs with splenic hemangiosarcoma.
  • Mapping sequencing reads to the Canfam3 canine reference genome to assess data quality and coverage.

Main Results:

  • Somatic mutations in PIK3CA, TP53, PTEN, and PLCG1 were identified in over half of the sequenced canine hemangiosarcoma samples.
  • These mutated genes are recognized as critical drivers in human cancers.
  • A PLCG1 mutation identical to one previously found in human visceral AS was observed in one canine case.

Conclusions:

  • The study identified conserved tumor driver genes between canine HSA and human AS, including PIK3CA, TP53, PTEN, and PLCG1.
  • Activating PIK3CA mutations represent promising therapeutic targets for precision medicine approaches in both canine and human cancers.
  • These findings establish a basis for developing targeted inhibitor clinical trials in canine HSA, potentially benefiting human AS research.