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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...

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Related Experiment Video

Updated: Jun 11, 2026

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
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Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Subtype-specific genomic alterations define new targets for soft-tissue sarcoma therapy.

Jordi Barretina1, Barry S Taylor, Shantanu Banerji

  • 1Department of Medical Oncology, Harvard Medical School, Boston, Massachusetts, USA.

Nature Genetics
|July 6, 2010
PubMed
Summary

This study maps genomic alterations in soft-tissue sarcomas, identifying frequently mutated genes like TP53 and NF1. Findings suggest new therapeutic targets for diverse sarcoma subtypes.

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A Mouse Model of Incompletely Resected Soft Tissue Sarcoma for Testing (Neo)adjuvant Therapies
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A Mouse Model of Incompletely Resected Soft Tissue Sarcoma for Testing (Neo)adjuvant Therapies
07:15

A Mouse Model of Incompletely Resected Soft Tissue Sarcoma for Testing (Neo)adjuvant Therapies

Published on: July 28, 2020

Area of Science:

  • Oncology
  • Genomics
  • Molecular Biology

Background:

  • Soft-tissue sarcomas exhibit significant histologic diversity with over 50 subtypes.
  • Current knowledge of genomic alterations in these diverse tumors remains limited.
  • Approximately 10,700 new cases and 3,800 deaths occur annually in the US.

Purpose of the Study:

  • To conduct an integrative analysis of DNA sequence, copy number, and mRNA expression across seven major sarcoma subtypes.
  • To identify frequently mutated genes and their clinical associations.
  • To explore potential therapeutic targets based on molecular alterations.

Main Methods:

  • Integrative analysis of DNA sequence, copy number, and mRNA expression data.
  • Analysis of 207 tumor samples from seven major soft-tissue sarcoma subtypes.
  • Gene knockdown experiments using short hairpin RNA (shRNA).

Main Results:

  • Identified frequent mutations in TP53, NF1, and PIK3CA across different subtypes.
  • PIK3CA mutations in myxoid/round-cell liposarcomas (MRCs) correlated with Akt activation and poor outcomes.
  • NF1 mutations (point mutations and deletions) were found in myxofibrosarcomas and pleomorphic liposarcomas.
  • Knockdown of amplified genes like CDK4 and YEATS4 in dedifferentiated liposarcoma reduced cell proliferation.

Conclusions:

  • Provides a comprehensive molecular landscape of diverse soft-tissue sarcoma subtypes.
  • Highlights PIK3CA and NF1 as key genes with significant mutations and clinical relevance.
  • Suggests that targeting amplified genes such as CDK4 and YEATS4 may be a viable therapeutic strategy for specific sarcoma subtypes.