Pan-Cancer Analysis of Potential Synthetic Lethal Drug Targets Specific to Alterations in DNA Damage Response

Shaoli Das1, Kevin Camphausen1, Uma Shankavaram1

  • 1Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States.

Frontiers in Oncology
|November 12, 2019
PubMed

Insights

This study identifies three cancer subtypes based on DNA damage response (DDR) alterations. It predicts synthetic lethality (SL) partners for targeted therapies, offering new strategies for cancer treatment.

Area of Science:

  • Oncology
  • Genomics
  • Computational Biology

Background:

  • DNA damage response (DDR) pathway alterations are a hallmark of cancer, leading to genomic instability and treatment resistance.
  • Synthetic lethality (SL) offers a promising therapeutic strategy by exploiting DDR defects in cancer cells, but clinical applications are limited.
  • A comprehensive understanding of DDR alterations across various cancer types is crucial for developing effective targeted therapies.

Purpose of the Study:

  • To perform a pan-cancer analysis of alterations in 10 DNA damage response (DDR) pathways.
  • To identify distinct DDR mechanisms and associated somatic mutations across different cancer types.
  • To predict novel synthetic lethality (SL) partners and potential drug targets for DDR-altered cancers.

Main Methods:

  • Unsupervised clustering of DDR pathway enrichment in 7,272 tumor samples from TCGA.
  • Machine-learning algorithms to predict SL partners for key DDR genes.
  • Analysis of FDA-approved drugs and drug screening data for sensitivity in cell lines with DDR mutations.
  • Kaplan-Meier analysis to assess clinical relevance of identified SL interactions.

Main Results:

  • Identified three prominent clusters associated with specific DDR mechanisms and distinct somatic mutations.
  • Predicted druggable SL partners for key genes in each DDR cluster.
  • Demonstrated clinical relevance of targeted SL interactions through improved disease-free survival in patient data.

Conclusions:

  • A computational framework for identifying clinically actionable SL drug targets in DDR-altered cancers has been established.
  • This approach provides a basis for developing personalized therapies based on specific DDR pathway alterations.
  • The findings support the potential of SL strategies to overcome treatment resistance in various malignancies.

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...
8.6K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.9K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
3.0K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.6K
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...
5.8K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
8.1K