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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...
Treatment Resistent Cancers02:56

Treatment Resistent 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...
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...
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: May 14, 2026

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models
09:58

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models

Published on: December 9, 2016

Targeting PRMT9 Overcomes Venetoclax Resistance in AML by Modulating Splicing and Inhibiting Translation.

Yang Li1, Xin He1, Lei Zhang2

  • 1City of Hope, United States.

Blood
|May 12, 2026
PubMed
Summary
This summary is machine-generated.

Protein arginine methyltransferase 9 (PRMT9) drives resistance to venetoclax in acute myeloid leukemia (AML). Inhibiting PRMT9 re-sensitizes AML cells to venetoclax, offering a potential therapeutic strategy.

Related Experiment Videos

Last Updated: May 14, 2026

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models
09:58

Using RNA-sequencing to Detect Novel Splice Variants Related to Drug Resistance in In Vitro Cancer Models

Published on: December 9, 2016

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Arginine methylation by protein arginine methyltransferases (PRMTs) is crucial for cancer cell proliferation.
  • The role of PRMTs in mediating therapeutic resistance, particularly to venetoclax (VEN) in acute myeloid leukemia (AML), is not well understood.

Purpose of the Study:

  • To investigate the role of PRMTs in venetoclax resistance in AML.
  • To identify potential therapeutic targets for overcoming VEN resistance in AML.

Main Methods:

  • Loss-of-function screens were performed in VEN-resistant (VEN-R) AML patient-derived xenograft (PDX) cells.
  • Genetic ablation and pharmacologic inhibition of PRMT9 were employed in preclinical models.
  • Mechanistic studies explored the impact of PRMT9 on RNA splicing, gene expression, and protein synthesis.

Main Results:

  • PRMT9 was identified as a critical factor promoting VEN resistance in AML.
  • VEN-R AML samples showed elevated PRMT9 levels; its inhibition re-sensitized cells to VEN.
  • PRMT9 ablation synergized with VEN to eradicate AML cells in preclinical models.
  • PRMT9 inhibition disrupted RNA splicing (ALG13 exon-skipping), downregulated the VEN-efflux transporter ABCC1, and suppressed oncoprotein synthesis (MCL1).

Conclusions:

  • PRMT9-mediated arginine methylation is linked to poor VEN responsiveness in AML.
  • Targeting PRMT9 represents a promising strategy to overcome VEN resistance in AML.
  • Combined inhibition of PRMT9 and VEN demonstrates therapeutic potential for resistant AML.