Konstantin Budagyan studies how genetic mutations, particularly the KRAS G12V mutation, affect the way cancer cells grow and respond to treatments. He looks at how these cells metabolize nutrients and utilize specific proteins to thrive. His studies reveal that cancer cells with the KRAS G12V mutation depend on a protein called ACSS2 for their survival. By inhibiting ACSS2, he shows that these cancer cells become more susceptible to certain therapies, thereby highlighting a potential way to enhance treatment for patients suffering from this type of colorectal cancer.
Key findings
Cells with the KRAS G12V mutation depend on the protein ACSS2 for growth, which makes them vulnerable to ACSS2 inhibition.
Targeting ACSS2 could significantly improve treatment effectiveness for colorectal cancer patients with the KRAS G12V mutation.
The metabolic requirements of KRAS G12V mutant cells may differ from those of other colorectal cancer types, highlighting the need for tailored therapies.
Frequently asked questions
Does Dr. Budagyan study KRAS mutations?
Yes, he focuses on the KRAS G12V mutation and how it affects colorectal cancer treatment.
What treatments has Dr. Budagyan researched?
He has researched how blocking the ACSS2 protein can enhance the effectiveness of treatments for patients with KRAS G12V colorectal cancer.
Is Dr. Budagyan's work relevant to colorectal cancer patients?
Yes, his research is particularly relevant to those with the KRAS G12V mutation, as it offers insights into more effective treatment options for them.
Publications in plain English
KRAS G12V mutation-selective requirement for ACSS2 in colorectal adenoma formation.
2025
Cell reports
Budagyan K, Cannon AC, Chatoff A, Benton D, Kurimchak AM +6 more
Plain English This study focused on how a specific type of KRAS mutation, called KRAS G12V, affects cell metabolism in colorectal cancer. Researchers discovered that cells with this mutation rely heavily on a protein called ACSS2 for growth, making them more vulnerable to certain treatments when ACSS2 is blocked. They found that targeting ACSS2 could help improve treatment effectiveness for patients with this mutation, which is important because different mutations can respond differently to therapies.
Who this helps: This research benefits patients with KRAS G12V colorectal cancer.
Unique vulnerability of RAC1-mutant melanoma to combined inhibition of CDK9 and immune checkpoints.
2024
Oncogene
Cannon AC, Budagyan K, Uribe-Alvarez C, Kurimchak AM, Araiza-Olivera D +5 more
Plain English This study looked at a specific type of skin cancer called melanoma that has mutations in a gene called RAC1, which makes it harder to treat. Researchers found that blocking a protein called CDK9 not only slowed down the growth of these RAC1-mutant melanoma cells but also made them more responsive to an immune therapy. In experiments, this combination treatment significantly reduced tumor growth, showing that targeting CDK9 could improve outcomes for patients with this type of melanoma.
Who this helps: Patients with RAC1-mutant melanoma.
A Facile Method to Append a Bio-ID Tag to Endogenous Mutant Kras Alleles.
2024
Methods in molecular biology (Clifton, N.J.)
Budagyan K, Cannon AC, Chernoff J
Plain English This research focused on KRAS mutations, which are found in about 50% of colorectal cancers and make the disease harder to treat. The study developed a new method to tag these mutations using a technique called BioID, which helps identify nearby proteins that interact with the mutated KRAS genes. The findings could lead to a better understanding of how different KRAS mutations affect cancer development and may open up new targeted treatments.
Who this helps: This helps patients with colorectal cancer and their doctors by providing insights for more effective therapies.
Unique vulnerability of-mutant melanoma to combined inhibition of CDK9 and immune checkpoints.
2023
bioRxiv : the preprint server for biology
Cannon AC, Budagyan K, Uribe-Alvarez C, Kurimchak AM, Araiza-Olivera D +5 more
Plain English This study focused on a specific type of melanoma with a RAC1 mutation, which is linked to worse outcomes and resistance to treatment. Researchers discovered that blocking a protein called CDK9 slowed the growth of these cancer cells and made them more responsive to an immune therapy called anti-PD-1. Specifically, combining CDK9 inhibition with anti-PD-1 treatment significantly reduced tumor growth in RAC1-mutant melanoma.
Who this helps: This benefits patients with RAC1-mutant melanoma who may have limited treatment options.
A Facile Method to Engineer Mutant Kras Alleles in an Isogenic Cell Background.
2021
Methods in molecular biology (Clifton, N.J.)
Budagyan K, Chernoff J
Plain English This study focused on creating specific KRAS gene mutations in a type of colon cell to better understand how these mutations affect cancer development and treatment. The research found a way to efficiently introduce different KRAS mutations into cells, which can help scientists investigate how these mutations impact cancer behavior and response to therapies. Understanding these differences is important because it could lead to more personalized cancer treatments for patients.
Who this helps: This helps cancer patients and doctors by providing insights for more tailored treatment options.
Devalaraja S, To TKJ, Folkert IW, Natesan R, Alam MZ +12 more
Plain English This study examined how a substance called retinoic acid, produced by tumor cells, helps to create an environment that suppresses the immune response against tumors. Researchers found that when retinoic acid levels were reduced, the immune system was better able to recognize and attack tumors, increasing the presence of cells that stimulate immune activity and enhancing the effectiveness of existing cancer treatments. This is important because it suggests a new strategy for improving cancer therapies by targeting how tumors manipulate immune cells.
Who this helps: This helps patients with cancer by potentially making treatments more effective.
Cytosine Deaminase APOBEC3A Sensitizes Leukemia Cells to Inhibition of the DNA Replication Checkpoint.
2017
Cancer research
Green AM, Budagyan K, Hayer KE, Reed MA, Savani MR +2 more
Plain English This study looked at a protein called APOBEC3A (A3A) in leukemia cells, particularly in patients with acute myelogenous leukemia (AML). Researchers found that high levels of A3A make these cancer cells more vulnerable to treatments that block a specific part of the cell's DNA repair process, leading to increased cell death. In their experiments, leukemia cells with A3A were killed by these treatments about 85% of the time, highlighting A3A's potential as a target for therapy.
Who this helps: This benefits patients with acute myelogenous leukemia and their doctors by providing a new treatment option.
APOBEC3A damages the cellular genome during DNA replication.
2016
Cell cycle (Georgetown, Tex.)
Green AM, Landry S, Budagyan K, Avgousti DC, Shalhout S +2 more
Plain English This study focused on a protein called APOBEC3A, which can damage DNA when cells are dividing. Researchers found that when APOBEC3A is present, it causes more DNA damage in active (dividing) cells than in resting (non-dividing) ones. Essentially, they discovered that replicating cells are more susceptible to mutations due to APOBEC3A, which might play a role in the instability of cancer genes.
Who this helps: This helps patients with cancer, as understanding these mechanisms could lead to better treatments.