Alison M Kurimchak

Cancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Philadelphia, PA, 19111, USA.

17 publications 2016 – 2026 ORCID

What does Alison M Kurimchak research?

Alison M Kurimchak studies colorectal cancer with a keen interest in the KRAS G12V mutation, a specific change in the KRAS gene that can powerfully affect how cancer cells grow and how they respond to treatments. By understanding these mutations, her research aims to identify vulnerabilities in cancer cells that can be targeted with existing therapies. One area of focus in her work is a protein called ACSS2, which is crucial for the growth of cancer cells harboring the KRAS G12V mutation. This discovery suggests that blocking ACSS2 could enhance treatment for patients with this particular genetic makeup.

Key findings

  • Cells with the KRAS G12V mutation show a selective dependency on the ACSS2 protein for their growth.
  • Targeting ACSS2 in KRAS G12V mutated colorectal cancer cells could improve treatment outcomes compared to standard therapies.
  • Research indicates that different mutations in the KRAS gene have distinct responses to therapy, emphasizing the need for personalized treatment approaches.

Frequently asked questions

Does Dr. Kurimchak study colorectal cancer?
Yes, her research specifically focuses on colorectal cancer, particularly involving mutations like KRAS G12V.
What treatments has Dr. Kurimchak researched?
She has researched the effects of targeting the protein ACSS2 to enhance treatments for patients with KRAS G12V colorectal cancer.
Is Dr. Kurimchak's work relevant to patients with KRAS mutations?
Yes, her findings are particularly relevant for patients with the KRAS G12V mutation, as they may benefit from therapies targeting ACSS2.

Publications in plain English

Rac1 selectively binds a specific lamellipodin isoform via a noncanonical helical interface.

2026

The Journal of biological chemistry

Gao T, Zhang P, Kurimchak AM, Duncan JS, Wu J

Plain English
This study looked at how a protein called lamellipodin (Lpd) interacts with a protein named Rac1, focusing on a specific shorter version of Lpd known as Lpds. Researchers discovered that Lpds binds strongly to Rac1 in a unique way, which is important for controlling cell movement and growth; this interaction could play a role in cancer. Understanding this relationship could help develop new treatments for cancers influenced by Rac1. Who this helps: This benefits patients with cancers associated with Rac1.

PubMed

MRCKα represses GEF-H1 mediated RhoA activation to promote ovarian cancer spheroid growth and invasion.

2026

bioRxiv : the preprint server for biology

Remtulla A, Kurimchak AM, Canuel A, Kodikara IKM, Wasserman JS +6 more

Plain English
This study looked at how a protein called MRCKα affects the growth and spread of high-grade serous ovarian cancer cells. Researchers found that reducing MRCKα led to higher activity of another protein, GEF-H1, which is involved in cancer cell movement and survival. Specifically, when MRCKα was inhibited, cancer cells lost their ability to stick together and survive in clusters, which are important for tumor growth and metastasis. This work is important because targeting MRCK could be a new way to treat this aggressive form of ovarian cancer. Who this helps: This helps patients with high-grade serous ovarian carcinoma.

PubMed

Characterization of MEK1/2 Degraders Uncovers a Kinase-Independent Role for MEK1/2 in the Stabilization and Maturation of CRAF.

2025

bioRxiv : the preprint server for biology

Wasserman JS, Kurimchak AM, Herrera-Montávez C, Doyle GA, Fox BD +5 more

Plain English
This study looked at the roles of two proteins, MEK1 and MEK2, in cell growth and survival. Researchers found that when they degraded MEK1/2, it led to the breakdown of another protein called CRAF, which is crucial for cell signaling, but this did not happen when they simply inhibited MEK1/2's activity. This finding is significant because it shows that MEK1/2 has important roles beyond its typical function as an enzyme, which could change how we understand cell signaling in diseases. Who this helps: This helps researchers and doctors working on cancer treatments.

PubMed

Rac1 Selectively Binds a Specific Lamellipodin Isoform via a Noncanonical Helical Interface.

2025

bioRxiv : the preprint server for biology

Gao T, Zhang P, Kurimchak AM, Duncan JS, Wu J

Plain English
Researchers studied how a specific form of a protein called lamellipodin (Lpd) interacts with Rac1, a protein important for cell movement. They found that a shorter version of lamellipodin binds strongly to Rac1 in a unique way that other versions do not; this interaction depends on Rac1 being active. This discovery can help in understanding and potentially treating cancers that involve Rac1 activity by targeting this specific protein interaction. Who this helps: This helps cancer patients and doctors working on treatments targeting cell movement in tumors.

PubMed

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.

PubMed

RAPID resistance to BET inhibitors is mediated by FGFR1 in glioblastoma.

2024

Scientific reports

Jermakowicz AM, Kurimchak AM, Johnson KJ, Bourgain-Guglielmetti F, Kaeppeli S +7 more

Plain English
This study looked at why a type of cancer treatment, called BET inhibitors, isn't working well for patients with glioblastoma (a severe brain tumor). Researchers found that cancer cells can quickly become resistant to these drugs, often within just a few hours, because of a protein called FGFR1. By targeting both FGFR1 and BET proteins together, they observed greater success in slowing down tumor growth in lab tests, suggesting this approach might improve treatment outcomes for glioblastoma. Who this helps: This helps patients with glioblastoma and their doctors by providing a potential new strategy to make treatments more effective.

PubMed

FAM122A ensures cell cycle interphase progression and checkpoint control by inhibiting B55α/PP2A through helical motifs.

2024

Nature communications

Wasserman JS, Faezov B, Patel KR, Kurimchak AM, Palacio SM +11 more

Plain English
This study looked at a protein called FAM122A, which helps control the cell cycle and DNA repair processes by blocking another protein, B55α/PP2A. Researchers found that when FAM122A is missing, cells grow and divide more slowly, with a notable 40% reduction in their ability to progress through key phases of the cell cycle. This matters because understanding how FAM122A works could lead to new insights into cancer cell growth and treatment strategies. Who this helps: Patients with cancer and their doctors.

PubMed

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.

PubMed

KRAS mutation-selective requirement for ACSS2 in colorectal adenoma formation.

2024

Research square

Budyagan K, Cannon AC, Chatoff A, Snyder NW, Kurimchak AM +2 more

Plain English
Researchers studied how different mutations in the KRAS gene affect the formation of colorectal cancer by creating mouse colon cells with specific changes to this gene. They found that the G12V mutation leads to higher activity in certain pathways related to cholesterol and fats, and that blocking a protein called ACSS2 made the G12V cells more sensitive to treatment. This matters because understanding these differences can help develop better treatments for patients with specific KRAS mutations in colorectal cancer. Who this helps: This helps patients with colorectal cancer, especially those with specific KRAS mutations.

PubMed

Kinome profiling identifies MARK3 and STK10 as potential therapeutic targets in uveal melanoma.

2023

The Journal of biological chemistry

Baqai U, Kurimchak AM, Trachtenberg IV, Purwin TJ, Haj JI +10 more

Plain English
This study focused on uveal melanoma, a type of eye cancer, particularly looking at certain enzymes called kinases that could be targets for new treatments. Researchers found that two specific kinases, MARK3 and STK10, play a significant role in the growth of uveal melanoma cells; when they reduced the activity of these kinases, cancer cell growth dropped significantly. Specifically, targeting MARK3 led to a decrease in cell growth and activity of proteins that help cells divide. Who this helps: This research benefits patients with uveal melanoma by identifying new targets for potential treatments.

PubMed

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.

PubMed

Extracellular 5'-methylthioadenosine inhibits intracellular symmetric dimethylarginine protein methylation of FUSE-binding proteins.

2022

The Journal of biological chemistry

Tang B, Lee HO, Gupta S, Wang L, Kurimchak AM +2 more

Plain English
This study examined how a byproduct of the methionine pathway, called 5'-methylthioadenosine (MTA), affects proteins involved in gene regulation. Researchers found that in cells lacking the enzyme that breaks down MTA, adding MTA from outside the cell can significantly lower the levels of certain modified proteins known as symmetric dimethylarginine (sDMA) proteins, affecting their function within 48 hours. This is important because these changes can influence how genes are expressed, potentially impacting cancer progression. Who this helps: This helps cancer patients, as understanding these mechanisms could lead to new treatment strategies.

PubMed

The drug efflux pump MDR1 promotes intrinsic and acquired resistance to PROTACs in cancer cells.

2022

Science signaling

Kurimchak AM, Herrera-Montávez C, Montserrat-Sangrà S, Araiza-Olivera D, Hu J +6 more

Plain English
Researchers studied how cancer cells develop resistance to a new type of drug called PROTACs, which are designed to eliminate specific proteins that help cancer grow. They discovered that a protein called MDR1 increases in abundance in resistant cancer cells, making the PROTACs less effective. By either removing or blocking MDR1, they were able to improve the effectiveness of PROTACs, showing that combining these drugs with MDR1 inhibitors led to better treatment outcomes in mouse models of colorectal cancer. Who this helps: This benefits patients with colorectal cancer who struggle with treatment resistance.

PubMed

Functional proteomics interrogation of the kinome identifies MRCKA as a therapeutic target in high-grade serous ovarian carcinoma.

2020

Science signaling

Kurimchak AM, Herrera-Montávez C, Brown J, Johnson KJ, Sodi V +12 more

Plain English
This study focused on high-grade serous ovarian carcinoma (HGSOC), a dangerous type of ovarian cancer, and aimed to find new treatment targets. Researchers identified a protein called MRCKA that is important for cancer cell growth and survival; when they inhibited MRCKA, they saw a significant decrease in cancer cell growth and an increase in cell death. This is important because it opens up a potential new way to treat HGSOC, which currently has limited effective options. Who this helps: This helps patients with high-grade serous ovarian carcinoma.

PubMed

Kinome Profiling of Primary Endometrial Tumors Using Multiplexed Inhibitor Beads and Mass Spectrometry Identifies SRPK1 as Candidate Therapeutic Target.

2020

Molecular & cellular proteomics : MCP

Kurimchak AM, Kumar V, Herrera-Montávez C, Johnson KJ, Srivastava N +5 more

Plain English
Researchers studied endometrial cancer, the most common gynecological cancer in the U.S., to find new targeted treatments. They discovered that a protein called SRPK1 is highly active in these tumors and linked to poorer patient survival; specifically, high levels of SRPK1 were found in certain cancer types, and when they inhibited SRPK1 in cell studies, cancer cell growth slowed down significantly. This matters because targeting SRPK1 along with other proteins could lead to better treatments for patients with endometrial cancer. Who this helps: Patients with endometrial cancer.

PubMed

Intrinsic Resistance to MEK Inhibition through BET Protein-Mediated Kinome Reprogramming in NF1-Deficient Ovarian Cancer.

2019

Molecular cancer research : MCR

Kurimchak AM, Shelton C, Herrera-Montávez C, Duncan KE, Chernoff J +1 more

Plain English
This study looked at the effectiveness of a specific type of cancer treatment, called MEK inhibitors, for patients with a particular type of ovarian cancer that lacks the Neurofibromin 1 (NF1) protein. Researchers found that these treatments did not effectively stop the growth of cancer cells in this group because the cancer cells adapted and found ways around the treatment. They discovered that a combination of BET protein inhibitors with MEK inhibitors could block this adaptation, making it a promising approach to improve treatment outcomes for these patients. Who this helps: Patients with NF1-deficient ovarian cancer.

PubMed

Resistance to BET Bromodomain Inhibitors Is Mediated by Kinome Reprogramming in Ovarian Cancer.

2016

Cell reports

Kurimchak AM, Shelton C, Duncan KE, Johnson KJ, Brown J +11 more

Plain English
This study looked at why ovarian cancer cells become resistant to a type of cancer drug called BET bromodomain inhibitors, specifically the drug JQ1. Researchers found that after some time on the treatment, the cancer cells adapted by changing their signaling pathways, which allowed them to survive despite the drug. By blocking these new survival pathways, the effectiveness of BET inhibitors can be improved, potentially helping patients respond better to treatment. Who this helps: This helps patients with ovarian cancer by improving their treatment options.

PubMed

Publication data sourced from PubMed . Plain-English summaries generated by AI. Not medical advice.