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Publications

The publications within the last eight years have given way to breakthroughs in metabolic pathways, PDAC TME's, drug treatments, therapies, etc. What we know most is this field is ever changing and we are on a mission to combat that with basic science approaches in collaboration with some valuable statistics.

A systems mechanism for KRAS mutant allele–specific responses to targeted therapy

 

CRC EGFR's are responsive to certain inhibitors in KRAS mutant patients

Controversial approaches point to breakthroughs in certain patient treatment

Genomic therapy is going to pave the way for future cancer therapies

Discernment between candidate mechanisms for KRAS G13D colorectal cancer sensitivity to EGFR inhibitors

Recent discovery of drug sensitivity in patients with KRAS G13D

Using a wildtype RAS is proposed to give way to better response of inhibition

Other isoforms of G12 KRAS would be good subjects for further research 

Identification of RAS mutant biomarkers for EGFR inhibitor sensitivity using a systems biochemical approach

 

EGFR inhibitors have been found to be really effective for certain CRC patients

NF1 binding affinity is critical for the proliferation of these CRC cells

Emergence of differences in structural biology of these mutations may open new conclusions

Co-targeting KRAS G12C and EGFR reduces both mutant and wild-type RAS-GTP

Using EGFR inhibitors along with KRAS G12C inhibitors in CRC patients

A comprehensive overview of combining Cetuximab and AMG-510

Transcriptomic-Based Microenvironment Classification Reveals Precision Medicine Strategies for Pancreatic Ductal Adenocarcinoma

Microenvironment of PDAC is indicative of the type of treatment administered

Certain patients under classical and classical adjacent PDAC suffer from the worst prognosis

Knowing the PDAC TME is dynamic gives limitations but puts us on the right track for future clinical trials

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