I have mentored a patient with a starting CA19.9 value of 818,000 that peaked at 1,200,000 during the first few cycles of (m)Folfirinox and then dropped to 200,000 as treatment progressed. There are two other first-line chemotherapies of Nalirifox being the latest FDA approved drug which is better than Gemzar/Abraxane (Gemcitabine nab-Paclitaxel. Nalirifox was slightly better in progression-free survival up to 25 months in comparison to (m)Folfirinox. At that point, overall survival was the same. An abstract on comparison of Nalirifox to (m)Folfirinox was just presented at the ASCO meeting in Chicago two weeks ago. The title of the abstract is “Comparative Effectiveness of NALIRIFOX vs. FOLFIRINOX in pancreatic cancer” by Xiayu Jiao of the Department of Pharmaceutical and Health Economics, USC Schaeffer Center, Los Angeles, CA and Afsaneh Barzi, City of Hope Comprehensive Cancer Center, Duarte, CA.

There are targeted therapies that are successful, however molecular profiling of the tumor needs to be performed to determine if specific mutations and actionable biomarkers are present. I have the germline form of the BRCA2 mutation and the PARP inhibitor Rucaparib has been extremely successful for me. I am the longest former pancreatic cancer patient that was diagnosed with metastatic disease taking this drug at 9 3/4 years. I achieved No Evidence of Disease and have since been declared cured. To get to the point of NED required very aggressive chemotherapy using full dose Folfirinox. I was on the original FDA approved formulation used from 2011-2018. I received treatment every 15 days for 24 months without pause. I had a total of 46 cycles of chemo with 24 cycles being Folfirinox and 22 of 5-FU/Leucovorin. Dosing was in alternating groups of six. This is used for PDAC and PACC forms of the disease and not for PNET tumors. You need to find out which cell type has been diagnosed as PNET tumors are treated with different regimens.

Keytruda requires a patient to have the somatic KRAS G12C mutation which occurs at a very low frequency in pancreatic cancer patients of 1-3%. It also requires the patient have the actionable biomarker of PD-1. These markers require molecular profiling of the tumor.

CRISPR/Cas9 is currently a research tool and only pancreatic cell lines have been looked at for gene editing. It has not been used in clinical trials and not developed enough for human trials at this point in time.

QUESTIONS TO ASK
https://pancan.org/facing-pancreatic-cancer/diagnosis/choosing-your-healthcare-team/questions-to-ask-your-healthcare-team/
.

https://pancreaticcanceraction.org/about-pancreatic-cancer/pancreatic-cancer-diagnosis/what-questions-should-i-ask-my-doctors/ .

https://www.cancer.org/cancer/types/pancreatic-cancer/detection-diagnosis-staging/talking-with-doctor.html .

.
https://pathology.jhu.edu/pancreas/questions-to-ask
.
https://www.cancer.org/cancer/pancreatic-cancer/detection-diagnosis-staging/talking-with-doctor.html
With late stage disease, one should consider clinical trials sooner than later These offer patients to potential for a better outcome over standard of care protocols by providing the latest drugs and treatments before availability to the general patient population. All cancer drugs began as clinical trials and those in trials where the drug is successful are already ahead in deriving benefit. Clinical trials have eligibility criteria where the prospective participant needs to be in better physical condition and meet the requirements of hematology and blood chemistry parameters. This is why clinical trials should not be looked at as a last resort. Deterioration of a patients health can lead to not being accepted into a trial.