Does Dostarlimab Really Cure Colorectal Cancer 100%?
Justin Lee 2025-01-22
In recent months, the miraculous efficacy of dostarlimab (Jemperli) has garnered widespread attention online, with some users claiming that the drug has achieved "cure for colorectal cancer" in the U.S. One user, identified as @Lawrenc09874431, even asserted that every patient taking this medication has been cured of colorectal cancer without the need for chemotherapy or surgery. Faced with such exciting claims, a friend reached out to me via WeChat for help. However, we cannot overlook the need for a thoughtful examination of such impressive yet unverified statements.
First, it is important to clarify that dostarlimab is neither a chemotherapy nor a radiotherapy drug; it is an antibody therapy, which we can generally understand as an immunotherapy drug. Initially developed by pharmaceutical company GSK, dostarlimab is a monoclonal antibody originally used for treating endometrial cancer, marketed as Jemperli. GSK has even established a dedicated website (jemperli.com), where many FAQs focus on endometrial cancer. As research progressed, scientists gradually discovered the drug's potential in treating other cancer types, particularly in certain gastrointestinal tumors, leading to recommendations for dostarlimab in treating colorectal cancer associated with DNA mismatch repair deficiency (MMR-D). This gradual process highlights the importance of continuously exploring and discovering new indications in pharmaceutical research.
It's worth emphasizing that clinical cases show a 100% efficacy and improvement rate of dostarlimab in specific colorectal cancer patients, but this situation is limited to certain individuals. In reality, dostarlimab targets patients with MMR-D colorectal cancer. In these patients, the drug effectively combats cancer cells by blocking the PD-1 pathway and activating the immune system. The success of this treatment strategy reflects the significance of personalized medicine. Therefore, to thoroughly understand the targeted use of this drug, one must grasp two technical terms: DNA mismatch repair and PD-1.
What is DNA mismatch repair (MMR-D)?
Simply put, DNA repair refers to the cellular response to DNA damage, which can restore the original structure of DNA and re-enable its functions. Cells can have different repair responses to various types of DNA damage. In mammalian cells, four relatively well-established DNA repair pathways have been identified, one of which is called DNA mismatch repair (MMR). The MMR system is a mechanism within cells designed to fix errors that occur during DNA replication. When this mechanism is defective, the genomic stability of the cell is compromised, leading to cancer. Tumor cells in MMR-D patients typically exhibit a high mutational burden, making them more recognizable and vulnerable to immune system attacks. Dostarlimab enhances immune function by participating in this process, potentially leading to significant improvements for some patients after treatment.
What is PD-1?
PD-1, or programmed death-1, is related to programmed cell death and apoptosis, referring to the orderly death of cells under genetic control to maintain environmental stability. Unlike cell necrosis, apoptosis is an active process involving a series of gene activations, expressions, and regulatory actions—it is not a pathological phenomenon but rather an adaptive death process for better environmental adaptation. PD-1 is an inhibitory immune checkpoint protein commonly expressed in T cells. Its primary function is to reduce immune responses and prevent autoimmune diseases. However, this mechanism is exploited by cancer cells in the tumor microenvironment to inhibit immune attacks. By blocking PD-1, dostarlimab lifts this suppression, allowing the patient's immune system to recognize and attack tumor cells again. Therefore, dostarlimab can have more pronounced therapeutic effects for MMR-D colorectal cancer patients.
In conclusion, dostarlimab indeed demonstrates powerful anticancer efficacy in certain populations, particularly in colorectal cancer patients with DNA mismatch repair deficiencies. However, this does not mean it can universally cure all late-stage colorectal cancer patients. Effective treatment requires precise patient selection; only individuals confirmed as MMR-D through current FDA-approved testing standards can receive effective treatment. Thus, patients should follow professional medical advice and make scientific and reasonable treatment choices to achieve optimal results. While dostarlimab is promising, it must be approached with caution and not seen as a panacea for the pursuit of a "cure."
