Complete Remission in All 12 Colorectal Phase 2 Cancer Trial Patients

A total of 12 patients have completed treatment with dostarlimab and have undergone at least 6 months of follow-up. All 12 patients (100%; 95% confidence interval, 74 to 100) had a clinical complete response, with no evidence of tumor on magnetic resonance imaging, 18F-fluorodeoxyglucose–positron-emission tomography, endoscopic evaluation, digital rectal examination, or biopsy. At the time of this report, no patients had received chemoradiotherapy or undergone surgery, and no cases of progression or recurrence had been reported during follow-up (range, 6 to 25 months). No adverse events of grade 3 or higher have been reported.

They used lab-made antibody called dostarlimab. It inhibits a protein known as programmed death receptor-1 (PD-1) found in many cancer cells. This inhibition then allows the immune system to recognize the cancer cells as harmful and target them for destruction. The drug was developed by GlaxoSmithKline, and it was given an accelerated approval by the Food and Drug Administration last year for cases of endometrial cancer linked to a mismatch repair deficiency.

The treatment exposes the cancer to the immune system.

Mismatch repair–deficient, locally advanced rectal cancer was highly sensitive to single-agent PD-1 blockade. Longer follow-up is needed to assess the duration of response.

The study involved researchers at the Memorial Sloan Kettering Cancer Center as well as Yale University, and it was sponsored by the pharmaceutical company GlaxoSmithKline.

The volunteers were all diagnosed with stage II or III rectal cancer, meaning their tumors had begun to grow larger and spread to nearby parts of the body.

New England Journal of Medicine – PD-1 Blockade in Mismatch Repair–Deficient, Locally Advanced Rectal Cancer

9 thoughts on “Complete Remission in All 12 Colorectal Phase 2 Cancer Trial Patients”

  1. Was announce the same day that fellow at Harvard mentioned his rejuvenation process — only problem mentioned was that it could cause cancer. Hmm.

  2. Not so fast.
    All of the patients in this trial had a certain genetic set-up that apparently allowed the drug to work as it did. Unfortunately, only 5-10% of all colon cancer patients have this genetic set-up.

    • But it worked. Just fine. I’m sure it can be tweaked for other genetic types as well. Custom medicine.

      • What makes you think it can be tweaked for the other 95% of the population that doesn’t have that defect?

        Not a be a killjoy but there’s zero indication that this will benefit the wider population.

      • If it is something that will save you from colorectal cancer, can you really call it a “defect?” Also, what exactly is it that it cannot be emulated by additional molecules which might enable or disable the molecular mechanisms involved in the so-called defect?

        • Can you call it a defect? Well….. that depends on whether that defect was the main reason you got the cancer in the first place…

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