Clinical Trial

Disease: Castration-Resistant Prostate Cancer, CRPC, (NCT02867345)

Disease info:

Prostate cancer is cancer that occurs in the prostate. The prostate is a small walnut-shaped gland in males that produces the seminal fluid that nourishes and transports sperm. Prostate cancer is one of the most common types of cancer. Many prostate cancers grow slowly and are confined to the prostate gland, where they may not cause serious harm. However, while some types of prostate cancer grow slowly and may need minimal or even no treatment, other types are aggressive and can spread quickly.

Prostate cancer may cause no signs or symptoms in its early stages. Advanced prostate cancer may lead to various symptoms, including:

  • Trouble urinating
  • Decreased force in the stream of urine
  • Blood in the urine
  • Blood in the semen
  • Bone pain
  • Losing weight without trying
  • Erectile dysfunction

Researchers have found several factors that might affect a man’s risk of developing prostate cancer. These include: age, race, ethnicity, family history, geography and genetic factors. Several heritable mutations have been linked to hereditary prostate cancer, including mutations in the following genes:

  • BRCA1 and BRCA2: These tumour suppressor genes normally help to repair errors in genomic DNA (or cause the cell to die if the error cannot be fixed). Inherited mutations in these genes more commonly cause breast and ovarian cancer in women, but changes in these genes (especially BRCA2) may also account for a small number of prostate cancers.
  • CHEK2ATMPALB2, and RAD51D: Mutations in these DNA repair genes might also be responsible for some hereditary prostate cancers.
  • DNA mismatch repair genes (such as MSH2MSH6MLH1, and PMS2): These genes normally help fix mismatches in genomic DNA that may occur during cell division. Men with inherited mutations in one of these genes have a condition known as Lynch syndrome (also known as hereditary non-polyposis colorectal cancer, or HNPCC), and are at increased risk of colorectal, prostate, and some other cancers.
  • RNASEL (formerly HPC1): The normal function of this tumour suppressor gene is to help cells die when something goes wrong inside them. Inherited mutations in this gene might allow abnormal cells to live for longer than they should, which can lead to an increased risk of prostate cancer.
  • HOXB13: This gene is important in the development of the prostate gland. Mutations in this gene have been linked to early-onset prostate cancer that runs in some families. Fortunately, this mutation is rare.

Other inherited gene mutations may account for some hereditary prostate cancers, and research is being done to find these genes.

Advanced prostate cancer has been known under a number of names over the years, including hormone-resistant prostate cancer (HRPC) and androgen-insensitive prostate cancer (AIPC). Most recently, the terms CRPC or castration-recurrent prostate cancer were introduced with the realisation that intracrine/paracrine androgen production is significant in the resistant of prostate cancer cells to testosterone suppression therapy. 

CRPC occurs when prostate cancer progresses under therapy-induced castration conditions. Several mechanisms have been proposed to explain this acquired resistance, many of which are driven by the androgen receptor (AR). Recent findings, however, sub-classified CRPC by downregulation/absence of AR in certain subtypes that consequently do not respond to anti-androgen therapies.

Prostate cancer that is detected early — when it's still confined to the prostate gland — is associated with the best chances for successful treatment.


The American Cancer Society’s estimates about 288,300 new cases of prostate cancer will be diagnosed in the U.S. in 2023, and about 34,700 deaths from prostate cancer.
Official title:
A Dose-escalation Phase I Trial of PD-1 Knockout Engineered T Cells for the Treatment of Castration Resistant Prostate Cancer

Peking University


Beijing, China
Department of Urology Peking University First Hospital, Beijing, Beijing, China, 100034

Study start:
Nov. 1, 2016
0 participants
Gene editing method:
Type of edit:
Gene knock-out
Programmed death 1 (PD-1)
Delivery method:
- Ex-vivo
Withdrawn due to no funding or financial support
IND Enabling Pre-clinical
Phase I Safety
Phase II Safety and Dosing
Phase III Safety and Efficacy

Status: Terminated


This is a dose-escalation study of ex-vivo knocked-out, expanded, and selected PD-1 knockout-T cells from autologous origin. Patients are assigned to 1 of 3 treatment groups to determine the maximal tolerant dose. After the lower number of cycles are considered tolerant, an arm of the next higher number of cycles will be open to next patients. Biomarkers and immunological markers are collected and analyzed as well.

Last updated: Feb. 9, 2024
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