Advances in Prostate Cancer Treatment – 2017 and 2018

Prostate cancer is the most common cancer in men. Cancer screening and oncological imaging methods have improved, allowing 90% of patients to be diagnosed early. Advances in local treatments and newly developed medications have brought the 5-year survival expectancy in prostate cancer to 99%. Looking at studies that have recently made an impact in this field:

1. Multiparametric MRI imaging is important in patients with suspected prostate cancer (March 2018)

Prostate biopsy is routinely performed in patients with elevated prostate-specific antigen (PSA) on blood testing or suspected prostate cancer on examination. Because the prostate lies next to the rectum at the bowel outlet, the biopsy is taken with transrectal ultrasound guidance. With advances in technology, newly developed MRI technology, multiparametric MR imaging combined with biopsy, has proved superior to the standard method of rectal ultrasound-guided biopsy. A study observed that biopsies performed following multiparametric MRI assessment detected clinically significant prostate cancers with a higher Gleason score . It also found that unnecessary biopsy procedures were avoided.

We believe that when we truly bring technology to our patients, we can combine the right diagnosis in the right patient with the most appropriate treatment.

2. A new treatment option in prostate cancer: Actinium alpha therapy

Technological innovations make it possible to image and treat cancerous areas by attaching radioactive substances to a receptor specific to a particular cancer. Most prostate cancer cells carry prostate-specific membrane antigen (PSMA) on their surface.

Treatment options are limited for men with advanced, metastatic castration (hormone suppression)-resistant prostate cancer.

Molecular applications of nuclear medicine provide both imaging and treatment by attaching radioactive substances to receptors specific to particular cells. Most prostate cancer cells carry prostate-specific membrane antigen (PSMA) on their surface. In actinium therapy, the actinium-225 isotope, which emits short-wavelength alpha radiation with cell-killing properties, binds to the prostate cancer cell through PSMA using a carrier molecule and destroys the cancer cell.

In a study of hormone-resistant cancer previously treated with multiple lines of therapy, metastatic prostate cancer showed both a survival benefit and a 50% reduction in PSA levels, establishing actinium therapy as a new treatment option for prostate cancer.

3. Enzalutamide and Apatinib showed efficacy in hormone-resistant, locally confined prostate cancer

In hormone-resistant prostate cancer that has not spread through the body, blood prostate-specific antigen (PSA) may continue to increase despite hormone suppression treatment. In this situation, the disease carries a high risk of spreading elsewhere in the body. Studies of two different drugs acting by suppressing the hormone at the receptor level in prostate cancer found that they prolonged the time until disease spread in these patients.

Enzalutamide had demonstrated efficacy and entered clinical use in hormone-resistant prostate cancer that had spread through the body. The PROSPER study, seeking the answer to "is it effective even before spread through the body?", found a significant extension in the time until spread (metastasis).

With a similar mechanism of action, apalutamide (Erleada) in a study including 1200 patients was shown to delay spread through the body by an additional 25 months. Based on this study, in February 2018 its use with standard hormone suppression drugs in hormone-resistant prostate cancer that had not spread through the body received FDA approval. This is the first treatment approved by the FDA for nonmetastatic, hormone-resistant prostate cancer

4. Abiraterone received FDA approval for hormone-sensitive metastatic prostate cancer (February 2018)

On 7 February 2018, the United States Food and Drug Administration, FDA, approved abiraterone (brand name Zytiga) for metastatic high-risk hormone-sensitive prostate cancer.

Male hormones (androgens) trigger the growth and proliferation of prostate cancer cells. Following discovery of this relationship in the 1940s, hormone suppression drugs preventing prostate cancer cells from encountering androgens (the best known being testosterone) or preventing testosterone production formed the basis of prostate cancer treatment. However, cancer cells do not have a stable structure; their biology can change over time and become resistant to treatments. Thus, although prostate cancer cells initially depend on male hormones, some tumor cells eventually begin proliferating independently of hormones; this is called castration- or hormone-resistant prostate cancer. Abiraterone is a new-generation hormone suppression treatment that works by suppressing androgen production in the adrenal gland. In 2011, it received FDA approval and entered use for hormone-resistant prostate cancer that had spread through the body. Following this success, the question was whether giving it before prostate cancer cells became resistant to hormonal therapies could improve disease outcomes. A study addressing this question evaluated 1200 patients with hormone-sensitive prostate cancer that had spread through the body and demonstrated both longer survival and a 38% reduction in cancer-related mortality risk. Following this study, in February 2018 the FDA approved abiraterone for hormone-sensitive prostate cancer.

- Related Topic: A story, a cancer, a drug, a team: Prostate cancer and Abiraterone

5. Caution with active surveillance in intermediate-risk prostate cancer with a low cancer burden 

In early-stage prostate cancer, for certain patient groups, observation and starting treatment only when there is a risk of progression is an option instead of surgery, equivalent radiotherapy or nonsurgical interventional methods. We know that in selected patients there is no difference in survival between the two approaches. However, retrospective screening studies found that intermediate-risk patients with low-volume disease who underwent immediate surgery had higher-risk pathological features than the low-risk group. It is important to select patients carefully for surveillance after a prostate cancer diagnosis, make the decision together with the patient, and use this option in those able to comply with surveillance protocols.

- Related Topic: What is prostate cancer risk classification?

6. The importance of genetic testing in prostate cancer

There are multiple cancer predisposition genes that can cause prostate cancer. Studies have found damage to DNA repair-related genes in 10% of these patients. Today's targeted drugs allow personalized treatments. In particular, if more than one first- or second-degree relative has a history of cancer, genetic tests should be performed. This result is important both for treatment decisions and for cancer screening of the patient's first-degree relatives.

- Related Topic: A new drug acting on DNA damage and repair in stage 4 prostate cancer resistant to standard treatments: Olaparib (Lynparza)

7. Surgery is no better than active surveillance in early-stage prostate cancer (July 2017)

According to the results of an important study lasting approximately 20 years, operating on low-risk, early-stage prostate cancers does not reduce mortality rates more than active surveillance alone. In other words, surgical outcomes for early-stage prostate cancer are no better than observation. Follow-up of 731 patients for an average of 12.7 years showed no difference in mortality between surveillance and surgery in early-stage prostate cancer.

According to approximately 20 years of follow-up in patients with localized / early-stage prostate cancer, surgery is not superior to active surveillance in reducing all-cause or prostate cancer-related deaths. Although surgery also appears to reduce the likelihood of local disease recurrence in this patient group, these recurrences mostly cause no complaints (are asymptomatic). Surgery for early-stage prostate cancer also has a higher side-effect rate than observation.

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