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Cancer in 2025: Treating the Cancer Patient of the Future

genetic code

You are a medical oncologist practicing in 2025 and your patient schedule for this sunny October morning includes two patients who present with different challenges. Improvements in cancer genomics have changed how physicians assess risk and how they diagnose and treat cancer.

The first patient is a 60-year-old man with prostate cancer that was identified when cancerous cells were found circulating in his blood. The genetic signature of these circulating cancer cells indicates that there is a 15 percent risk that his prostate tumor will metastasize to distant sites. The signature also reveals that a gene called WWOX has been amplified, meaning that the tumor cells contain many copies of this gene instead of the normal two copies. Moreover, WWOX is an oncogene, meaning that it helps turn normal cells cancerous. The good news: you can use this finding to learn whether the cancer is limited to the prostate or has already spread. So you inject the patient with an antibody that targets the protein that the WWOX gene expresses, and you send the patient for a whole-body scan.

On the scan, a small region of the prostate lights up. But fortunately, no distant metastatic sites are visible. Now you must decide whether this man is a candidate for watchful waiting (regularly conducting whole-body scans using the WWOX antibody to see if the cancer has spread) or for having his tumor surgically removed and then treating him with radioactive WWOX antibodies to destroy any remaining cancer cells.

To help you decide, you send the patient to a urologist for a laser-guided biopsy of the prostate tumor. Analysis of the biopsied tumor cells shows they have the same genetic signature that was detected in the circulating cancer cells—good news indicating that the risk of this cancer spreading to distant sites remains low. So you opt for active surveillance with regular whole-body scans—both to reveal whether the cancer has spread and to continue monitoring the genetic signature of circulating tumor cells to see if additional markers have appeared that might indicate more-aggressive disease.

The second patient is a 45-year-old woman with advanced (stage 4) ovarian cancer.

In 2012, patients with this type of ovarian cancer had a median survival of 2.95 years, but by 2025, new therapies have extended their life expectancy by another 8 years.

When the patient’s ovarian cancer was diagnosed, biopsied tumor tissue was sent to the molecular pathology laboratory for genomic sequencing. You review the lab report before seeing the patient and observe several promising targets for treatment:

  • An amplified potassium channel gene: extra copies of this gene are found in a high percentage of ovarian tumors, making it a useful target.
  • A MAP kinase gene run amok: kinases are enzymes that help regulate key cellular activities, including cell division. But when a MAP kinase gene goes awry—becomes continuously active, for example—cancer can result.
  • A microRNA gene that has been knocked out: microRNAs are short RNA molecules that help regulate gene expression. If a microRNA stops production of a protein that causes cells to divide, then the absence of that microRNA could allow uncontrolled cell division—cancer—to occur.

The amplified potassium channel could be targeted by a monoclonal antibody, similar to the way the anticancer drug Herceptin targets an amplified gene involved in breast cancer.

The activated MAP kinase could be turned off by using an inhibitor drug. The first successful kinase inhibitor, Gleevec, came into oncology practice in the early 2000s, and by 2025 there are hundreds of such drugs, each targeting a different kinase.

The missing microRNA could be restored by using gene therapy to replace the gene that codes for it—a cancer treatment strategy perfected in 2020 after many false starts.

Clinical trials have shown that a carefully timed regimen using all three of these approaches is more effective that any single approach and causes remarkably low toxicity—no hair loss, weight loss, vomiting, fevers or life-threatening infections. You explain the planned regimen to the patient and tell her that her cancer will probably recur. But when that happens, it too will be genetically analyzed to identify new molecular targets that can be exploited in re-treating the cancer.

In 2025, cancer has become a chronic, usually nonlethal, disease. While it cannot always be eradicated, it usually can be controlled. Preserving quality of life has become paramount, so patients no longer suffer the toxicities that they faced back in 2012.

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Harry Ostrer, M.D.

Harry Ostrer, M.D.

Harry Ostrer, M.D. is professor of pathology and of genetics at Albert Einstein College of Medicine and director of genetic and genomic testing at Montefiore Medical Center.

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  • ayush November 7, 2012, 3:49 PM

    What about nanoparticle therapy and gene therapy to correct underlying mutation/s and selective radioparticle ablation of cancer cells??