On a sweltering day in 2018 with temperatures soaring above 102 degrees, I found myself lying on a hospital bed, staring at the anesthesiologist, feeling somewhat dizzy.

I was being evaluated for lymphoma—a form of blood cancer. Although I didn’t have obvious signs, a persistent rise in my white blood cell counts over a period of several weeks couldn’t be explained easily. The less sinister causes of high counts were ruled out. Both I and my primary care doctor agreed this needed to be followed up by an oncologist. A lot of cancer diagnoses were incidental, I knew all too well.

“How’s it going, doc?” asked the anesthesiologist. “You just passed out!”

“Never been better!” I was jubilant. “Can’t really blame Michael Jackson for using that s—t”—that was my nod to Propofol—which was the agent used to knock me out for the procedure.

“Take it easy, my friend,” he said with a smile. “You will be confused for a while. Don’t marry or divorce anyone in the next few hours.”

I accepted the very sound advice and did none of that, although I vaguely remember asking a pretty nurse to go out to lunch with me later, to which she said, “I will write it down, Dr. Ahmed—in case you are confused!”

Then began the scariest period of my life: waiting for the results to come back. What would it show? Do I have lymphoma?

I was no stranger to cancer. I treated cancer patients, and I am a physician-scientist focused on battling cancer for a living. My professional life has been centered around identifying and testing new treatments for aggressive cancers, specifically, cancers of blood cells. And yet, through these moments of anxiety and dread, which started with my visit to the oncologist in my own workplace, I experienced for the first time what thousands of others experience every day in different parts of the world.

My bone marrow aspiration test results came back after about two weeks. I didn’t have lymphoma or other unusual cell. But I did have something: certain suspect mutations or changes in the cells collected from my biopsy.

I reviewed the results with my oncologist.

“What does it mean?” I was curious. It was not nothing.

“They tested your bone marrow aspirates for some commonly known genetic changes or mutations that are associated with cancers,” the oncologist, for whom I have the deepest respect, replied.

“Did we ask for them to test it?” I asked. Turns out, the oncologist did not ask for testing for potential cancer-causing mutations in my specimens, but the molecular pathologist did it anyway. They called it panel testing, which meant checking for certain high-risk mutations in patient samples.

Apparently, it was a routine procedure to run these genomic analyses in biopsy specimens. In my case, unfortunately, some hits were found. The abnormal genes were circled with a red marker in the test report. These genetic mutations were not actionable, meaning there wasn’t much I or the oncologist could do about it other than follow up routinely.

“And, needless to say, to you,” my oncologist stressed, “don’t sit around if you feel anything unusual.”

What these mutations really revealed was that deep in the DNA of my cells, in the marrow, there were possible roots of abnormal growth. Did it mean I would have cancer soon? Not really. Neither did it mean that I had no such risk. It all had to be correlated clinically. Since I had no abnormal cell identified, a diagnosis was not made. The decision to return for regular follow-ups was a no-brainer.

Thankfully, my high white blood cell counts started to drop in subsequent tests, and I went into a watchful waiting mode. But that didn’t leave me with much peace. What if the behavior of my lymphocytes changed drastically? What if they became aggressive? In essence, I became a citizen of “cancer land”: a constant state of anxiety for the unknown. It was like a killer lurking in the shadows, waiting to attack me. I became that spy who constantly looks over his shoulder, always looking for his assassin.

I couldn’t help thinking about my family. With three young children, my wife would be in a helpless situation if I wasn’t around. Several iterations of events continued to play in my mind constantly—what will I do if a diagnosis is reached? What remedy will I seek?

In the world of cancer treatment, chemotherapy is an essential tool. Whether it’s blood cancers such as lymphoma or leukemia or other forms of cancer in different organs (we call them solid tumors), treating with a chemical agent, or a few chemical agents together, is strongly considered. Of course, surgery and radiation are two major treatments.

The principle of using chemo to treat cancer depends on the main character of cancer cells: they grow rapidly. Chemo kills fast-growing cells and mounts a strong defense against the aggression of cancer cells, treating fire with fire. But some normal cells, which also grow fast, such as hairs, nails, and normal blood cells, became the collateral damage of this war between chemo and cancer.

This is where targeted treatment bursts into the cancer therapeutics scene. Instead of attacking all fast-growing cells by a chemical agent (or several agents), these newer treatments look for features that will ideally be present only in cancer cells and not in normal cells. The targeted treatments destroy the cancer cells preferentially without affecting the normal cells at all.

To create such a targeted treatment, scientists need to figure out the peculiarities of cancer cells—a change, or abnormality not always visible on the outside of the cells but present inside of them as an unmistakable identity. These peculiarities or cancerous changes can be mutations in genes, like what was found in my samples. But the trouble is, how do you know that the mutated genes are the driver of cancer and if they are, how will you target these with a drug? That requires sophisticated analysis and careful interpretation of genetic data, as well as a thorough understanding of the link between mutated genes and cancer.

Consider a library full of books as the genome, and each book in that library as an individual gene. Once we have a full library, we can then take out a book and compare that with the pirated copy. A mutated gene needs to be compared with an unmutated gene to understand the differences between them. Then comes the part of creating drugs to target these specific genetic abnormalities, if possible.

A significant challenge for researchers has been that no reference library for the human genome existed—at least not until the start of the new millennium. This changed with the successful completion of the human genome sequencing in the year 2000. What followed was, in my opinion, a golden period for targeted treatments in cancer care—from non-chemo drugs with relatively simpler chemical structures to versatile monoclonal antibodies to immunotherapy, including unique cell therapy.

This is a story of drug development adventures. Our tale will take you to the workshops of pioneering scientists like Paul Ehrlich and to the cutting-edge laboratories of modern-day drug makers. We will walk the halls of some of the finest hospitals in the world with cancer doctors and researchers who chaperoned revolutionary immunotherapy. Throughout this journey, our patients—survivors and warriors—will inspire you to embrace positivity.

Adapted from Race for a Remedy: The Science and Scientists behind the Next Life-Saving Cancer Medicine (Prometheus) by Makhdum Ahmed, MD. Published with permission.

Author Bio:

Makhdum Ahmed, M.D., Ph.D, is an award-winning physician-scientist and a drug development executive. He is an executive director in AstraZeneca’s research and development in blood cancers. A former director for the Cancer Moonshots program at the M.D. Anderson Cancer Center in Houston, he was the recipient of the Australian Leadership Awards (2009) and Global Health Corps Fellowship (2011).

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