Learn to Wait…Wait to Learn

I didn't hear anything today, so I am learning about the history of ADCs. Antibody-Drug Conjugates (ADCs) are a central part of the Clinical Trial I hope to join.

My application for the ADC MATCH Clinical Trial is still being reviewed by the Principal Investigator.

So... more waiting.

Cancer teaches you that waiting is rarely passive. Waiting for scans. Waiting for pathology. Waiting for blood work. Waiting for phone calls. Waiting for treatment decisions. Waiting becomes part of the disease.

I've decided that if I'm going to wait, I might as well learn.

Today I went back to the beginning.

I started reading about the history of Antibody-Drug Conjugates (ADCs), beginning with the original idea of a "magic bullet" proposed by Paul Ehrlich around 1900. His vision was remarkably simple: imagine a medicine that could find only the diseased cell, leave healthy cells alone, and destroy its target with precision.

More than a century later, that vision is finally becoming reality.

I've been watching recorded lectures from oncologists and researchers discussing ADC therapy. Several of them believe that, for some cancers, targeted antibody-drug conjugates may eventually replace portions of traditional chemotherapy.

Instead of flooding the entire body with chemotherapy—as we've done for decades—an ADC uses an antibody as a guided delivery vehicle. The antibody recognizes a specific marker on a cancer cell, attaches to it, enters the cell, and releases an extremely potent drug exactly where it's needed.

It's less like carpet bombing and more like guided delivery.

One idea that really caught my attention is that the future may involve combinations of ADCs carrying different payloads. Cancer is incredibly adaptable, and one reason treatments eventually stop working is that cancer cells develop resistance.

Imagine attacking the same cancer cell in multiple different ways at the same time.

One ADC might interfere with cell division.

Another might damage DNA.

Another might activate the immune system.

Instead of relying on a single weapon, future treatments may use several highly targeted approaches together.

What surprised me most was learning that today's ADC payloads are not the same chemotherapy drugs many of us received years ago.

The medicines I received during TIP chemotherapy in 2024 and 2025 circulated throughout my body because that was the only way to reach every possible cancer cell. And the cancer still found a hiding spot.

Modern ADC payloads work differently.

Most are extraordinarily potent cytotoxic molecules—far too toxic to safely give by themselves. In the old days, these compounds would have been unusable because they would damage healthy tissue along with cancer.

But attach only a few molecules to a carefully selected antibody, and suddenly those same compounds become powerful targeted therapies. In many cases, only a handful of payload molecules need to reach the cancer cell to kill it.

As I kept reading, I discovered that ADC payloads come in several different classes.

Microtubule inhibitors interfere with the tiny structural fibers that cells use to divide. Without functioning microtubules, cancer cells cannot complete cell division and eventually die. These payloads can be 100 to 1,000 times more potent than many traditional chemotherapy drugs, which is why targeted delivery is essential.

Topoisomerase I inhibitors are one of the hottest areas of ADC development today. Rather than attacking the cell's internal scaffolding, they interfere with DNA replication and prevent rapidly dividing cancer cells from successfully copying their genetic material.

Examples include SN-38 and deruxtecan (DXd), two payloads that are already being used successfully in modern ADC therapies.

Other ADC payload classes include:

• DNA-damaging agents, which break or cross-link DNA.

• RNA polymerase inhibitors, which stop cancer cells from making RNA.

• Protein synthesis inhibitors, which prevent cancer cells from producing the proteins they need to survive.

• Immune-stimulating payloads, designed to wake up the body's immune system directly inside the tumor.

• Targeted protein degraders (PROTACs), an emerging approach that causes specific cancer-driving proteins to be destroyed instead of simply blocked.

• Researchers are even exploring ADCs that could deliver gene-silencing molecules, epigenetic therapies, and other precision medicines.

The more I learn, the more I realize that ADCs are becoming something much bigger than "chemotherapy attached to an antibody."

They're becoming a precision delivery platform.

The clinical trial I'm hoping to join—the ADC MATCH study—matches patients to different ADCs based on the molecular characteristics of their tumors.

The treatments currently being studied include:

• Sacituzumab govitecan, which delivers SN-38, a topoisomerase I inhibitor. If I'm matched to this treatment, this is the payload I would receive.

• Trastuzumab deruxtecan, which delivers DXd (deruxtecan), another topoisomerase I inhibitor.

• Enfortumab vedotin, which delivers MMAE, a powerful microtubule inhibitor.

Although they're all called antibody-drug conjugates, they're carrying different payloads that kill cancer cells through entirely different biological mechanisms.

Understanding the payload helps explain why two ADCs can target different cancers, produce different side effects, and sometimes work when another ADC does not.

The exciting part is that this field is still evolving.

Researchers are already investigating new payloads, smarter linkers, dual-payload ADCs, and combinations designed to reduce resistance while improving precision.

That sounds a lot like progress.

So today there wasn't a phone call.

No decision.

No acceptance into the trial.

Just another day of waiting.

But it wasn't wasted.

Every day I understand a little more about the science that may someday help me—and hopefully many others.

Maybe that's another way of fighting cancer.

One page at a time.

—Ty