That possibility has become a major focus for Prof. John Kopchick and his team at Ohio University. Their work focuses on what happens if, instead of attacking a tumor using only conventional cancer drugs, they also block one of the biological signals that helps the tumor to resist treatment and grow?

The idea rests on an important distinction. Growth hormone does not act by itself. It binds to a growth hormone receptor, or GHR, on the surface of cells, rather like a key engaging a molecular lock. That interaction triggers signals inside the cell. Normally, those signals have useful roles. But cancer is extraordinarily good at exploiting normal biology. Tumors can express GH and its receptor, allowing GH-induced signals to operate locally within the tumor micro-environment as well as through the hormone circulating in the bloodstream.

This matters because one of the greatest challenges in cancer treatment is therapy resistance. A chemotherapeutic drug may initially kill large numbers but not all of the actual cancer cells, allowing the surviving cells to adapt and grow. Some become better at pumping the therapeutic drugs back out of the cell. Others change their characteristics in ways associated with invasion and spread or metastasis. Still others become less willing to activate apoptosis, the cellular self-destruct program that ordinarily removes badly damaged cells. Research reviewed by Kopchick and his colleagues places GH signalling within several of these survival strategies.

The implications are striking. If GH is helping a tumor to defend itself, then blocking the GH receptor could make an existing treatment work better. Instead of inventing an entirely new weapon against every feature of a cancer cell, researchers might weaken part of the tumor’s defensive system and allow established therapies to hit harder.

There is an unusual advantage to this strategy: a growth hormone receptor blocker already exists. Pegvisomant, marketed as Somavert, was developed to treat acromegaly, a disorder caused by excessive growth hormone action. Its origins lie in basic research in Kopchick’s laboratory into the structure of GH and the way it activates its receptor. They discovered that altering one of the one hundred ninety one amino acids in GH could transform GH from a molecule that stimulates its receptor resulting in growth into one that obstructs or inhibits its action and, thus, inhibits growth. Further engineering and development resulted in the compound called pegvisomant, designed to bind the receptor without allowing normal signaling to proceed and to inhibit the action of endogenous GH whether in the blood or in the microenvironment of a tumor.

That journey is a powerful example of “bench to bedside” science. An insight into molecular structure became an experimental antagonist, then a medicine for patients. Prof. John Kopchick has described the achievement with understandable pride because the discovery emerged from academic research at Ohio University. The story also contains an intriguing scientific return journey. A drug created from fundamental laboratory work, and established clinically for acromegaly, is now being investigated back at the laboratory bench for a very different purpose: helping treat cancer.

Why might this work? Imagine a cancer cell as a besieged fortress. Chemotherapy is trying to breach its walls, but the fortress has pumps that throw harmful compounds back outside, internal programs that repair or tolerate damage, and the ability to alter its identity when conditions become threatening. GH signaling appears to strengthen several of these cancer cell defenses. However, blocking the receptor may instead lower the drawbridge.

Pancreatic ductal adenocarcinoma offers a demanding test of that idea. This cancer is notoriously difficult to treat, in part because resistance involves more than one mechanism alone. Its tumor microenvironment, including drug-efflux systems, changing cellular states and altered metabolism, can contribute to its terrible potency. In experiments reported by Kopchick’s team, pancreatic cancer cells expressed both GH and its receptor, providing the machinery for local GH action that stimulates these horrible events ultimately resulting in tumour growth and metastasis. Also, as GHR levels get higher in a patient’s tumor, prognosis get worse.

The researchers then examined what happened when GHR antagonists were combined with gemcitabine, a chemotherapy used against pancreatic cancer. In mouse models carrying human pancreatic tumors, the combination of a GHR antagonist and gemcitabine markedly improved treatment outcomes compared with chemotherapy alone. The experiments pointed toward changes in pathways linked to drug resistance, including the molecular pumps that can remove chemotherapy from cells and the process known as epithelial-to-mesenchymal transition. That transition can give cancer cells traits associated with mobility, metastasis, adaptability and treatment resistance. Importantly, this treatment in mice has resulted in animals with shrinking pancreatic tumors and, in some animals, the tumour completely disappeared!

These findings are promising, but their stage of development matters. Results in cultured cells and mouse models are not proof that the same strategy will improve survival in people with pancreatic cancer. They are proof of concept: evidence strong enough to justify asking the next questions. The researchers themselves call for further preclinical work, careful dose studies and, ultimately, well-designed human trials.

The clues are provocative. Patients with acromegaly experience excessive GH action, while people with Laron Syndrome have short stature and have inherited GH resistance because their GHRs do not function normally. These conditions in Laron Syndrome individuals reinforce a theme from laboratory research: GH signaling may influence how cancers develop. Again and amazingly, Laron Syndrome patients demonstrate protection from all forms of cancer, with significantly lower incidences than the rest of the population! In fact, in an Ecuadorian cohort of these patients studied by Dr. Guevara, only 1 of approximately 100 developed cancer where their ‘normal’ relatives had approximately 20-25% of many kinds of cancers. And similar results were reported for an Israeli cohort of patients studied by Dr. Laron (for whom the syndrome was named).

That question is now being explored in another cancer, that is, non-small cell lung cancer. Here too, treatment resistance is central. The Ohio University group is asking whether the GHR is another escape route cancer cells can exploit.

Lung cancer is the leading cause of death in the cancer world. Kopchick’s team’s work on lung cancer strengthens the case because it asks whether the same biological logic involving GH action appears in another major cancer. Non-small cell lung cancer accounts for most lung cancers, and although surgery, chemotherapy, radiotherapy, targeted drugs and immunotherapies have transformed treatment, resistance remains a persistent problem.

The researchers found that GHR levels were higher in human non-small cell lung cancer tissue than in normal lung tissue. In patient datasets, high GHR expression was also associated with poorer overall survival and with genes involved in treatment-resistant behaviour.

Laboratory experiments then supplied a possible explanation. When lung cancer cells were exposed to GH, they became more resistant to cisplatin, a widely used chemotherapy drug. GH increased activity associated with ABC transporters, molecular pumps capable of removing drugs from cells. It also encouraged epithelial-to-mesenchymal transition, the adaptable cellular state leading to metastasis already implicated in pancreatic cancer. Pegvisomant, the GHR inhibitor or antagonist, counteracted these effects and significantly improved the response to chemotherapy in cultured cells as well as in mice that have undergone human non-small lung cancer cell implantation.

The repetition across different cancers is important. A pancreatic tumor and a lung tumor are different diseases, and nobody should expect a universal cancer treatment. Yet both can apparently exploit reduced GH signalling as part of a wider network that promotes cancer survival. This suggests that GH and the GHR may be like pieces of cellular infrastructure puzzle that some tumors learn to misuse.

There is another reason this approach attracts attention. Modern oncology increasingly relies on combination therapies. A tumor is genetically diverse and biologically adaptable, so blocking a single pathway can simply create pressure for another route to emerge. The work from Kopchick and team points toward GHR antagonism as a possible partner for existing treatments rather than a replacement for them. Their broader research considers combinations with chemotherapy, targeted therapy and immunotherapy, with the aim of removing some of the protection that GH signaling may provide.

This also changes how we might think about drug development. Pegvisomant was designed to stop excessive GH action in patients with acromegaly, rather than as a cancer treatment. Its established clinical use means scientists already know far more about the drug in humans than they would about a completely new experimental molecule. That does not make its use in cancer automatically safe or effective. Cancer patients, treatment combinations, doses and biological goals can be very different. But repurposing an existing medicine can give researchers a valuable head start.

The story also illustrates why basic science can have consequences that are impossible to predict at the beginning. Early experiments on GH structure might once have seemed remote from the urgent realities of oncology. By identifying how the hormone engages its receptor, however, researchers gained the ability to interfere with that interaction. Pegvisomant emerged from that knowledge as a safe and efficacious drug used world-wide for the treatment of acromegaly. Decades later, the same molecular tool is helping researchers test whether blocking GHR can expose vulnerabilities in tumors.

For Prof. John Kopchick, this creates a rare scientific arc. A discovery made at an academic laboratory travelled toward clinical medicine, became an approved drug, and is now returning to experimental cancer research with a new purpose. However, the journey is not complete. The pancreatic and lung cancer findings come largely from cells and animal models. Human cancer trials will be necessary to determine whether the encouraging effects translate into meaningful benefits for patients.

There are also fundamental questions still to answer. Which tumors depend most strongly on GH action? Could GHR levels help identify patients most likely to benefit? What dose of a GH antagonist would be required inside the complex environment of a human tumor? Which standard treatment makes the best partner? And could blocking the GHR also influence immune cells, connective tissue and other components surrounding a tumor?

That distinction is crucial for patients and the public. Promising preclinical results often mark the beginning of a difficult translational process, not its end. Researchers must establish which cancers truly depend on the pathway, whether benefits persist in living systems, and whether combinations produce unacceptable side effects. The strength of this program is that it connects a molecular mechanism of cancer with a drug that can test the mechanism directly. Each experiment can therefore refine a practical therapeutic hypothesis.

Those questions are precisely what make the research compelling. Cancer rarely succeeds through one trick. It survives by exploiting ordinary biological systems for extraordinary purposes. GH is essential to normal human development and physiology, yet in certain tumors its signalling may become part of a defensive network that helps malignant cells grow, change and withstand treatment.

The emerging strategy is therefore to identify cancers in which GH signalling is helping the enemy, then interrupt that assistance at the right moment and in the right patients. If future studies confirm the promise seen so far, a medicine born from decades of research into human growth could acquire a remarkable second role, by taking away one of the signals that helps cancer fight back.