Dr. Philip McMillan,  John McMillan

Cancer rates after the pandemic should be falling. In many cases they are not. During the pandemic, a cancer diagnosis made severe or fatal COVID outcomes much more likely. Many patients who would otherwise be filling oncology clinics today did not survive the worst waves. By the cold logic of population statistics, that loss should leave a visible gap in cancer numbers for years afterwards, a phenomenon epidemiologists call a mortality debt. Norway’s national cancer registry, together with matching hospital data from the United Kingdom, tells a stranger story. Some cancers did fall as expected. Others have climbed sharply, and the cancers that climbed share an unsettling biological feature.

Cancer in Norway 2025, based on the country’s national registry report, lays out a pattern that splits cleanly down the middle. Some cancers fell. Cervical cancer dropped by 21 per cent. Lung, uterine, prostate, and even colon cancer all slid downward, consistent with a mortality debt among older patients carrying multiple comorbidities. Other cancers refused to follow suit. Non-melanoma skin cancer rose 20 per cent in women and 13 per cent in men. Melanoma climbed roughly 12 per cent across both sexes. Thyroid cancer rose 11.4 per cent. Breast cancer climbed 10.5 per cent. The cohorts that should have been quietest after a respiratory pandemic are the ones doing the most talking.

Dr Philip McMillan, a British researcher and clinician, has been working through the Norway 2025 figures alongside UK hospital episode statistics from 2016 to 2025. His reading of the data is that the post-pandemic cancer signal is not a story about growth speed at all. It is a story about behaviour. Specifically, it is a story about a small protein called CD147 that sits on the surface of certain cells, and about the back door it opens to both viruses and tumours.

A Castle With Two Doors

Most readers will be familiar with the basic SARS-CoV-2 entry mechanism. The virus latches onto ACE2 receptors and slips inside the host cell. What is less widely discussed is a second entry point. CD147, also known as basigin, sits on the surface of many human cells and behaves like an auxiliary lock. Once the virus enters through ACE2, the cell upregulates CD147, giving the virus an accelerated route into already-infected cells and into nearby cells that carry the receptor.

Think of it this way. The cell is a castle. ACE2 is the front gate. CD147 is the back door. The trouble starts because the same protein that lets the virus in is the one certain cancers use to spread.

CD147 has a day job long before any viral context arrives. On cancer cells, it acts as a chaperone for lactate transport. Tumour cells run almost entirely on glycolysis, burning through glucose and dumping lactate as a waste product. If they cannot evacuate that lactate, they choke. CD147 escorts lactate out into the surrounding tissue, acidifies the local environment, breaks down the extracellular matrix, suppresses nearby immune cells, and drives the formation of blood vessels that let tumour cells reach circulation.

Some cancers express more CD147 than others. Melanoma is the textbook example, which is one reason it metastasises so early in its course.

The Reframing of “Turbo Cancer”

The phrase turbo cancer has become shorthand among worried lay audiences for what feels like a wave of aggressive, late-stage diagnoses in younger people. It is also a phrase that ends most scientific conversations before they start. Researchers hear it, infer a claim that tumours are growing faster on cell-biology timescales, and reach for the rebuttal that no such acceleration has been demonstrated.

Dr. McMillan offers a sharper way to put the same observation. “Post-pandemic, more cancers are behaving like melanoma. Melanoma spreads very early,” he argues, a parallel that puts the worry on firmer ground. His claim is not that cells divide at impossible speed. The claim is that more tumours are acting invasively early, breaching tissue planes early, seeding distant organs early. The newsworthy observation is not the doubling time of the tumour. It is the stage at presentation.

That distinction matters because it points to a mechanism researchers can actually test. If CD147 expression and signalling are driving more aggressive invasiveness across the cancers where CD147 already plays a structural role, the affected list should look strikingly like the list of cancers rising in both Norway and the UK. It does. Skin cancer, breast cancer, brain and central nervous system cancer, thyroid cancer, kidney cancer, liver cancer. An overlay of UK hospital episode trends from 2016 onward shows the same direction of travel as the Norwegian incidence curve, despite measuring different things. When two independent population datasets drift in the same direction, the prior probability of a real effect climbs steeply.

What the Mortality Debt Hides

The deeper trouble with reading these numbers is the camouflage layered on top. Older patients with prostate, lung, uterine, and colon cancer were disproportionately likely to die during the pandemic. Their absence pulls the headline incidence figures downward, masking the true direction of change. In a population that has lost a meaningful share of its higher-risk older patients, a flat curve in central nervous system tumours or breast cancer is actually a quiet rise. The neutral line is the warning sign.

Read that way, the Norwegian and UK numbers stop looking ambiguous. The cancers expected to fall did fall. The cancers expected to fall but didn’t have done something stranger: they held steady or climbed. And the other cancers expected to do nothing in particular rose by double digits.

The Obvious Counter-Explanations

A careful reader will reach for the standard alternatives before entertaining a new mechanism, and rightly so. The first is a screening rebound: cancers go undiagnosed during lockdown, then surface in a catch-up wave once clinics reopen. The second is demographic composition: an ageing or growing at-risk population can lift incidence without any change in underlying biology. The third is coding practice: registries periodically reclassify what counts as which cancer, and a quiet definitional shift can masquerade as a real signal.

None of these tidily accounts for what the numbers show. A screening rebound would be expected to peak and then subside, not persist into 2025 across multiple unrelated cancers; nor would it touch melanoma and non-melanoma skin cancer, where presentation does not depend on a screening programme in the same way as cervical or colon cancer. Demographic shifts are too slow to drive double-digit moves in three or four years. And coding changes that simultaneously elevated thyroid, breast, skin, kidney and liver cancer in two countries, on two different reporting systems, would be a remarkable coincidence. The conventional explanations cover some of the curve. They do not cover the shape of it.

The Question Patients Are Already Asking

There is an honest emotional core to this analysis that is worth keeping in view. Almost every reader knows the question Dr. McMillan puts into words. “Am I imagining it that my co-workers, friends, family, so many more people seem to be having cancer? Is it just coincidental?” he asks. People do not arrive at that question casually. They arrive at it after a colleague’s stage-four diagnosis in their mid forties, after a friend’s brain tumour discovered six weeks before death, after a parent’s melanoma already in the liver by the time the dermatologist takes a proper look.

What this analysis asks the medical community to do is unglamorous and unavoidable. Take the registry data seriously. Account for the mortality debt explicitly. Stratify cancer trends by CD147 expression status. Look at age, look at stage at diagnosis, look at metastatic burden at presentation. Stop measuring only what was easy to measure before 2020.

A test for an unfamiliar pattern only works if the prior probability has been built up honestly. Right now, the prior built into most public health reporting is that there is nothing unusual to find. So the data are not interrogated at the resolution that would reveal whether something unusual is there. That is a methodological choice, not a biological fact. Choosing to look harder is not a conspiracy. It is what epidemiology is supposed to do.

The CD147 hypothesis may or may not survive contact with the next decade of research. What deserves to survive is the discipline of asking questions. The cancers behaving like melanoma are not going to wait for the literature to catch up. Neither, frankly, are the patients.