Bladder cancer 'attacked and killed by common cold virus'

Authored by bbc.com and submitted by mvea

Image copyright Science Photo Library Image caption A virus of the common cold infected and killed bladder cancer cells in the study

A strain of the common cold virus can infect and kill bladder cancer cells, a small study suggests.

All signs of the disease disappeared in one patient, and in 14 others there was evidence that cancer cells had died.

University of Surrey researchers said the virus could "help revolutionise treatment" for the cancer and reduce the risk of it recurring.

A bladder cancer charity called the study "very exciting" if larger studies confirmed the findings.

Non-muscle invasive bladder is the 10th most common cancer in the UK, with around 10,000 new cases each year.

Current treatments for this type of bladder cancer are invasive or can cause serious, toxic side effects.

And constant, costly monitoring is needed to check that the cancer has not returned after treatment.

In this study, 15 patients with the disease were given the cancer-killing coxsackievirus (CVA21) through a catheter one week before surgery to remove their tumours.

When tissues samples were analysed after surgery, there were signs the virus had targeted and killed cancer cells in the bladder.

Once these cells had died, the virus had then reproduced and infected other cancerous cells - but all other healthy cells were left intact.

What the virus does is special, says study leader Prof Hardev Pandha, from the University of Surrey and Royal Surrey County Hospital.

"The virus gets inside cancer cells and kills them by triggering an immune protein - and that leads to signalling of other immune cells to come and join the party," he said.

Image copyright Science Photo Library Image caption No side effects were found in patients treated with the virus via a catheter to the bladder

Normally, the tumours in the bladder are "cold" because they do not have immune cells to fight off the cancer.

But the actions of the virus turn them "hot", making the body's immune system react.

Prof Pandha said the same virus had also been tested on skin cancer, but this was the first time it had been studied in a clinical trial on bladder cancer.

"Reduction of tumour burden and increased cancer cell death was observed in all patients, and removed all trace of the disease in one patient following just one week of treatment, showing its potential effectiveness," he said.

"Notably, no significant side effects were observed in any patient."

The plan is now to use the common cold virus with a targeted immunotherapy drug treatment, called a checkpoint inhibitor, in a future trial in more patients.

Dr Nicola Annels, research fellow at the University of Surrey, said viruses like the coxsackievirus "could signal a move away from more established treatments such as chemotherapy".

Allen Knight, chairman of Action Bladder Cancer UK, said the study findings were "very exciting".

Bladder cancer costs the NHS more per patient than nearly every other cancer, because of the high recurrence rate, he said.

"If the safety, tolerability, and efficacy data can be confirmed in larger clinical studies and trials, then it could herald a new era in the treatment for non-muscle-invasive bladder cancer patients, like me, who often feel that innovations in cancer therapies pass us by."

Dr Mark Linch, a bladder cancer expert at the Cancer Research UK Cancer Institute at University College London, said the initial results were "encouraging".

"It will be really interesting to see how this new virus-based therapy fares in larger trials in people with non-muscle invasive bladder cancer, particularly in combination with newer immunotherapies," he said.

mrslipple on July 5th, 2019 at 13:59 UTC »

The 60 minutes piece they did on this was fascinating. I didn't know our white blood cells can easily kill cancer but the problem is they never know it's there. By injecting the cancer with a disease they can see they are alerted to the cancer. (Sorry all white blood cells I see as Osmosis Jones).

DiogenesBelly on July 5th, 2019 at 12:53 UTC »

So we can't cure the common cold or cancer, but maybe one can cure the other?

mvea on July 5th, 2019 at 12:14 UTC »

The post title is a copy and paste from the title, subtitle, first and eleventh paragraphs of the linked popular press article here:

Bladder cancer 'attacked and killed by common cold virus'

A strain of the common cold virus can infect and kill bladder cancer cells, a small study suggests.

All signs of the disease disappeared in one patient, and in 14 others there was evidence that cancer cells had died.

"The virus gets inside cancer cells and kills them by triggering an immune protein - and that leads to signalling of other immune cells to come and join the party," he said.

Journal Reference:

Viral targeting of non-muscle invasive bladder cancer and priming of anti-tumour immunity following intravesical Coxsackievirus A21

Nicola E Annels, David Mansfield, Mehreen Arif, Carmen Ballesteros-Merino, Guy R Simpson, Mick Denyer, Sarbjinder S Sandhu, Alan Melcher, Kevin J Harrington, BronwYn Davies, Gough Au, Mark Grose, Izhar N Bagwan, Bernard A. Fox, Richard G Vile, Hugh Mostafid, Darren Shafren and Hardev Pandha

Clin Cancer Res July 4 2019

Link: http://clincancerres.aacrjournals.org/content/early/2019/06/29/1078-0432.CCR-18-4022

DOI: 10.1158/1078-0432.CCR-18-4022

Abstract

Purpose:

The CANON (CAVATAK in NON-muscle invasive bladder cancer) study evaluated a novel ICAM-1-targeted immunotherapeutic-coxsackievirus A21 as a novel oncolytic agent against bladder cancer.

Experimental Design:

Fifteen patients enrolled on this 'window of opportunity' phase 1 study, exposing primary bladder cancers to CAVATAK prior to surgery. The first nine patients received intravesical administration of monotherapy CAVATAK; in the second stage, six patients received CAVATAK with a sub-therapeutic dose of mitomycinC, known to enhance expression of ICAM-1 on bladder cancer cells. The primary endpoint was to determine patient safety and maximum tolerated dose. Secondary endpoints were evidence of viral replication, induction of inflammatory cytokines, anti-tumour activity and viral-induced changes in resected tissue.

Results:

Clinical activity of CAVATAK was demonstrated by induction of tumour inflammation and haemorrhage following either single or multiple administrations of CAVATAK in multiple patients, and a complete resolution of tumour in one patient. Whether used alone or in combination with mitomycinC, CAVATAK caused marked inflammatory changes within NMIBC tissue biopsies by up-regulating interferon-inducible genes including both immune checkpoint-inhibitory genes (PD-L1 and LAG3) and Th1-associated chemokines as well as induction of the innate activator RIG-I, compared to bladder cancer tissue from untreated patients. No significant toxicities were reported in any patient, from either virus or combination therapy.

Conclusions:

The acceptable safety profile of CAVATAK, proof of viral targeting, replication and tumour cell death together with the virus-mediated increases in "immunological heat" within the tumour microenvironment all indicate that CAVATAK may be potentially considered as a novel therapeutic for NMIBC.