We learn something new about cancer from a great website called The Scientist

One thing we value here is a well‑written science story that tells us something we didn’t know — and does so in a trustworthy, responsible way. Not the sensationalist, attention‑grabbing material that flashes across our screens all too often. So when our researchers came across Colorectal Cancer and Childhood Exposure to a Common Gut Bacterium by Laura Tran in The Scientist[1], we decided to look at the source itself, to see whether it deserves a place among the canon of science‑news providers we consider worthy of your attention, gentle readers.

As you might expect, The Scientist specialises in clear, sober reporting: across the biosciences, speaking very broadly. The style is terse and informative, closely aligned in spirit with the journals and institutions it covers. There’s a strong news section, a quarterly print magazine, topic‑based browsing, and a generous set of resources. Our test search — naturally, Antibiotics — produced several well‑illustrated, highly informative pieces.

If pressed, we’d say the ideal reader is intelligent, graduate or postgraduate, and probably working somewhere in the life sciences. But there is plenty here for teachers preparing a good science lesson too. Or even two.

Our verdict: not as bite‑sized as Nature Briefing, nor as magazine‑like as New Scientist, The Scientist nevertheless earns a worthy place alongside them as a provider of news and ideas for the educated and reasonable community (that’s us, gentle readers). And in an age when so much content is shaped for attention rather than understanding, that’s a very important thing indeed.

And having satisfied ourselves that The Scientist is indeed a sober and reliable chronicler of the biosciences, we can turn to the story that brought us there in the first place. It is a quietly important one: evidence that early‑life exposure to certain strains of that perfectly ordinary gut bacterium — Escherichia coli carrying a particular genetic island — may leave a mutational fingerprint that shows up years later in colorectal tumours. No melodrama, no scare‑stories, just the steady accumulation of data: mutational signatures, epidemiology, and the slow, careful work of linking mechanism to disease. This is exactly the sort of thing the scientific enterprise does well, and exactly the sort of thing we like to bring to your attention.

[1] https://www.the-scientist.com/childhood-exposure-to-bacterial-toxin-tied-to-early-onset-colorectal-cancer-72952?fbclid=IwY2xjawSxsvNleHRuA2FlbQIxMABicmlkETBVNUo0ekNo

#cancer #medicine #science #life science #research #laboratory #start up #biotechnology

Gene Megacluster: a really big moment in antibiotic research

The idea of whole and unexpected possibilities in antibiotic research excites our highest hopes-and those of readers who have accompanied us on this journey for years. None more so than this report from Nature Briefing Gene Megacluster boosts antibiotic arsenal. We’ve set up their usual summary, plus links: and then we’ll try to answer a few of your questions as best we are able

A newly discovered gene ‘megacluster’ in Streptomyces bacteria enables them to produce a variety of potent antibiotic compounds. These compounds act as a multi-pronged offensive weapon against other species, with each targeting different stages of the bacterial metabolic process. It’s more difficult for bacteria to develop resistance to attacks that hit several targets, so the discovery could lead to the development of new antibiotics, experts say. The research has “discovered something new in a system so extensively studied — hidden in plain sight,” says medicinal chemist Mark Blaskovich

Nature | 4 min read
Reference: Nature paper

So, what is this gene megacluster? An unusual stretch of DNA in Streptomyces that encodes four distinct families of natural-product antibiotics, including: one compound entirely new to science, another never previously recognised as an antibiotic, and two known families deployed in a new coordinated fashion. Not a bad haul for one discovery, we think.

What does it do in Streptomyces? All four molecules target biotin (vitamin B7)—a universal cofactor required for growth, cell division, and metabolic enzyme function in most bacteria. They attack different points in the biotin pathway: production, uptake, use, and availability, aided by flanking streptavidin genes that bind up free biotin.

Why is this discovery genuinely new? Well , all sorts of reasons: here are a few of the best

–Co-location is unheard of: Antibiotic biosynthetic pathways are usually scattered across the genome. Here, four unrelated antibiotic families sit side-by-side, implying intentional evolutionary selection.

–Coordinated multi-antibiotic strategy: Natural antibiotics typically act alone. This cluster encodes a team of molecules that hit the same vulnerability from different angles—something not previously documented.

–Hidden in plain sight :Streptomyces genomes have been mined for decades, yet this megacluster was overlooked because genome-mining tools historically focused on single-product clusters. We love this bit, as regular readers will have already discerned

–It appears to be widespread. The megacluster is present across multiple Streptomyces species, suggesting an ancient, conserved strategy rather than a rare curiosity.

Could similar clusters exist in other organisms? Likely, yes. The discovery provides a road map for genome mining that looks for coordinated multi-pathway clusters, not just single biosynthetic islands Early research might do better to focus on procaryotes rather than eucaryotes-but who knows?

How could it help us to develop new antibiotics? This is the Big One for us , isn’t it? Lots of ways potentially, but as of late June 2026 three practical routes suggest themselves:

1. Direct development of the four biotin-targeting molecules. Because they attack different steps in the same essential pathway, they could be: used individually, combined as a cocktail, or engineered into hybrid molecules. Multi-target antibiotics are inherently harder for pathogens to resist. So that will teach them we’re serious this time.

2. Synthetic biology reconstruction. The megacluster’s architecture can be transplanted into: Streptomyces strains, E. coli or yeast expression systems, or modular cell-free platforms, permitting all sorts of scaling and production advantages

3. Drug discovery by analogy The discovery provides a template: look for clusters that coordinate attacks on other essential pathways (e.g., folate, isoprenoid synthesis, lipid II). Genome mining guided by this logic could uncover dozens of new multi-pronged antibiotic families.

4. Biotin-pathway inhibitors as a new class Biotin metabolism is conserved across many pathogens, including Gram-negatives—historically hard to target. These molecules could seed a new class of antibiotics that bypass existing resistance mechanisms

At this blog we tend to rate discoveries by the possibilities they open rather than the questions they answer. By that metric, this one is big indeed-and we think you’ll al agree with that.

#antibiotic research #antibiotic resistance #health #medicine #biotechnology #genetic engineering #research #bacteria

Diabetes: another benefit of the BCG Vaccine?

A couple of years ago we did a piece called Did your long-ago BCG Vaccine save you from dementia? In which we reported that the famous BCG (Bacillus Calmette-Guérin) vaccine was also proving efficacious in cases of bladder cancer and certain types of dementia. (LSS 2 12 24) Well today things just became even more intriguing. Read this from Nature Briefing, Century Old Vaccine helps control diabetes;

A tuberculosis vaccine developed in the 1920s helps to regulate blood sugar in people with certain types of diabetes, enabling them to reduce their insulin use. The findings demonstrate yet another beneficial off-target effect of the Bacillus Calmette–Guérin vaccine, derived from a weakened form of the bacterium that causes tuberculosis in cows. The shot has been approved to treat bladder cancer in the United States and is being investigated against conditions such as Alzheimer’s disease. The results were presented at the American Diabetes Association meeting on 7 June.

Nature | 5 min read

And the Learning Point? When we did Training and Teaching, they always told us that we had to have a learning point. So we think it’s this:

Vaccines are one of civilisation’s quiet miracles:[2] you design them for one threat, and decades later they’re still paying unexpected dividends — BCG for TB, then bladder cancer, then dementia, and now hints of protection against diabetes. That’s what real science does: it compounds. You invest once, and the benefits echo for generations. But if you decide, like the climate denier or the old‑school smoker, that evidence is optional and expertise a nuisance, you’re effectively betting your long‑term future against the only tool that has ever reliably improved it. Reality is not something you can pick and choose.

[1] BCG vaccine – Wikipedia

[2] Vaccines and immunization

#vaccination #BCG #tuberculosis #cancer #dementia #diabetes #health #medicine #research

More on AI and Antibiotics-and it’s good news

Once again, the source for our blog today comes from the excellent Nature Briefing, who are always in the forefront of scientific research in every field. Today we are showcasing their piece AI is taking on antibiotic resistance because we think they’re picking up on some real game-changing developments, and we really want you to know about them.

Let’s start with their usual helpful summary, as it’s a good general overview. But this time we earnestly beg you to click on the link they have provided: read below to find out why.

Antibiotics are an effective, but somewhat indiscriminate solution to some gut infections. Helpful species of gut bacteria get caught in the crossfire, which increases the likelihood that drug-resistant bacterial strains will evolve. Researchers are now designing drugs to selectively target disease-causing species with the help of artificial intelligence. Some teams are using AI to screen drug molecules for the most promising candidates quickly and cheaply. Others have developed tools that predict how drug molecules bind to protein targets to reveal a drug’s mechanism of action, reducing the need for wet-lab experiments.

Nature | 15 min read

Because if you do, you will step into a world of research where Information Science and Biological Science are meeting: which of course is more and more these days isn’t it? You will learn about:

Jonathan Stokes of McMaster University in Canada who have pioneered the use of AI to test their newest molecule called enterololin and thereby strip out all kinds of old-skool testing processes.

Regina Barzilay of MIT who with her team have done much of the AI work to set this up for Jonathan She is a remarkable woman who has been hunting down the link between antibiotics and AI since 2018-how’s that for far sightedness, folks?

You’ll be able to name check tools like Diffdock , RdKit and Chemprop which these people use to do all this-how’s that going to sound in the pub?

And a woman called Molly Bartlett who’s something called a Chemical Informatician at London’s Imperial College. As we still have a tenuous connection to that august institution we sometimes write in to their alumnus mag and tell them what a good job they’re doing, knowing we speak for all of you, gentle readers.

And much more besides, Especially if you do the decent thing and sign up to go behind the paywall.

Funny, isn’t it? If our first name were Donald (it isn’t) we might note how much this progress a) seems to come from despised places like Canadia and Englandland b) how somehow these evil foreigners still find ways to work with Unitedstatespersons c) maybe if you want to find cures for important things you may have to look at other methods in addition to earnest prayer d) if I were getting bigly older, perhaps approaching my eightieth birthday for example, I might like to have a few antibiotics around. Just a thought.

# Antibiotic research #Artificial Intelligence ~medicine #health #bacteria

Progress on Multiple Sclerosis: When Big Data meets Molecular Genetics

Photo by Fayette Reynolds M.S. on Pexels.com

Few of us have not met someone who is suffering from Multiple Sclerosis, that terrible wasting disease wherein the immune system seems to turn on its own body, especially in the fatty sheaths around the neurons. Leading to a progressive deterioration in mobility before confining victims finally to a wheelchair-or even worse. The experience for families and victims was extra-bad because for many years the cause seemed unknown, making hope of any cure quite unlikely. Michael Marshall of the New Scientist has been covering this story most assiduously. And so we are pleased to showcase it, because it celebrates achievements in two our our favourite fields-big data and molecular biology-and the benefits which accrue when scientists from both work together.

We urge you to read Michael’s article either by buying the hard copy mag (there’s tons else to read inside it) or paywalling past the link below [1] Suffice it to say: #1 The molecular evidence that the Epstein Barr virus (which can cause glandular fever) is involved. #2 That this has a strong effect on both B cells and T cells in the immune system, which ,when they go rogue, are essentially responsible for the terrible lesions of MS #3 That not all hosts of Epstein Barr virus go on to develop MS, because the chances of that depends on certain genetic propensities and variants and, best of all #4 the above and more, which we report so glibly, has been elucidated by the use of huge data studies : 10 million people in one, 617, 186 in another, even 471 000 B cells in another-how’s that for numbers, folks?-which were only possible because: #5 places like the UK and USA have worked to build big collaborative things the the UK Biobank and All of us. Well some of the people in those countries have anyway.

All of which leads us to few reflections, some of which will not be uncongenial to regular readers. Firstly, it seems a pretty good idea to spend money on science, especially basic research, instead of cutting it. Secondly scientists these days work best in large teams whose members come from all sorts of backgrounds and this is especially true when you throw multidisciplinarygroups of them together. And that this also seems to be true of football teams: how far would Arsenal FC. for example, have enjoyed their current success if they had insisted on retaining a staff entirely composed of plucky British lads? [2] The implications in turn for visa systems, cultural openness and plain common sense are clear in turn.

[1]Huge study reveals how Epstein-Barr virus may cause multiple sclerosis | New Scientist

[2]‘Everything can happen’: Trossard confident of Arsenal’s chances in final | Arsenal | The Guardian

#multiple sclerosis #Ebpstein-Barr virus #T cells #B cells #autoimmune disease #medicine #health

WHO has a Cunning Plan to speed antibiotic development

“The scientific community has developed and approved new antibiotics in recent years. This is good, but unfortunately not sufficient to catch up with evolving drug-resistance bacteria, especially against those of greatest concern. We need a reliable pipeline with new antibacterial agents that are innovative, affordable, accessible to all those who need them.”

Dr Yvan Hutin, Director of Antimicrobial Resistance at WHO

Says it all really, everything that we’ve been banging on about here for the last six years and more. The problem is simple, but deadly. Although more than 90 new antibiotics are now in development, very of few of them target the really high-priority organisms that worry health care professionals: and even fewer of these are really innovative (in the way that penicillin was in its day for example) And so the World Health Organization, that most noble of entities has come up with a Cunning Plan to really get things moving. They gave divided it into three Target Product Profiles:

-our old friends the multidrug resistant gram negative bacteria such as enterobacteriales, Acinobacter baumanii and Pseudomonas aeruginosa, who’ve shown up in so many old LSS blogs we won’t bother to list them.

–Gram positives like Enterococcus faecium. We have wondered why the gram negatives have been getting all the attention, and seeing no Darwinian reason why the gram positives should not evolve resistance too, are extremely glad someone is at last paying attention to them.

-their third trope for action is bacterial meningitis, caused by organisms such as Neisseria meningitidis and Streptococcus pneumoniae among others. Particularly welcome, for of those who incur such dreadful infections, one out of six will die and of the survivors, about one in five will be left with some long term disimpairment.

Hats off to Dr Hutin in particular and the World Health Organization in general. The World Health Organization is often treated as a mere federation of its member states, but in practice it is something larger and more coherent than the sum of its parts. Individual nations see only their own budgets, their own pathogens, their own political cycles; the WHO sees the whole epidemiological chessboard. Its strength lies in that cooperative vantage point — the ability to gather data from Lagos and Lima, to convene experts from Seoul and Stockholm, and to turn a hundred local anxieties into a single, rational blueprint for global action. In a field as fragmented and under‑powered as antibiotic development, that kind of coordination isn’t bureaucracy; it’s civilisation defending itself. There’s your glass-raiser for Friday Night Cocktails, gentle readers.

WHO releases new target product profiles for urgently needed antibiotics

#antibiotics #penicillin #world health organisation #epidemiology #microbiology #health #medicine

Breakthrough for blindness, an old lesson re-learned: and a mystery question

Leber congenital amaurosis, called LCA for short, is the most common form inherited sight loss in children[1] It’s caused by defects in a cluster of genes including RPE65 and until recently was quite untreatable. Now, as Ian Sample reports for the Guardian,[2] a team of researchers have effected a major new treatment called Luxturna: a gene‑replacement therapy delivered by injecting a working copy of the RPE65 gene directly under the retina. By giving retinal cells the functional gene they’re missing, it restores the visual cycle and can improve light sensitivity, visual function, and navigation ability in people with RPE65-related Leber congenital amaurosis. Interestingly the team comprises a husband and wife called Jean Bennett and Albert Maguire who share the prestigious Breakthough Prize [3] with their colleague Katherine High.

Regular readers will share our admiration for the work of this remarkable trio. They may note moreover that the researchers have something else to teach us, something that strongly concurs with opinions often expressed in this blog:

Bennett said it was a “tremendously exciting time” for scientific and medical research, but warned that the US administration’s attacks on science could “cause damage for generations to come”, leading her to fear a brain drain that the country would struggle to recover from.

“Agendas have become politicised, government agencies that support basic and applied research have been undermined, knowledgeable advisers and experts have been dismissed or have fled and revised guidelines contradict decades of rigorous research,”

Says it all really. But don’t just sit around reading it here:tell your friends and neighbours. For us there still remains outstanding question. Is Albert Maguire by any chance a relation of Ken Maguire, one of the best pub landlords of the 1990s, being sometime manager of the superb Latymers in Hammersmith Road London W14?

[1]Leber congenital amaurosis – Moorfields Eye Hospital

[2]‘Oscar of science’ awarded to team behind gene therapy that restores lost vision | Science | The Guardian

[3]Breakthrough Prize – Wikipedia

#LCA #Blindness #gene therapy #medicine #health #science #research #pub #beer

Humble little herb may have mighty role as antibiotic

Could a humble little wildflower growing unnoticed in bog and marshland be a key player in the science of antibiotic resistance? According to an article by researchers Ronan McCarthy John J. Walsh and Kavita Gadar for the Conversation[1], yes it could. For they have discovered that Tormentil (Potentilla erecta) [2] not only has intriguing antibiotic properties of its own, it may help us to retread and recycle some old human made antibiotics which are sadly reaching the end of their effective lives.

Tormentil has appeared for centuries in the herbariums of traditional folk medicine. It has been used variously to treat ailments as diverse as gum disease, diarrhoea and wounds. Noting this, our resourceful researchers put it into a cross study against 70 other plant species in their Laboratory. It came out tops, hacking into the biofilms that bacteria use to defend themselves and thereby shortening the lives of these creatures by more than somewhat. They even identified the active agents in the tormentil which are ellagic acid and agrimonem. But you probably guessed that, being such an erudite and well-informed bunch of readers. Even more remarkably they:

…. combined low levels of the antibiotic colistin – an antibiotic that is only used as a last-resort against severe infections due to its potential toxicity to patients – with the tormentil extract. The low-level antibiotic dosage wasn’t enough to kill the bacteria when used on its own. But when combined with the tormentil extract, the plant compound enhanced the antibiotic’s efficacy.

You don’t need to be an old LSS hand to realise our worries about the declining effectiveness of colistin and some of the other older antibiotics.[3]

And our conclusions? We’ve written over twenty blogs on the theme of antibiotics or other medicines which may be hidden in nature. And therefore to destroy wildlands in order to grow food which no one really needs, or to build shopping malls of aching vacuity, is biologically insane, whatever the short term economic benefits. That probably half of all wild plants contain something useful, if only to the secret services of certain well known governments . As Shakespeare had it

“Within the infant rind of this small flower / Poison hath residence and medicine power.”
— Romeo and Juliet, Act 2, Scene 3

[1] https://theconversation.com/wildflower-once-used-to-treat-wounds-and-sore-throats-shows-promise-in-fighting-dangerous-superbugs-279406?utm_mediu

[2] Potentilla erecta – Wikipedia

[3] Liu, Y.-Y. et al. (2016). “Emergence of plasmid-mediated colistin resistance mechanism MCR-1 in animals and human beings in China.” The Lancet Infectious Diseases, 16(2), 161–168.
DOI: 10.1016/S1473-3099(15)00424-7

#health #medicine #antibiotic resistance #wild flowers #tormentil #bacteria #microbiology

VIR 5500: Promising new treatment for Prostate Cancer

Immunotherapy, which involves training the body’s own defence systems such as T-cells to attack cancerous tissues, has been one of the medical success stories of the last twenty years. Yet some cancers still demonstrate a certain recalcitrance in the face of the new ministrations. Unfortunately, one of them is Prostate cancer, the most common form of cancer in men, killing up to 1.5 million of them annually. But not only does this report by Nicola Davis of the Guardian [1] offer hope of real progress, it has some deeper lessons for those of us in the evidence-based thought-modulated community(EBTM). Which means you, gentle reader.

All immunotherapy depends on T Cell engagers (TCEs) which form a bridge between certain sites on the T Cell and on the tumour cell. Anyone working with them to try to cure prostate cancer encounters two difficulties. Generally, traditional TCEs can be pretty indiscriminate, leading to side issues like massive cytokine storms and problems with dose toxicity. Specifically, prostate cancer cells have a knack of resisting T cells, making immunotherapy especially hard to apply. Now a team led by the admirable Professor de Bono in collaboration with Vir Biotechnology[2] is trialling a new form of molecular cloaking treatment called VIR-5500 which masks the T-cells right up to the moment when they are in contact with the prostate cancer cells. A protease in the malign cells then activates the T-cells, unleashing their curative effect. We won’t spoil Nicola’s summary of the results, which you can read in her article. But you will find them impressive to say the least.

All of which goes to show what curiosity-driven basic science can achieve when money is spent on it. VIR -5500 could not have existed without decades of molecular immunology, protein engineering, tumour cytology and many other disciplines hidden away in unmanly places like university departments and research institutes. Which is ironic, because many of the butch types at the Dog and Duck, who routinely perform their masculinities by loudly decrying scientific research into things like climate change, will be the first to suffer when prostate cancer comes along. But History always teaches the same lesson to the deluded in the end.

[1] Researchers praise ‘stunning’ results of new prostate cancer treatment | Prostate cancer | The Guardian

[2] Our Strategy | Vir Biotechnology

#prostate cancer #immunotherapy #t cells #health #medicine #science #molecular biology

Food: is it quite as good as you thought?

Food is everywhere these days. Shelves groan with glossy cookbooks, restaurants and gastropubs queue up for tax breaks, and the airwaves are thick with chirpy kitchen‑dwellers—some dropping their aitches with theatrical enthusiasm, others sounding as if they’ve just strolled out of a rowing club bar. Everywhere you look, there’s another beaming evangelist waving a saucepan and assuring us that their latest ‘blend’ is nothing short of a revelation. One could be forgiven for thinking that food itself has become a national moral project, a jolly good thing in which we are all expected to take an interest.

However the readers of our little blog being a thoughtful lot, we thought we’d put up two stories which might provide a little counter-balance to the general merriment. The first from the indefatigable Kat Lay of the Guardian (clearly she knows about more than just antibiotics) does not suggest food is bad per se. But it does suggest that being extremely careful about what you eat, and who is selling to you might be a very good idea[1] Her headline tells you exactly what we mean: Ultra-processed foods should be treated more like cigarettes than food – study

“OK, OK”. you say, “but wot I eat is my choice, innit, guvnor? If I ain’t doin’ no one else no ‘arm, wosser problem?” Well according to Nature Briefing, Eating Well is about more than your health, this might be:

Debates over what to eat — more protein, say, or less ultra-processed food — often neglect any mention of how our food systems affect the biosphere that keeps us alive. But nutrition doesn’t exist in a vacuum, notes Earth-systems scientist Johan Rockström. He co-chaired the latest update to the Planetary Health Diet, which aims to optimize human health globally and reduce environmental and social harms. It notes that “global greenhouse-gas emissions could be cut by 20% by 2050 by eating healthily, reducing food waste and adopting sustainable production practices”, writes Rockström. “If diets remain unchanged, however, emissions will increase by 33%.”Nature | 7 min read
Reference: The EAT-Lancet Commission on healthy, sustainable, and just food systems report

We want humanity to survive, really we do. If you went extinct there would be no one to man the check out tills at supermarkets and we’d have to use those ghastly check-out-yourself tills that are so slow, complicated and inconvenient. Yeah food is alright, sometimes. But as the old saying goes-be careful what you wish for.

[1]https://www.theguardian.com/global-development/2026/feb/03/public-health-ultra-processed-foods-regulation-cigarettes-addiction-nutrition

#food #nutrition #climate change #obesity #health #fat #protein #fast food #processed food