Many of the efforts to improve on the first generation of CAR-T therapies such that they can reach solid tumors had focused on tweaks inherent to the cancer killing agent — specifically, utilizing more potent T cells as their base, from stem memory T cells to virally associated T cells to marrow infiltrating lymphocytes. But what if just amplifying CAR-T cells can do the job? Darrell Irvine and his team at MIT have some intriguing mouse data for one such tech.

As Conservative Party leaders face off in a bid to become the UK’s next Prime Minister, scientists from a range of specialties — from cancer to climate — are sounding louder alarms about the threats of a looming no-deal Brexit for their research work.

Citing an analysis by the University College London of the latest EU research funding data, the Guardian reported that UCL and eight other Russell Group universities ran only 20 big European research collaborations in 2018, a steep drop from around 50 in 2016. And individual researchers are feeling the cloud of uncertainty snuffing out prospects.

When Hal Barron unveiled his grand plan to turn GlaxoSmithKline’s R&D group around, he championed genetics as one of two key focuses for the UK pharma giant, announcing a discovery deal with 23andme and pledging to focus more on CRISPR tech as well as machine learning. A year later, the R&D chief is building on that promise as he seals a new pact with two prominent CRISPR researchers in his neighborhood in San Francisco.

If Denis Rebrikov has his way, the world could be expecting more CRISPR babies soon.

The Russian scientist has told Nature he is considering following Jiankui He’s example in knocking out the CCR5 gene in embryos and implanting them into women — except doing it in a better way. It marks the first declaration of interest in continuing the work when researchers around the world are calling for suspension of human germline editing and stricter standards, following a global backlash against He’s claims that he facilitated the birth of twin girls who had been CRISPR-ed as embryos.

Scientists the world over have found plenty of reasons to condemn their Chinese colleague Jiankui He’s experiment with the world’s first CRISPR babies late 2018: The alleged medical need to confer HIV immunity was unfounded, the consent process seemed dubious, the actual gene editing appeared spotty, just to name a few. But a new research paper may have uncovered the most staggering of them all.

A Singaporean biotech looking to break into the big NASH field has offered a glimpse of the preclinical data that’s stoked its confidence in targeting an oft-overlooked cytokine.

Researchers from Duke-NUS Medical School and National Heart Centre Singapore started with hepatic stellate cells, which “are pivotal in the pathogenesis of NASH and give rise to up to 95%” of disease driving cells known as liver myofibroblasts. Here’s how they summarized the current NASH landscape, from their new paper in Gastroenterology:
A number of factors are implicated in HSC activation and transformation, including the canonical pro-fibrotic factors transforming growth factor-B1 (TGFB1) and platelet derived growth factor (PDGF) and also pro-inflammatory factors such as CCL2, TNFA and CCL5.. Perhaps reflecting this complexity and implicit redundancy, no single upstream initiating factor has been targeted successfully in NASH and there are no approved NASH drugs. Currently, there are a number of drugs in clinical trials for NASH but many of these target metabolism and it is not clear if they will improve liver fibrosis, which predicts clinical outcomes.
To simultaneously get at the fat accumulation, inflammation and scarring present in NASH, they need a better target. And the scientists believe they have found the answer in interleukin 11, or IL11.

AstraZeneca’s cediranib may not have made the cut as a single agent to treat ovarian cancer, but Yale researchers think it could serve as a powerful add-on to amplify the effects of PARP inhibitors.

The theory has been that cediranib works by blocking the formation of new blood vessels, thus depriving tumors of the nutrition and oxygen necessary to live and grow. But in a mouse trial, a team out of Peter Glazer’s lab found that the drug also directly affects pathways involved in DNA repair — a potentially more useful function.

Parvus Therapeutics has just scored a discovery deal with Genentech on autoimmune diseases, putting them in alliance with one of the most sought-after partners in the business.

We don’t know what the upfront is — and typically Genentech isn’t known for splurging big on discovery bets — but the whole deal, biobucks included, weighs in at a prospective $800 million.

Whatever they’re anteing up, Genentech will now hop on the Burlingame, CA-based biotech’s Navacim platform, which converts effector cells into regulatory T cells, Tregs, that in turn whip up immune regulator cells to mob the inflammatory cells that trigger autoimmune diseases like rheumatoid arthritis and multiple sclerosis.

British scientists want to counter cancer by using an approach that worked for HIV and tuberculosis: by creating treatments to preclude cancer’s ability to become resistant to existing drugs and recur.

The drug discovery program, orchestrated by the Institute of Cancer Research (ICR) in London, will be launched at a facility in the British capital with an initial £75 million (roughly $85 million) injection.

At Tessa Therapeutics, the big idea has been to adapt virus-specific T cells (VST) to target virally-associated tumors, and swarm cancer cells. Researchers believe these VSTs can be versatile, making superior CAR-Ts that can then be combined with an oncolytic virus and a checkpoint inhibition strategy. In its latest preclinical trial, the Singapore-based biotech has spotlighted one such “all-in-one” approach that they are now taking into the clinic.