Good morning, everyone, and welcome to another working week. We hope the weekend respite was relaxing and rewarding, because that oh-so-familiar routine of meetings, online calls, and deadlines has predictably returned. But what can you do? The world keeps spinning no matter how much we push back. So time to get on with it. Please join us for a cup of stimulation — hot buttered rum is our choice today — as we cast about for items of interest. Speaking of which, here are some tidbits. Hope your day goes well…

Weight-loss drugs may eventually reach only about 50% of the overweight ‌and obese people who could benefit from them due to complexities of health care systems and financial constraints, Reuters writes, citing comments made by Eli Lilly chief executive officer David Ricks said at a conference. Lilly and Novo Nordisk are competing for share in the global market for ​GLP-1 drugs, which analysts see topping $100 billion per year in the next decade. But ​just one in 10 people who are overweight or obese are using GLP-1s. “It’s never going to be a hundred,” Ricks said. “For institutional reasons ​in health care and some other complexities in managing health, it’s never going to be that high.” He pointed to low-cost statins, ​the most commonly prescribed cholesterol drugs, as a comparable example. “Between 40 and 50% of people who should be on them, are on them. I think of that as maybe a ceiling,” he said.

The Trump administration’s desire to pry open the black box of prescription drug prices is facing stiff opposition from the phalanx of lobbyists representing pharmacy benefit managers and health insurers, STAT notes. In January, the U.S. Department of Labor proposed a rule that would mandate PBMs disclose a wide range of drug pricing information to employers and make it easier to be audited. The public had until last week to submit comments. A review of the more than 500 letters reflects varying interests: predictable resistance from PBMs and health insurers; enthusiasm from Mark Cuban’s pharmacy and others in the business community who want middlemen to face more accountability; and drug companies cheered PBMs being in the regulatory crosshairs but wanted pullback on disclosure of drug pricing data. 

Continue to STAT+ to read the full story…

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ATCC and the Broad Institute report the development of engineered isogenic cancer models designed to replicate resistance to targeted therapies, beginning with osimertinib, the latest-generation epidermal growth factor receptor (EGFR) inhibitor used to treat non-small cell lung cancer (NSCLC) with EGFR mutations.

According to the researchers, the work addresses a critical challenge in oncology—treatment resistance that emerges over time. EGFR-mutant lung cancer was among the first subsets of a major epithelial cancer where directly targeting an oncogene was associated with marked clinical benefit. While targeted therapies have significantly improved overall survival, resistance inevitably develops.

Developing resistant models directly from patient tumors can take years due to the scarcity of samples. In contrast, engineering resistance mechanisms in controlled laboratory models allows researchers to systematically study multiple escape pathways much faster.

To accelerate discovery, scientists from ATCC and the Broad Institute collaborated to engineer a panel of drug-resistant NSCLC models using CRISPR gene editing and gene overexpression techniques. These models systematically model the resistance mechanisms that arise in patients treated with osimertinib, note the researchers.

“With this powerful new set of tools, drug-sensitive and drug-resistant cancer cells can be studied side by side to understand therapeutic resistance and the underlying drivers,” says Roth Cheng, PhD, CEO of ATCC. “By creating and providing these cancer models along with a rich data-set to the global research community, our hope is to reveal hidden targets and combination strategies that turn today’s treatment failures into tomorrow’s breakthrough. We look forward to extending this approach to additional cancer types.”

Engineering drug-resistant lung cancer models

Led by William R. Sellers, MD, director of the cancer program at the Broad Institute, Fang Tian, PhD, director of biological content at ATCC, and Francisca Vazquez, PhD, director of the Cancer Dependency Map (DepMap) at the Broad Institute, the team identified representative classes of resistance mechanisms to osimertinib. They then selected three disease-representative, osimertinib sensitive NSCLC cell lines as the foundation for developing the new isogenic drug-resistant cell models.

ATCC engineered the selected authenticated cell lines with resistance mechanisms using CRISPR-based methods. The six resistance mechanisms included: PIK3CA E545K mutation, KRAS G12D mutation, BRAF V600E mutation, EGFR C797S mutation, CCDC6-RET fusion, and TPM3–NTRK1 fusion.

In addition, scientists at the Broad Institute are generating additional resistant cell lines driven by gene amplification mechanisms using overexpression methods.

These engineered isogenic model systems allow researchers to compare genetically matched cancer cells that differ only by a specific resistance alteration—providing a powerful framework to study how tumors evolve under targeted therapy.

The models will be integrated into the DepMap, a global effort to identify genetic vulnerabilities across hundreds of cancer cell models. The collaboration also contributes to the development of a Response and Resistance Map (ResMap), an emerging framework designed to systematically characterize how cancers respond to therapy and how resistance evolves.

“Drug resistance remains one of the most significant barriers to durable cancer treatment,” said Kirsty Wienand, PhD, senior research scientist in DepMap at the Broad. “Systematically engineering resistance mechanisms in well-characterized cell models allows us to study how tumors adapt to targeted therapy. Integrating these models into DepMap will help researchers worldwide identify new vulnerabilities and potential therapeutic combinations.”

The collaboration ensures that both the biological models and the associated data will be widely accessible to the scientific community, says the research team. Data will be integrated into the DepMap portal, with links to the corresponding ATCC cell line identifiers. In addition, the engineered cell lines will be distributed globally through ATCC following authentication and quality control.

Systematically engineering clinically relevant resistance mechanisms in lung cancer models, the collaboration establishes a scalable framework for studying how tumors escape targeted therapies, explain the scientists, adding that the resulting models and datasets will help researchers identify new vulnerabilities and therapeutic strategies to overcome drug resistance and improve outcomes for patients with cancer.

By combining advanced cell engineering, functional genomics, and computational biology, the collaboration should provide an important resource for studying drug resistance, cancer vulnerabilities, and precision oncology strategies.

ATCC and the Broad Institute will present the research findings at the American Association for Cancer Research^® (AACR) Annual Meeting 2026, April 17–22 in San Diego:

Title: Engineering isogenic models harboring resistance mechanisms to the latest-generation EGFR inhibitor in non-small cell lung cancer

Session Category: Experimental and Molecular Therapeutics; Session Title: Drug Resistance 2: Tyrosine Kinase Inhibitors

Date: April 22, 2026, 9:00 AM–12:00 PM, Poster Section 11, Poster Board: 8, Poster Number: 7029

The post Decoding Resistance to Targeted Therapy via New Cancer Models appeared first on GEN – Genetic Engineering and Biotechnology News.

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