Tag: Genomics

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The State of Multiomics & NGS

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Next-generation sequencing (NGS) has never been cheaper or more accessible. In turn, spatial biology, single-cell, and proteomics are fueling exciting advances in biology. The rapidly declining cost of whole-genome sequencing is empowering researchers to ask questions that were beyond reach just a few years ago. 

In The State of Multiomics & NGS virtual summit—sponsored exclusively by Illumina—GEN invites you to watch a superb line-up of presenters covering key topics in the world of multiomics, spatial biology, and NGS. This year’s summit features a broad selection of talks and panel discussions from renowned experts that offers our audience rich insights into the latest NGS platforms, spatial biology applications in neurodegenerative diseases and cell biology, and a critical look at data management challenges and solutions.

Among the highlights are:

  • A keynote presentation from Miranda Orr, PhD, on the use of spatial biology in studying Alzheimer’s and other neurodegenerative diseases

  • A deep dive into the latest NGS platforms and applications with veteran genomics analysts Keith Robison, PhD, and Shawn Baker, PhD

  • Modeling the proteome architecture of human cells with Noorsher Ahmed, PhD (Lundberg lab)

  • Chris Dwan on data management strategies for multiomics

  • And a sponsored breakout conversation featuring Illumina’s chief medical officer, Eric Green, MD, PhD, and cancer biologist Bodour Salhia, PhD (USC)

We look forward to seeing you on April 29. Registration is absolutely free! !

Guest Speakers Include

The State of Multiomics & NGS speakers

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TRACERx MRD Results Showcase ppmSeq’s Ultra-Sensitive ctDNA Detection at AACR

Minimal residual disease (MRD) continues to be a central focus at the AACR meeting. The small numbers of cancer cells that remain in the body after treatment helps gauge the effectiveness of a treatment and relapse risk. The ability to detect those cells, even in tiny amounts, is an ongoing goal of the cancer community.

At this year’s AACR, the sequencing company Ultima Genomics is announcing new findings in this area using its ppmSeq technology. The data will be presented across six abstracts, including a plenary session.

Highlighting the program will be initial TRACERx (TRAcking Cancer Evolution through therapy (Rx)) MRD data showcasing performance of ppmSeq relative to ultrasensitive bespoke panels.

TRACERx is a long-term study—one of the largest tumor evolution studies—funded by Cancer Research UK. The program analyzes how cancer evolves, spreads to other parts of the body, and develops resistance to treatments. Instead of taking just one biopsy, researchers sample different parts of the same tumor and metastases; the program involves sequencing multi-region and multi-time-point genetic data from over 3,200 tumor samples from over 800 lung cancer patients.

The data will be presented at a plenary session by Charles Swanton, FRCP, BSc, PhD,  professor at The Francis Crick Institute in the U.K. He will present an early validation pilot of ppmSeq across 50 plasma samples—using tumor-specific variants identified from prior whole genome sequencing—achieved high analytical sensitivity for ctDNA detection at low single-digit parts-per-million.

“TRACERx has always followed the science of cancer evolution wherever it leads,” said Swanton. “Improving the sensitivity of ctDNA detection is central to the wider ambition for MRD monitoring, and expanding studies across a broader patient population will give us the statistical power and clinical context to determine how whole genome MRD monitoring can be deployed at NHS scale and beyond.”

Data from collaborators will also be presented at the conference. Labcorp will present data from an independent analytical study of an assay developed in coordination with ppmSeq technology, including the performance across multiple solid tumor types in pre-surgical, treatment-naive plasma samples. This analysis of 120 non-cancerous donor samples showed specificity exceeding 99.9%, underscoring the ability of ppmSeq whole genome sequencing to accurately differentiate between cancerous and non-cancerous samples, minimizing false positives. Additional analysis across three commercially available cancer cell lines spanning 13 concentration levels from 0.5 to 500 parts per million showed a 95% limit of detection below 3 ppm, demonstrating the assay’s capacity to detect ultra-low levels of circulating tumor DNA (ctDNA).

“For a long time, the question has been whether you can get truly ultra-sensitive MRD detection from a whole genome approach without all the complexity of bespoke assays,” notes Gilad Almogy, PhD, CEO of Ultima Genomics. “What these AACR data show is that the answer is yes. We’re seeing ppmSeq deliver the level of sensitivity needed to make whole genome MRD practical, scalable, and much easier to deploy globally.”

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Brain Gene Variations Help Explain Neurological and Psychiatric Sex Differences

Thousands of genes are expressed differently in the brains of men and women, researchers have discovered.

The findings could help explain differences in neurodevelopmental, psychiatric, and neurodegenerative disorders between the sexes.

While men are more likely to experience schizophrenia, attention deficit hyperactivity disorder, and Parkinson’s disease, women are more prone to mood disorders and Alzheimer’s disease.

The U.S. study, in Science, is the first systemic single-cell survey of sex differences in gene expression across multiple regions of the human brain.

“Together, these findings provide a comprehensive map of molecular sex differences in the human brain and offer initial insight into their underlying mechanisms and potential functional consequences,” Alex DeCasien, PhD, from the National Institute of Mental Health in Bethesda, Maryland, told Inside Precision Medicine.

DeCasien and co-workers conducted a high-resolution analysis of gene expression in tissue samples from the brains of 15 men and 15 women using single-nucleus RNA sequencing.

They then used data from earlier large neuroimaging studies to select six cortical regions to sample, four of which showed sex-related differences in grey matter volume and two in which no such differences were found.

The team found subtle but widespread differences in gene activity between men and women. Biological sex explained very little of the variance in gene expression across the brain, at less than 1%, but differences were widespread—with more than 3000 genes showing different expression according to sex in at least one cortical region.

The greatest sex-related differences in gene expression were on the sex chromosomes. However, most of the genes showing sex-related variations in expression were autosomal—carried on one of the 22 numbered non-sex chromosomes.

The predominant driver for sex-biased expression of genes on these autosomal chromosomes were sex steroid hormones such as estrogen and testosterone.

Surprisingly, more than half the X chromosome genes in women were expressed in both alleles for at least one cell type. This indicated that many had escaped X chromosome inactivation—a female phenomenon in which one of the two X chromosomes is switched off early in development to stop women producing double the number of X-linked gene products to men.

“That finding has implications for understanding sex-biased disease susceptibility because several genes implicated in neurodevelopmental disorders reside on the X chromosome,” commented Jessica Tollkuhn, PhD, from Cold Spring Harbor Laboratory, and S Marc Breedlove, from Michigan State University, in an accompanying Perspective article.

They noted that autosomal genes showing sex-biased expression were substantially enriched for extracellular matrix components, hormone signaling pathways, and metabolic processes. “Genes with greater expression in women were enriched for mitochondrial and synaptic functions, whereas male-biased genes were associated with metabolic and structural pathways,” the editorialists added.

“By pinpointing these sexually differentiated processes, the data provide a treasure trove for the discovery of biomarkers of and/or therapeutic targets for differential disease risk in men and women.”

DeCasien and team added: “These findings raise the possibility that sex differences in gene expression modulate the magnitude of genetic effects at risk loci, contributing to differences in disease vulnerability and to reduced portability of polygenic risk prediction across sexes.”

The post Brain Gene Variations Help Explain Neurological and Psychiatric Sex Differences appeared first on Inside Precision Medicine.

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Integrated Sample Preparation System Standardizes and Streamlines Pre-Analytical Workflows

Invivoscribe launched the PrepQuant™ sample preparation platform that integrates nucleic acid extraction, concentration, and quantification with a single automated instrument. The product is designed to standardize sample preparation and simplify pre-analytical workflows to reduce costs and eliminate a primary source of inconsistency in molecular testing.

Developed in collaboration with Hitachi High-Tech Corporation, PrepQuant combines Invivoscribe’s experience in developing standardized molecular assays, providing global clinical testing services, along with Hitachi High-Tech’s technological and manufacturing capabilities

The PrepQuant system is assay agnostic, generating highly concentrated genomic DNA and cell free DNA (cfDNA) yields for next-generation sequencing (NGS), qPCR, and digital PCR (dPCR) assays. By consolidating multiple steps in a single platform, the system can lab operating costs, sample variability, and lab bench space, while optimizing tests results.

“PrepQuant represents a significant advancement in our commitment to standardize the entire testing process, starting with the pre-analytical workflow,” said Jeff Miller, CEO and CSO of Invivoscribe. “This is particularly important in the era of precision medicine, where reliability of measurable residual disease and liquid biopsy results depend markedly on the quality and consistency of the starting material.”

“The concept for the was driven directly by insights from LabPMM, our global network of testing laboratories,” added Jordan Thornes, vice president, global clinical lab operations. “Our teams recognized the limitations of currently available automated instruments, particularly the labor-intensive nature and increased risk of errors associated with running three separate protocols across multiple instruments. This all-in-one system was designed to reduce costs, while addressing those challenges and significantly improving operational efficiency.”

The PrepQuant is designed and validated for use with blood, plasma, and bone marrow specimens, with ongoing development for additional specimen types. Invivoscribe will officially unveil the product at the American Association for Cancer Research (AACR) Annual Meeting in San Diego, at booth #3459 from April 19–22.

 

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An inducible base editing platform for cancer functional genomics in vivo

Nature Biotechnology, Published online: 15 April 2026; doi:10.1038/s41587-026-03079-3

We developed a functional genomics platform using a small-molecule-controllable base editor that enables gene editing with reduced cellular toxicity and minimal transcriptional perturbation. The resulting high efficiency of the method potentiates in vivo inducible genetic screening, allowing systematic identification of critical residues in cancer therapeutic targets.

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Can psychiatric genetics advance without incorporating a lifecourse perspective?

Psychiatric disorders unfold over the lifecourse, yet genomic studies of these conditions overwhelmingly rely on phenotypes collected at a single time point, often in adulthood. Genome-wide association studies (GWAS) of psychiatric conditions may therefore miss genetic variants with time-varied relevance to etiology, prevention and treatment, such as those that influence trajectories of symptoms and behaviors, age-at-onset, course of treatment response, and co-evolution of comorbidities. With recent advances in longitudinal biobanks and analytic tools, we posit that incorporating a lifecourse perspective in psychiatric genetics will enable critically relevant insights into each of these areas of investigation.

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Pregnancy Sickness Study Identifies New Genetic Links

The University of Southern California (USC) research team that identified the hormone-encoding gene GDF15 as a key driver of pregnancy sickness has identified nine additional genes linked to its most severe form, hyperemesis gravidarum (HG). Six of the identified genes had not been previously linked to the condition.

The Keck School of Medicine of USC team and international collaborators conducted a genome-wide association study (GWAS), scanning the entire genome for differences between women who developed HG during pregnancy and those who did not. They analyzed data from more than 10,000 women with the condition and more than 450,000 controls across European, Asian, African, and Latino ancestries. Their findings offer new clues about the condition and new hope for those affected.

Marlena Fejzo, PhD, a clinical assistant professor of population and public health sciences in the Center for Genetic Epidemiology at the Keck School of Medicine, led the present study and earlier research linking GDF15 to HG. Fejzo told GEN, “The study is much larger than previous studies and on a more diverse population allowing for identification of new genes associated with HG … The new genes give us new directions to explore for prediction, diagnosis, treatment, and response to therapies.”

Fejzo is first author of the team’s published report in Nature Genetics (“Multi-ancestry genome-wide association study of severe pregnancy nausea and vomiting”), in which the team stated, “Potential roles for candidate genes in appetite, insulin signaling, and brain plasticity provide pathways to explore etiological mechanisms and therapeutic avenues.”

HG, which affects about 2% of women, causes nausea and vomiting so severe that eating can become extremely difficult. “Most pregnancies are affected by nausea and vomiting (NVP), but in 0.3–10.8% of pregnancies the symptoms can be severe enough to cause maternal weight loss and adverse maternal and fetal outcomes,” the authors wrote. HG in its most severe form can even be life threatening.

HG was long misunderstood and often dismissed as psychological, growing evidence shows that it has a strong biological and genetic basis and can lead to severe malnourishment, putting both mother and baby at risk. Current treatments for HG are frequently ineffective in improving patient symptoms, the authors further pointed out, and so increase the risk of pregnancy termination, postpartum depression, and suicidal ideation, along with other maternal and offspring comorbidities. “Therefore, understanding of HG etiology is critical to begin to address the negative impact severe NVP has on maternal and child health.”

While historical hypotheses have previously centered around human chorionic gonadotropin (hCG), recent large-scale genetic studies have implicated the GDF15 gene encoding growth differentiation factor-15—a hormone associated with nausea and vomiting, the authors further pointed out. Earlier research by Fejzo and an international team had shown that the link between HG and GDF15 lies in women’s sensitivity to the hormone. They found that women exposed to lower levels of the hormone before pregnancy because of a mutation in the gene experience more severe symptoms, while women exposed to higher levels of the hormone before pregnancy have less severe nausea and vomiting symptoms.

“GDF15 was identified as the greatest genetic risk factor for HG in both a genome-wide and an exome-wide association study, and a rare mutation in GDF15 was associated with a greater than tenfold increased risk for HG,” the scientists noted in their newly reported study. Fejzo explained to GEN, “The mutation in GDF15 is rare. People who carry the mutation have abnormally low levels of GDF15 when they are not pregnant and that increases their risk of being hypersensitive to it during pregnancy when it is produced in massive amounts by the placenta.”

Commenting on their prior work implicating a role for GDF15 and HG, Fejzo further explained to GEN, “In our first GWAS study we found the association between the GDF15 gene and HG. Next, we published a whole-exome sequencing study that identified a mutation in GDF15 associated with HG. Then we published our study in Nature which provided strong evidence that hypersensitivity to the rise of GDF15 in pregnancy (due to low pre-pregnancy GDF15 in circulation) is the main driver of the condition.”

For their newly reported study the researchers carried out a multi-ancestry genome-wide association study of 10,974 HG/excessive vomiting in pregnancy cases and 461,461 controls across European, Asian, African, and Latino ancestries from nine contributing studies.

The results identified 10 genes that were linked to HG, including four that had previously been identified, and six new genes. “Because this is the largest study of HG ever conducted, we’ve been able to tease out important new details that were previously unknown,” said Fejzo. “The fact that we’ve studied women from multiple ancestry groups suggests that these results may be generalizable across a broad population.”

The four genes previously identified were growth differentiation factor 15 (GDF15), GFRAL, which produces the receptor for the GDF15 hormone of the same name, and IGFBP7 and PGR, both of which are involved in development of the placenta. The strongest link by far was to GDF15, which rises sharply during pregnancy. “We know that GDF15 and it’s receptor GFRAL are the main drivers and are in a signaling pathway that causes aversions, nausea, and vomiting,” Fejzo told GEN. “More work needs to be done to explore the other associations, but since studies suggest manipulating progesterone and/or IGFBP7 may not be safe in pregnancy, current studies are focusing on the GDF15 pathway.”

The six newly identified genes offer further clues that might help explain the basis of HG or point to new ways of treating it. They include FSHB, TCFL72 SLITRK1, SYN3, IGSF11, and CDH9. “Now that we’ve more than doubled the genes associated with HG, we can dig deeper into the biology behind this condition, as well as new possible pathways for treating it,” Fejzo said. Speaking to GEN, the researchers noted, “Because the new associations are novel, we need to understand the roles they may play in normal pregnancy and then compare that to pregnancies affected by HG.”

Of the newly identified genes, TCF7L2 stands out because it is one of the strongest genetic risk factors for type 2 diabetes and is also associated with gestational diabetes. “This is a brand-new target, and it’s not yet clear what it’s doing in pregnancy,” Fejzo said. In further commentary to GEN, Fejzo added, “The TCF7L2 gene is a type 2 diabetes-associated gene and a transcription factor that may control glucagon-like peptide-1 (GLP-1) expression and has been associated with liraglutide effects resulting in greater weight loss in obesity. So understanding its role in that rapidly evolving therapeutic arena has potential.”

Several of the other genes identified are involved in appetite and nausea, as well as brain plasticity, or how the brain learns and adapts to new information. Fejzo suggests the brain may learn to associate certain foods with feeling sick, leading to strong, lasting aversions during pregnancy. More research is needed to explore this possibility. “Other genes are associated with learning flexibility so we hypothesize that they may play a role in conditioned taste aversion and may provide new targets to alter or dampen learned aversions,” Fejzo told GEN. Historically, people believed the pregnancy hormone hCG was the cause, but we found no evidence to support that and instead, fascinatingly, we found a link to the follicle stimulating hormone receptor.”

Of the ten candidate genes six—GDF15, GFRAL, IGFBP7, PGR, TCF7L2 and SYN3—have been linked with cachexia—a wasting condition with similar symptoms to HG, including loss of appetite, weight loss and muscle wasting, the scientists noted. “Manipulation of GDF15, GFRAL, IGFBP7, PGR and TCF7L2 in animal models has shown effectiveness in reducing symptoms of cachexia. Thus, assuming analogous functions for these factors in HG, there is both genetic and biological support for causal and potentially reversible contributions for these genes in NVP.”

The researchers also found that some genes linked to HG were associated with other pregnancy outcomes. “This study also identified individual associations between risk genes and adverse outcomes including shorter pregnancy duration, pre-eclampsia, and birth weight,” they noted.

Several medications are available for treating HG, but even the most effective, Zofran, only partly relieves symptoms for about half of patients. The new findings reveal new potential treatment targets and could possibly also help match existing medications to patients based on their genetic profiles. “The ten genetic associations provide intriguing avenues to advance our understanding and pursue therapeutic pathways for a common pregnancy condition that in its most severe form is associated with substantial morbidity and even mortality for mothers and exposed offspring,” the scientists concluded.

Fejzo and her team just received approval to launch a clinical trial of metformin, a widely used diabetes medicine that increases GDF15 levels. The study will test whether taking metformin before pregnancy can desensitize women to the hormone, potentially reducing nausea and vomiting or preventing HG in women who have had it before. GEN was told, “We will be initiating a clinical trial to increase GDF15 prior to pregnancy in patients with a history of HG and planning to conceive to desensitize them to the hormone’s rapid rise in early pregnancy. We and others have shown preliminary evidence that this approach may work as in our retrospective study pre-pregnancy metformin use was associated with a significant reduction in HG risk.”

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Epigenetic Target Could Sensitize Pancreatic Cancer to Immunotherapy

Researchers have found an epigenetic switch that pancreatic cancer cells use to protect themselves against genomic instability. In a study published in Cancer Research, the team reports that blocking the epigenetic regulator DPY30 triggered immune cell infiltration into pancreatic tumors in mice, sensitizing them to immunotherapy. 

Frequently diagnosed at advanced stages, pancreatic cancer is often resistant to conventional therapies and shows limited response to immunotherapy. This leaves patients with few effective treatment options. 

“As cancer biologists, we are intrigued by the remarkable ability of pancreatic cancer cells to tolerate genomic instability and sustained replication stress while continuing to proliferate and evade immune surveillance,” said Francesca Citron, PharmD, PhD, instructor of genomic medicine at The University of Texas MD Anderson Cancer Center and lead author of the study. “This paradox led us to investigate the adaptive mechanisms that enable cancer cells to buffer genomic instability, particularly by protecting replication forks and preventing catastrophic DNA damage.” 

The researchers were interested in finding out whether epigenetic regulators may play a direct role in safeguarding the integrity of replication forks, where DNA is copied as cells divide. Under stress, DNA replication is typically disrupted, for instance as cancer cells continue dividing and accumulating mutations that result in genomic instability. However, Citron’s team discovered that pancreatic cancer cells rely on DPY30 to protect DNA replication forks under stress and continue multiplying in spite of genomic instability. 

DPY30 belongs to a group of proteins that together form the WRAD/COMPASS complex, which is involved in epigenetics regulation. The study found that this component was able to switch the entire complex from playing a global epigenetics function to a localized role at stressed replication forks, where DPY30 stabilized.

“Historically, WRAD core components, particularly DPY30, have been primarily studied in the context of histone methylation and transcriptional regulation,” said Citron. “Our findings significantly expand this paradigm by demonstrating that these factors play a direct role in maintaining replication fork stability under conditions of stress. Importantly, we also establish a link between this mechanism and modulation of the tumor immune microenvironment, providing a conceptual bridge between replication stress and immune response.”

In a mouse model of pancreatic cancer, DPY30 inhibition destabilized replication forks, leading to increased genomic instability and activating inflammatory signaling pathways. This then triggered the recruitment of tumor-infiltrating lymphocytes and turned previously immunologically “cold” tumors into “hot” tumors that responded to immunotherapy. 

“Inhibiting DPY30 leads to increased replication-associated DNA damage, which in turn robustly enhances immune signaling pathways,” said Citron. “This dual effect, on genome stability and immune activation, opens new therapeutic opportunities to impair replication fork protection while simultaneously stimulating anti-tumor immune responses.”

Furthermore, biopsies from pancreatic cancer patients showed that higher levels of DPY30 expression were associated with higher tumor grades, a poorer prognosis and lower response rates to immunotherapy. Together, these findings point at DPY30 as both a therapeutic target and a biomarker to stratify patients who are most likely to benefit from immunotherapy. 

Going forward, the researchers plan to dive deeper into how HPY30 influences immune cell recruitment and activation within the tumor microenvironment. In parallel, they will be exploring pharmacological strategies to inhibit DPY30 and testing their efficacy in preclinical studies. Citron added: “Ultimately, our goal is to develop rational combination therapies that drive more effective and durable responses in patients.”

The post Epigenetic Target Could Sensitize Pancreatic Cancer to Immunotherapy appeared first on Inside Precision Medicine.

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Novel Targets for Complex Cancer Revealed by Genetic Regulatory Node Mapping

In a new study published in Nature titled, “Mapping convergent regulators of melanoma drug resistance by PerturbFate,” researchers from The Rockefeller University have developed a platform called PerturbFate that can systematically map how diverse disease-associated genetic variations reshape cells. By tracking gene regulation in single cells over time, the team identified regulatory nodes common to diverse variations. Using melanoma drug resistance as a proof-of-concept, results showed that these shared points of control offer a path toward combination therapies that can target disease across many genetic causes. 

“Once you know that a disease is associated with hundreds of genes, how do you design one therapy to target it?” posed Junyue Cao, PhD, head of the Laboratory of Single-Cell Genomics and Population Dynamics at Rockefeller. “We wondered whether all these different genes may be mediated by some shared downstream signaling that we can discover and target instead.” 

Advances in genomic sequencing and genetic screening have allowed researchers to identify hundreds of genetic mutations linked to disease. Yet these genes often span diverse pathways with broad functionalities, from gene regulation to cell signaling, making them difficult to target collectively.  

Cao proposed that if these mutations converge on shared downstream programs, the key challenge is not to target each mutation individually, but to identify the common control points known as regulatory nodes.  

PerturbFate allows researchers to observe how different genetic changes reshape a cell in real time by tracking DNA accessibility, and RNA production and processing. By capturing these changes in the same single cell, the system reveals the networks of genes that control cell behavior and how different genetic variations can have the same effect. 

“This technology lets us perturb hundreds to thousands of genes in parallel and then measure the detailed molecular changes in each individual cell,” says Cao. “That allows us to link many different genetic perturbations to their downstream effects and identify regulatory nodes.” 

To test the platform, the authors focused on melanoma drug resistance. Using PerturbFate, they selected 143 genes linked to resistance to the common melanoma drug, Vemurafenib. PerturbFate then tracked how deactivating each of these genes reshaped the cell. Cao explains the platform captures gene expression, RNA dynamics and chromatin state, all critical components when identifying upstream regulators that drive these disease states. 

After analyzing more than 300,000 cells, the researchers found that diverse genetic perturbations pushed melanoma cells into the same drug-resistant state. Drug resistance dropped significantly when these common control points were targeted, pointing to a promising strategy for combination therapies. 

The platform also revealed an important nuance involving the transcriptional coactivator, Mediator Complex. Disrupting different parts of this same complex could trigger drug resistance through routes that ultimately converged on the same survival signal in melanoma cells, called VEGFC. Resistant cells could no longer proliferate after blocking that signal. 

The team has made both the experimental and computational tools behind PerturbFate openly available, and plans to extend the approach from cultured cells to living systems. Cao and colleagues are currently applying PerturbFate to conditions, such as aging and Alzheimer’s disease, to uncover shared vulnerabilities that can guide more effective treatments. 

“This is just a starting point,” says Cao. “Now that we’ve demonstrated the approach in a simple model, we’re working to extend it into living systems to study even more complex diseases.” 

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