Office of STEM Engagement Initiatives at the Broad Institute supports students and early-career trainees entering and succeeding in STEM careers. By building and sustaining partnerships within the community and training members of the Broad in relevant skills like scientific communication and mentorship, we empower Broadies to be ambassadors for their science. Together, these efforts prepare the next generation of scientific leaders.
The OSEI team is looking for a program coordinator to help organize and implement existing programming in our K-12 portfolio including, but not limited to: Educational Tours, Bio-Coding Club, Bio-Coding Club Educator Program, and Broad Scientists in the Classroom. The coordinator will work with the OSEI Associate Director to develop, oversee and deliver curricula and training programs that leverage the resources and strengths of the Broad community and its partners. The coordinator will also spend a smaller portion of time providing support for administrative tasks such as scheduling, travel arrangements, and other logistics. The program coordinator will join an office that employs a team-based approach to developing and delivering programming.

Principal Duties and Responsibilities

Coordinate all activities related to existing in-school STEM awareness programming, including Broad Scientists in the Classroom and local Bio-Coding Club chapters.
Provide professional development and support for educators to start Bio-Coding Clubs at their school or organization.
Attend annual Science Educators Conference; recruit Educators to expand local Bio-Coding Club and provide support and training to designees.
Oversee the NetPals and KeyPals collaboration with Cambridge School Volunteers (CSV); recruit on-site volunteers to coordinate communication and onsite experience. Work with CSV coordinators and Cambridge Public Schools contacts set up visits and engage students in fun and educational activities on their visit days.
Manage collaborations with Broad scientific groups to develop new curriculum for the Bio-Coding Club.
Assist the BSSP program manager in the coordination, planning, and support of the Broad Summer Scholars Program, working with rising high school seniors during the 6-week program.
Recruit, coordinate, and provide training to program volunteers from the Broad community.
Create and maintain calendars for programs requiring regular communication with other Broad staff and partners.
Oversee administrative tasks as needed, such as scheduling, catering, data entry, and event planning and support.
Maintain relationships with key stakeholders, including educators and STEM practitioners at other organizations and institutions.
Assist in coordination and planning of all OSEI events and programs.
Assist with scheduling and facilitating educational tours for local school groups.
Other duties as assigned.

Qualifications

BS in biology, computer science, science education, or other related scientific discipline with 2+ years of related experience; or an advanced degree without experience; or equivalent work experience.
Experience working with middle and/or high school students through informal STEM educational programming (in and/or out of school).
Demonstrated ability to develop and deliver curricula in STEM areas.
Ability to facilitate interactions with students, educators, and other administrative partners inside and outside of the Broad.
Ability to multi-task in a fast-paced environment.
Must be able to use sound judgment to handle a variety of tasks and effectively anticipate and solve problems.
Must possess a high level of initiative and the ability to work creatively and independently, as well as in a team environment.
Excellent communication skills required, including public speaking, writing, teaching, and presentations; ability to communicate with and support individuals with a wide variety of different social identities, backgrounds and experiences.

Logistics

Hybrid role: 2 days per week on-site during the academic year, increasing to 5 days per week on-site during summer program dates.
Requires regular local travel to schools
Ability to work a flexible schedule

The Broad Institute will not offer visa sponsorship for this opportunity.

The expected base pay range for this position as listed above is based on a 40 hour per week schedule. Broad provides pay ranges representing its reasonable and good faith estimate of what the organization reasonably expects to pay for a position at the time of posting. Actual compensation will vary based on factors including but not limited to, relevant skills, experience, education, qualifications, and other factors permissible by law.

At Broad, your base pay is just one part of a comprehensive total rewards package. From day one, this role offers a competitive benefits package including medical, dental, vision, life, and disability insurance; a 401(k) retirement plan; flexible spending and health savings accounts; at least 13 paid holidays; winter closure; paid time off; parental and family care leave; and an employee assistance program, among other Broad benefits.

The Broad Institute is an equal opportunity employer. All qualified applicants will receive consideration for employment without regard to race, national origin, religion, age, color, sex, disability, protected veteran status, or any other characteristic protected by local, state, or federal laws, rules, or regulations.

Should you need a reasonable accommodation to complete the application or interview process, please contact [email protected] for assistance.

About the company

What Broad Institute does: The Broad Institute conducts biomedical and genomic research to understand and treat diseases, focusing on genetic and molecular approaches. How its products work: It runs large collaborative research projects, analyzes genetic data, and develops educational tools and resources (including pandemic simulations and STEM materials) that are shared with researchers, schools, and educators. How it differs from competitors: It combines multidisciplinary collaboration with access to large-scale genomic datasets and a mix of government grants, philanthropy, industry partnerships, and intellectual property licensing to accelerate discovery, often working across academia, industry, and education sectors. What its goal is: To advance human biology and disease knowledge, translate genetic insights into diagnostics and therapies, and improve education in science and biomedical research.

Company Size

1,001-5,000

Company Stage

Late Stage VC

Total Funding

$182.5M

Headquarters

Cambridge, Massachusetts

Founded

2003

Get referred to Broad Institute

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Simplify's Take

What believers are saying

Novo Nordisk Foundation renewed $53 million on September 30, 2026 for Broad collaboration.
ARPA-H awarded up to $34.5 million on July 9, 2026 for PERC.
Broad launched CTG on July 21, 2026, institutionalizing repeatable rare-disease gene therapy.

What critics are saying

CTG and PERC remain founding-phase platforms; patients receive no clinical care yet.
Broad depends on NIH, ARPA-H, and philanthropy; funding shocks freeze translational programs.
Drug companies capture clinical upside; Broad risks becoming a discovery shop without durable royalties.

What makes Broad Institute unique

David Liu's editing platforms power over 25 clinical trials today.
Broad's DepMap now integrates nearly 150 3D cancer models, expanding target discovery.
Broad and Finland mapped immune mechanisms across 10 million cells in Nature, October 2026.

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Benefits

Health Insurance
Dental Insurance
Vision Insurance
Life Insurance
Disability Insurance
Health Savings Account/Flexible Spending Account
401(k) Retirement Plan
Paid Holidays
Paid Vacation
Parental Leave

Growth & Insights and Company News

Headcount

6 month growth

1 year growth

2 year growth

Morning Top News

Oct 1st, 2026

One drug, many rare diseases.

One drug, many rare diseases. Advertisements CNBC Advisory Board member Dr. Anna Greka has built her career on finding connections between different rare diseases. Greka, a Harvard professor and physician at Mass General Brigham, is also a member of the Broad Institute. At her lab, she oversees the Ladders to Cures Accelerator, an initiative designed to speed up the development of treatments for rare disease patients. It's a model she hopes is able to attract more investment to the space. Greka and her team are working on identifying where different rare diseases converge and share a single biological mechanism. Greka calls this approach "nodal biology". By identifying areas where rare diseases overlap, Ladders to Cures hopes to develop new types of drugs that can be used to treat multiple conditions. By developing single drugs capable of treating multiple diseases, the addressable patient population of those drugs becomes much bigger. That can make a drug more profitable, which Greka says is key to building a rare drug development model that is economically sustainable. Greka has already shown that the nodal approach can work. In 2019, she and her team published a paper outlining a mechanism they discovered for a rare kidney disease that also plays a role in diseases that impact the eye and brain. With the Ladders to Cures Accelerator, Greka hopes to discover even more nodal connections and start to develop drugs that can treat them. On October 27th, the Broad Institute will host the 3rd Annual Ladders to Cures Symposium. Greka will be there, along with her colleagues Dr. David Liu, Dr. Winston Yan, and MIT economist Andrew Lo. Ahead of the event, Becky Quick sat down with Greka to ask about the work being done at Ladders to Cures and the impact she hopes the accelerator can have on the rare community. CNBC Cures is underwritten by Alexion, AstraZeneca Rare Disease.

Technology Networks

Oct 1st, 2026

Atlas of immune cells explains how genetic variants cause disease.

Atlas of immune cells explains how genetic variants cause disease. A new method reveals which genetic variants are most important in disease and how cells "buffer" the expression of genes critical for health. Published: October 1, 2026 Read time: 4 minutes Scientists have identified thousands of genetic differences that change a person's risk of disease, but working out how they actually impact biology - an important step toward creating new treatments - has been much more challenging. One reason is that many of the genetic variants associated with disease aren't found in genes themselves, but within the vast stretches of DNA that regulate gene activity. Now, scientists have developed a new approach to connecting disease-linked regulatory variants to the actual genes they control. Their results, in Nature, reveal that these variants are more likely to influence disease risk if they alter chromatin accessibility - the openness of a section of the genome - in a way that then changes expression of a specific gene, compared to variants that affect only chromatin accessibility or gene expression alone. The finding could help other scientists prioritize the genetic variants that are most important in a particular disease. The research team applied their method to millions of immune cells from more than 1,100 blood donors enrolled in FinnGen, a large medical research project in Finland. The resulting atlas revealed likely molecular mechanisms by which tens of thousands of genetic variants cause hundreds of different diseases and health traits - including autoimmune hypothyroidism, inflammatory bowel disease, asthma, Alzheimer's disease, and skin cancer. * Daily Breaking Science News * Tailored newsletters * Exclusive eBooks, infographics and online events The new work was led by researchers at the Broad Institute, Massachusetts General Hospital, and the Institute for Molecular Medicine Finland (FIMM) at the University of Helsinki, in collaboration with the Finnish Red Cross Blood Service and BioBank Japan. "Immune dysregulation sits at the root of an enormous range of human diseases, from autoimmunity to cancer to neurodegeneration," said Ramnik Xavier, a co-senior author of the study, a core institute member at the Broad Institute, and Kurt Isselbacher Professor at Massachusetts General Hospital and Harvard Medical School. "What excites me about this work is that it doesn't just tell us that a gene matters; it tells us the molecular mechanism, which can point toward therapeutic strategies." The team also found that many of the genes most critical to health and survival are wired to dozens of regulatory elements in the genome at once, each contributing only a small change to gene expression. That redundancy, they found, keeps the expression of these important genes relatively stable and is also why these genes have been so hard to study using traditional methods. "One of the biggest gaps in human genetics has been between finding a disease-associated variant and understanding its function," said Mark Daly, co-senior author, an institute member at the Broad Institute, co-director of Broad's Program in Medical and Population Genetics, and founding chief of the Analytical and Translational Genetics Unit at Massachusetts General Hospital. "This atlas provides reliable evidence that we can now systematically connect genetic association signals to molecular switches affecting specific genes and cells at scale. With confirmatory editing experiments now possible, we have a path to unlocking the power of human genetics to provide novel insights into causal disease mechanisms." Open or closed. Daly, Xavier, and their colleagues had previously analyzed data from FinnGen - a research project that integrates genomic information and health records for more than 500,000 people in Finland. The 2023 study using FinnGen data pinpointed hundreds of genomic regions linked to diseases. In this new work, they wanted to connect those risk variants to their molecular consequences. In the millions of immune cells from FinnGen donors, the researchers measured both gene expression and chromatin accessibility in the same cells. This let them connect whether a genetic variant was correlated to a change in that openness in a particular cell type, and then whether that change in openness was also correlated with a change in gene expression. By collecting and analyzing this data from each of the millions of individual cells, the team had enough statistical power to show how cells maintain stable expression of genes that are important for life: by hooking these genes up to many weak regulatory switches rather than a single strong one. That explained why studies looking only at gene expression often missed the full story: a switch that matters for disease may move expression only slightly - too little for those studies to detect. "We think the body wants precise control over the expression of its most important genes; it doesn't want any single genetic variant to be able to swing that expression too far on its own," said Masahiro Kanai, first author of the study, a postdoctoral scholar at the Broad Institute and an instructor in medicine at the Center for Computational and Integrative Biology, Massachusetts General Hospital and Harvard Medical School. "So instead of relying on one strong switch, these genes are controlled by many weaker ones. We call this regulatory buffering, because it dampens the effect of any single chromatin change before it reaches gene expression, like a shock absorber." From signal to mechanism. The researchers chose to build their atlas from immune cells because immune dysregulation is at the root of many seemingly different diseases affecting different tissues. Across eight broad types of immune cells, the team carried out the full analysis of chromatin accessibility and gene expression for thousands of different disease-linked genes. They then traced the precise molecular mechanisms behind several disease-linked genetic variants. One, inside a gene called TNRC18, had been flagged in the 2023 FinnGen study as being linked to inflammatory bowel disease, with no known mechanism. The new data show the variant reduces TNRC18 expression in T cells, and it does this most strongly in a subset called T helper 1 cells, pushing those cells toward a more inflammatory state. Another example, involving the genes IL4R and IL21R, helped explain why one variant lowers the risk of asthma while another variant in the same genetic region instead raises the risk of autoimmune hypothyroidism. The thyroid-risk variant turns up IL21R, the receptor for an immune signal called IL-21, and mice lacking that receptor on their T cells are protected from the same thyroid complication. The finding points toward blocking IL-21 as a potential way to treat a similar thyroid complication that can occur as a side effect of cancer immunotherapy. The team has made its data and methods freely available to spur new research. They caution that many of the connections they've mapped are still hypotheses rather than confirmed mechanisms. They are now working to profile immune cells from diseased tissue directly rather than relying only on samples from healthy individuals. "This is a launching pad for future research," said Daniel Graham, a study co-author and an institute scientist at Broad. "There's a lot of reason to be optimistic about the power of using this type of data to uncover mechanisms of disease." Reference: Kanai M, Delorey TM, Honkanen J, et al. Population-scale immune multiome atlas reveals regulatory disease mechanisms. Nature. 2026:1-15. doi: 10.1038/s41586-026-11078-2 This article has been republished from materials linked above. Note: material may have been edited for length and content. For further information, please contact the cited source. Add Technology Networks as a preferred Google source to see more of its trusted coverage. Chosen for you

Broad Institute

Sep 30th, 2026

Atlas of immune cells explains how genetic variants cause disease.

Atlas of immune cells explains how genetic variants cause disease. A new method reveals which genetic variants are most important in disease and how cells "buffer" the expression of genes critical for health. By Sarah C.P. Williams September 30, 2026 Highlights. * Geneticists have long struggled to find the mechanisms by which many disease-linked genetic variants actually cause disease. * A new atlas of more than 10 million immune cells from more than 1,100 Finnish blood donors provides a way to connect disease-associated regulatory variants with the genes they control. * The approach relies on looking at chromatin accessibility - the openness of the DNA around a certain genetic variant - and how that openness correlates with the expression of nearby genes. Scientists have identified thousands of genetic differences that change a person's risk of disease, but working out how they actually impact biology - an important step toward creating new treatments - has been much more challenging. One reason is that many of the genetic variants associated with disease aren't found in genes themselves, but within the vast stretches of DNA that regulate gene activity. Now, scientists have developed a new approach to connecting disease-linked regulatory variants to the actual genes they control. Their results, in Nature, reveal that these variants are more likely to influence disease risk if they alter chromatin accessibility - the openness of a section of the genome - in a way that then changes expression of a specific gene, compared to variants that affect only chromatin accessibility or gene expression alone. The finding could help other scientists prioritize the genetic variants that are most important in a particular disease. The research team applied their method to millions of immune cells from more than 1,100 blood donors enrolled in FinnGen, a large medical research project in Finland. The resulting atlas revealed likely molecular mechanisms by which tens of thousands of genetic variants cause hundreds of different diseases and health traits - including autoimmune hypothyroidism, inflammatory bowel disease, asthma, Alzheimer's disease, and skin cancer. The new work was led by researchers at the Broad Institute, Massachusetts General Hospital, and the Institute for Molecular Medicine Finland (FIMM) at the University of Helsinki, in collaboration with the Finnish Red Cross Blood Service and BioBank Japan. "Immune dysregulation sits at the root of an enormous range of human diseases, from autoimmunity to cancer to neurodegeneration," said Ramnik Xavier, a co-senior author of the study, a core institute member at the Broad Institute, and Kurt Isselbacher Professor at Massachusetts General Hospital and Harvard Medical School. "What excites me about this work is that it doesn't just tell us that a gene matters; it tells us the molecular mechanism, which can point toward therapeutic strategies." The team also found that many of the genes most critical to health and survival are wired to dozens of regulatory elements in the genome at once, each contributing only a small change to gene expression. That redundancy, they found, keeps the expression of these important genes relatively stable and is also why these genes have been so hard to study using traditional methods. "One of the biggest gaps in human genetics has been between finding a disease-associated variant and understanding its function," said Mark Daly, co-senior author, an institute member at the Broad Institute, co-director of Broad's Program in Medical and Population Genetics, and founding chief of the Analytical and Translational Genetics Unit at Massachusetts General Hospital. "This atlas provides reliable evidence that we can now systematically connect genetic association signals to molecular switches affecting specific genes and cells at scale. With confirmatory editing experiments now possible, we have a path to unlocking the power of human genetics to provide novel insights into causal disease mechanisms." Open or closed. Daly, Xavier, and their colleagues had previously analyzed data from FinnGen - a research project that integrates genomic information and health records for more than 500,000 people in Finland. The 2023 study using FinnGen data pinpointed hundreds of genomic regions linked to diseases. In this new work, they wanted to connect those risk variants to their molecular consequences. In the millions of immune cells from FinnGen donors, the researchers measured both gene expression and chromatin accessibility in the same cells. This let them connect whether a genetic variant was correlated to a change in that openness in a particular cell type, and then whether that change in openness was also correlated with a change in gene expression. By collecting and analyzing this data from each of the millions of individual cells, the team had enough statistical power to show how cells maintain stable expression of genes that are important for life: by hooking these genes up to many weak regulatory switches rather than a single strong one. That explained why studies looking only at gene expression often missed the full story: a switch that matters for disease may move expression only slightly - too little for those studies to detect. "We think the body wants precise control over the expression of its most important genes; it doesn't want any single genetic variant to be able to swing that expression too far on its own," said Masahiro Kanai, first author of the study, a postdoctoral scholar at the Broad Institute and an instructor in medicine at the Center for Computational and Integrative Biology, Massachusetts General Hospital and Harvard Medical School. "So instead of relying on one strong switch, these genes are controlled by many weaker ones. We call this regulatory buffering, because it dampens the effect of any single chromatin change before it reaches gene expression, like a shock absorber." From signal to mechanism. The researchers chose to build their atlas from immune cells because immune dysregulation is at the root of many seemingly different diseases affecting different tissues. Across eight broad types of immune cells, the team carried out the full analysis of chromatin accessibility and gene expression for thousands of different disease-linked genes. They then traced the precise molecular mechanisms behind several disease-linked genetic variants. One, inside a gene called TNRC18, had been flagged in the 2023 FinnGen study as being linked to inflammatory bowel disease, with no known mechanism. The new data show the variant reduces TNRC18 expression in T cells, and it does this most strongly in a subset called T helper 1 cells, pushing those cells toward a more inflammatory state. Another example, involving the genes IL4R and IL21R, helped explain why one variant lowers the risk of asthma while another variant in the same genetic region instead raises the risk of autoimmune hypothyroidism. The thyroid-risk variant turns up IL21R, the receptor for an immune signal called IL-21, and mice lacking that receptor on their T cells are protected from the same thyroid complication. The finding points toward blocking IL-21 as a potential way to treat a similar thyroid complication that can occur as a side effect of cancer immunotherapy. The team has made its data and methods freely available to spur new research. They caution that many of the connections they've mapped are still hypotheses rather than confirmed mechanisms. They are now working to profile immune cells from diseased tissue directly rather than relying only on samples from healthy individuals. "This is a launching pad for future research," said Daniel Graham, a study co-author and an institute scientist at Broad. "There's a lot of reason to be optimistic about the power of using this type of data to uncover mechanisms of disease." Paper cited: Kanai M, Delorey TM, et al. Population-scale immune multiome atlas reveals regulatory disease mechanisms. Nature. Online September 30, 2026. DOI: 10.1038/s41586-026-11078-2 Support for the study was provided in part by the National Institutes of Health (DK043351, DK062432, R00HG012222, R01HG014518), the Klarman Cell Observatory, the FinnGen Project, the Department of Molecular Biology at MGH, the Masason Foundation, JSPS KAKENHI (25H01057), AMED (JP24km0405217, JP24ek0109594, JP24ek0410113, JP24kk0305022, JP223fa627001, JP223fa627002, JP223fa627010, JP223fa627011, JP22zf0127008, JP24tm0524002, JP24wm0625504, JP24gm1810011), JST Moonshot R&D (JPMJMS2021, JPMJMS2024), Ono Pharmaceutical Foundation for Oncology, Immunology, and Neurology, a Baelz Research Grant, and the RIKEN TRIP initiative (AGIS).

Position Hire

Sep 4th, 2026

MIT scientists develop technique to track gene activity over time in individual cells.

MIT scientists develop technique to track gene activity over time in individual cells. On September 1, the Broad Institute of MIT and Harvard announced a new method for tracking gene activity in cells over time. Previously, scientists had to destroy cells to access their RNA, providing only a one-time snapshot of a cell's genetic activity. The new technique allows living cells to report their own transcriptomes, enabling analysis without cell death. Detailed in the journal Cell, the method involves virus-like particles that cells use to package and release RNA into the surrounding culture medium. Researchers can repeatedly sample this medium to observe changes in gene activity in the same cell population as they develop or respond to stimuli. This approach has been tested on various cellular models, offering insights into disease progression and drug effects. Paul Blainey, a senior author of the study and a professor at MIT, emphasized the importance of developing practical tools for the scientific community. The concept, once considered science fiction, demonstrates the potential of long-term, high-risk research. The effort began over a decade ago, aiming to create a non-destructive RNA sequencing method. The team drew inspiration from retroviruses, which naturally package RNA genomes for cell-to-cell transmission. They engineered cells to produce a retroviral protein capable of encapsulating cellular RNA. This protein helps form virus-like particles that release RNA into the culture medium, allowing scientists to sequence the RNA without harming the cells. Co-first author Mohamad Najia highlighted the broader applicability of this molecularly encoded solution compared to traditional methods involving robotics or mechanical biopsies. The study, led by Najia, Jacob Borrajo, and Anna Le, demonstrated the method's effectiveness in various cell types, including human cancer and stem cells. The researchers also tested the method on complex systems like human endothelial cell spheroids and organ-on-a-chip devices. The technique revealed short-term transcriptional changes and gene expression dynamics related to tissue formation. Collaborating with MIT's Linda Griffith, they showed the method's utility in monitoring gene activity in organ models. The Broad team is exploring further applications and refining the technique for single-cell studies. They encourage scientists interested in cellular and tissue changes over time to adopt their innovative method.

Labroots

Sep 2nd, 2026

CRISPR pooled libraries: optimizing knockout library design.

CRISPR pooled libraries: optimizing knockout library design. * Laura Drepanos Computational Associate III, Broad Institute of MIT and Harvard BIOGRAPHY * Andrew Hempstead, PhD Associate Director of Scientific Engagement and Success, Addgene BIOGRAPHY Date & Time Date: July 22, 2026 Time: 9:00 AM PT, 12:00 PM ET CRISPR-Cas9 knockout pooled libraries have allowed researchers to conduct screens to identify genes important in varying cellular functions for further study. Addgene has played an important role in the dissemination of this technology, distributing CRISPR pooled libraries to thousands of researchers around the world. The Genetic Perturbation Platform (GPP) at the Broad Institute of MIT and Harvard has recently developed the Julianna and Jacquere knockout pooled libraries for screens in human and mouse cells. These pooled libraries have balance off-target and on-target considerations for an optimized design. This webinar will be co-presented by Addgene and the GPP. Addgene will provide a introduction to CRISPR pooled libraries, the landscape of types available, their applications, and design considerations. The Doench Lab will then describe the considerations for the construction of these new pooled libraries, a comparison to other available tools, and their work to validate the new optimized libraries. We'll conclude with information about how to access these new resources, including their availability as ready-to-use lentiviral preparations. At Addgene, we are committed to supporting researchers both by providing the high-quality materials you need and by equipping you with the knowledge and resources to use them successfully. If you are new to using pooled libraries, or embarking on a CRISPR screen in your lab, this webinar provide you with the information you need to use an optimized tool for your research. Learning Objectives: * Describe CRISPR pooled libraries and their research applications * Identify considerations for CRISPR-Cas9 knockout library design * Explain the optimization of the Julianna and Jacquere pooled libraries You May Also Like Sep 2, 2026, 09:00 AM PDT C.E. CREDITS Las infecciones congénitas continúan siendo una causa importante de morbimortalidad fetal y neonatal, lo que hace fundamental contar con estrategias diagnósticas oportun... Speaker: Dr. Daniel Aguirre Chavarría 8 Sept 2026 10:30am IST |1:00pm SGT | 2:00pm KST | 3:00pm AEST | 6:00pm NZDT Understanding the tissue microenvironment in tumour samples is an important factor for predicting response to different treatment regimens. Highly multiplexed imaging of tenfolds of protein... Speaker: Charlotte Stadler, PhD, Adyary Fallarero, PhD, MBA Sep 8, 2026, 07:00 AM PDT Circulating calprotectin has emerged as a sensitive and clinically valuable biomarker reflecting inflammatory activity across a range of rheumatic diseases. Unlike traditional acute-phase ma... Speaker: Dirk Föll, Univ.-Prof., Dr., Marija Jelusic, Prof., MD, MSc, PhD, Tomáš Milota, Assoc. Prof., MD, PhD Sep 8, 2026, 08:00 AM PDT Understanding how cells consume oxygen is fundamental to biology, yet most researchers capture this only at a single time point, missing the full metabolic picture. The Resipher measures oxy... Speaker: Dr. William Hotham, PhD, MRes, BSc (Hons) Sep 15, 2026, 07:00 AM PDT C.E. CREDITS The Plachta lab has pioneered the use of live-imaging approaches to discover how the preimplantation embryo forms in real time. Our recent findings help to transform the field of preimplanta... Speaker: Nicolas Plachta, Ph.D Sep 15, 2026, 08:00 AM PDT Join us for an interactive webinar focused on the practical analysis of Next Generation Flow(TM) measurable residual disease (MRD) in Multiple Myeloma through a real case example. We will... Speaker: Javier Pérez Peña, PhD