Celebrated by a recent exhibition at its new building in White City, London, the MRC LMS has launched a book and website with over 100 interpretations of the phrase ‘A Picture of Health’ gathered from a broad cross-section of society.
As his Picture of Health, Professor Juanma Vaquerizas, head of the MRC LMS Developmental Epigenomics group, chose this image of a fruit fly embryo. Read why:
“Animals of all kinds must go through zygotic genome activation: After fertilisation the first developmental steps are enabled from the maternally inherited material. Then a switch occurs to full control of the developmental programme which will form a new individual using their own genome. Here this transition is happening in a fruit fly embryo. We can see the majority of nuclei in the embryo undergoing nuclear division (in blue), with a special compartment of cells called pole cells (pink) that will lead to the formation of the germline. It represents fundamental aspects of life, among them evolution – the very same mechanisms that lead to the generation of the enormous cellular complexity of an organism will also lead to mutations that can become fixed in the genome of the species driving their evolution. Zygotic genome activation is an amazing time point in the life of any organism, one that we should marvel at how nature managed to orchestrate it.”
Image by Liz Ing-Simmons
Developmental Epigenomics group, MRC London Institute of Medical Sciences, London, UK
Image copyright held by Liz Ing-Simmons
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Non-invasive blood test can detect cancer four years before diagnosis.
Non-invasive blood test can detect cancer four years before diagnosis. Thoughts health innovators?
The leading cause of death worldwide, cancer killed at least 7.6 million people in 2008, accounting for a staggering thirteen percent of all deaths globally. With no signs of abating, the number of international cancer deaths is projected to increase by forty-five percent in the next decade. The majority of deaths involving this disease are caused primarily by lung, breast, colorectal, stomach,…
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Whole Genome Bisulfite Sequencing
Whole Genome Bisulfite Sequencing (WGBS) is a bisulfite sequencing method that enables the detection of DNA methylation at the whole-genome level. This encompasses the analysis of methylation at CpG sites and less common non-CpG sites, including CNG. The detection and quantification of methylation are of critical importance for the understanding of gene expression and other processes that are subjected to epigenetic regulation.
Reduced Representation Bisulfite Sequencing
Reduced representation bisulfite sequencing (RRBS) is an efficient and high-throughput technique for analysing the genome-wide methylation profiles on a single nucleotide level. It combines restriction enzymes and bisulfite sequencing to enrich for areas of the genome with a high CpG content. Given its cost-effective and productive nature, RRBS is employed extensively across a range of fields.
Assay for Transposase-Accessible Chromatin Sequencing (ATAC-seq)
ATAC-seq (Assay for Transposase Accessible Chromatin using sequencing) is a high-throughput sequencing technology that uses the transposase Tn5 to investigate chromatin accessibility. The core principle of ATAC-seq is to use the transposase Tn5 to cleave open chromatin regions and, in doing so, to incorporate sequencing adapters into the DNA at these regions. These adapter-tagged DNA fragments are then subjected to high-throughput sequencing to identify open chromatin regions in the cell nucleus. These regions are typically sites in the genome that are readily accessible to transcription factors and other regulatory proteins. Therefore, ATAC-seq is a powerful tool for studying epigenetic changes in gene expression regulation, cell differentiation, and disease
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Advancing Leukemia Research & Treatment — Submit Your Abstract Today, Track 10: Cancer Epigenetics
Join global hematologists, oncologists, researchers, molecular biologists, and clinicians at the 12th International Cancer, Oncology & Therapy Conference, taking place April 09–11, 2026, in Dubai, UAE.
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A new method for creating induced pluripotent stem (iPS) cells includes a memory reset that puts the cells in a more embryonic-like state.
« Australian researchers have found a way to reprogram cells from adults so that they’re more like embryonic stem cells. These memory-less cells can be reprogrammed to become any kind of cell, potentially unlocking an endless supply of stem cells for research or treatment. »
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Epigenomic and transcriptomic analyses reveal differences between low-grade inflammation and severe exhaustion in LPS-challenged murine monocytes
Naler et al., Commun Biol. 2022; 5: 102.
Next-gen Precision Medicine Market to Witness Surge in Demand Owing to Rising End-use Adoption
The precision medicine market report provides extensive competitive analysis and profiles of key market players, such as, Roche Holding AG, Illumina Inc., Thermo Fisher Scientific Inc., QIAGEN, Quest Diagnostics, Laboratory Corporation of America Holdings, Novartis AG, AstraZeneca, Bristol-Myers Squibb, and Eli Lilly & Company.
The other players in the value chain include Abbott Laboratories, Almac Group, Ltd, Asuragen, Inc., Cepheid Inc, Cetics Healthcare Technologies GmbH, Ge Healthcare, Glaxosmithkline Plc, Intomics A/S., Biocrates Life Sciences Ag, and Pfizer Inc.
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The precision medicine market was valued at $3,516 million in 2016, and is estimated to reach at $7,746 million by 2023, registering a CAGR of 11.9% from 2017 to 2023. Precision medicine is based on a unique concept that states, two people infected with same disease dont need to have same physical response toward the disease. However, it depends on the surrounding environment and influence of genes and symptoms of patient. Moreover, it also depends on patients ability of responding to that particular disease, which enables the doctors and researchers to organize the required treatment.
Precision medicine commonly includes use of system biology and panomics to determine the reason for an individual patient's illness at the molecular level. Followed by the use of concentrated medications to address individual patient's illness. Precision medicine offers many advantages such as efficient treatment customized to patients needs and category of disease. Moreover, precision medicine can reduce cost of treatment and help decrease repeated administration of medications.
The precision medicine market is segmented based on technology, sequencing technology, product, application and geography. Based on technology, it is divided into genomics, transcriptomics and epigenomics. Based on sequencing technology, the market is bifurcated into sequencing by synthesis, ion semiconductor sequencing, sequencing by ligation, pyrosequencing, single molecule real time sequencing, chain termination sequencing and nanopore sequencing. Based on product, the precision medicine market is subdivided into consumables, instruments and services. Based on applications it is classified into oncology, CNS, immunology, respiratory medicine, infections, and other applications. Based on end users, it is categorized into diagnostic tool companies, pharma & biotech companies, clinical laboratories, and healthcare IT/big data Companies. Geographically, it is analyzed across North America, Europe, Asia-Pacific, and LAMEA.
The precision medicine market is expected to grow at a productive rate during the forecast period. Surge in global incidence of cancer and increase in ageing population susceptible to disease are expected to boost the demand of precision medicines. Government initiative & grants and private companies investing in R&D of precision medicines is expected to boost the market growth.
Can the study of epigenomics lead to personalized cancer treatment?
- By Fabian V. Filip , The Conversation -
Molecular insight into our own DNA is now possible, a field called personal genomics. Such approaches can let us know when we might have cancer-causing alterations in our genes.
Well-known examples are the melanoma oncogene BRAF kinase, the breast cancer gene BRCA1 and the prostate specific antigen PSA.
But there is more to cancer and other diseases than our genes. In addition to the DNA code, there is a hidden layer of regulation controlling the activity of genes – while not changing the DNA itself. This field, called epigenetics, is the study of how genes are regulated to express themselves, even though they rely on the same genetic information. A gene is still a gene, but it responds differently to many facets of its chemical environment.
For example, have you thought about why identical twins are different? How it is possible that the lifestyle of our grandparents can affect our lives today? Something beyond our DNA is at work. This is epigenetics.
The hidden layer responsible for fine-tuning alongside our DNA is called epigenomic regulation. Epigenomics is the field of quantifying epigenetic marks on a genome-wide scale, thereby capturing a snapshot of our epigenetic state.
Recently, the systems biology and cancer metabolism lab at UC Merced published discoveries about an epigenetic factor called Jumonji. This factor not only affects how an entire network of cancer genes behaves; it actually takes on the role of a cancer gene, bringing uncontrollable cell growth.
Epigenomics captures how gene activity is controlled
Already, doctors and others who diagnose diseases can, to some degree, use personal genomics tests that integrate our unique genetic makeup into clinical decision-making. However, there is more to our genome than what such tests can reveal.
Epigenetics makes sense of chemical modifications that can switch genes on or off. Importantly, none of these modifications changes the DNA sequence. Alternatively, our own cells use epigenomic regulators to control the activity of genes. If the right chemistry is in place, the right gene products are expressed at the right time.
Environmental influences like nutrition or cigarette smoke as well as our own hormones have strong epigenetic impact and affect how active our genes are.
In a disease such as cancer, epigenomic regulators such as Jumonji are often mistuned, causing them to affect gene activity. One thing they may do is to fail to put the right chemical modifications on their target genes, which rely on many factors to switch their activity on or off. This can lead to altered metabolism, which promotes unlimited cellular growth. Once cells have unlimited ability to divide, a tumor forms.
The researchers found that Jumonji is overabundant in cancer cells and promotes uncontrolled division of cancer cells, which leads to unstoppable tumor growth. Jumonji takes the role of an epigenetic master regulator of cancer genes.
In addition, Jumonji teams up with hormone-dependent regulators that are responsible for treatment-resistant cancers.
Systems biologists can help to understand how we can overcome resistances. Systems biology opens possibilities to understand regulatory signals and circuits that govern our cells. If we are able to comprehend these signals, we can design drugs to break unwanted circuits and overcome resistances. Given its hidden, complex nature, epigenomics benefits from a systems biology approach that lays open critical wiring of our cells.
Toward personalized epigenomics
Epigenomics has a lot of promise for cancer treatments, but there are still many more questions that we need to answer. What does the epigenome of a healthy person look? And how does the epigenome change as we age? How does the epigenome of a sick person differ? In the future, these important questions will be addressed by personalized epigenomics, which tries to extract information out of a comprehensive picture of a person’s epigenome.
You may ask: Why can we not create a simple test that tells us if we have good genes but an unfavorable epigenome?
Our epigenome is highly dynamic. Epigenomic regulators are nonstop at work, including Jumonji, removing or adding chemical marks allowing for transient gene readouts while blocking it in the next minute.
Is it too early for consumers to think about personalized tests? Is the information still too cryptic or too unreliable to draw conclusions?
Personal gene tests for cancer exist. Hollywood actor Ben Stiller claims a simple genetic test for abnormally high levels of the prostate antigen saved his life.
Abnormally high levels of the prostate specific antigen in the blood can mean that a man has prostate cancer, but not always. That is why the test is not FDA-approved. And this test does not take epigenetic factors into account.
Artistic illustration of an epigenomic handprint capturing regulation of a person beyond changes in DNA. In background research campus with art statue ‘New Beginnings,’ symbolizing hope for cure. Credit: Systems Biology and Cancer Metabolism Laboratory, Fabian V. Filipp
Cancer drugs against epigenomic factors promise hope
Drugs targeting the epigenomic machinery raise optimism as a viable direction of clinical research. Present-day clinical questions relevant to epigenetic research address which drug molecules modify the epigenome and which specifically kill cancer cells. It is open whether epigenetics is on the good or on the bad side of cancer. Researchers found that epigenetics can even assist the cancer cells to manipulate our own immune system and to evade the drug targeting approaches.
According to recent genomic insights, researchers compare the delicate equilibrium to Yin and Yang, complementary forces that keep each other in check. If one force overtakes the systems, it is out of equilibrium. For the cells this means either unlimited growth, cancer or death. Without doubt, once we have a better understanding of epigenetic regulation, we can design drugs that counterregulate these factors.
This is beginning to happen with some cancers. Recent breakthroughs in melanoma research identified a genetic mutation of an epigenetic player. Cancer resistance to treatment is a major obstacle. However, epigenetic drugs, on their own or in combination with other drugs, can be a viable alternative.
The epigenetic drug used in the laboratory study stops the ability of cancer cells to hide from the immune system and makes the tumor vulnerable. For cancer patients with epigenetic activation, epigenetic drugs promise hope.
Fabian V. Filipp, Assistant Professor of Systems Biology and Cancer Metabolism, University of California, Merced
This article was originally published on The Conversation. Read the original article.