Daily Archives: December 22, 2021

Genetic Tests Prompt Therapy Adjustments in Epilepsy – Medscape

Posted: December 22, 2021 at 1:36 am

Physicians at a Boston hospital adjusted medical management for nearly three-quarters of patients with infantile- or childhood-onset epilepsy who were diagnosed with genetic epilepsy, researchers reported at the annual meeting of the American Epilepsy Society. The findings provide new insight into the usefulness of genetic tests in children with epilepsy of unknown cause.

Genetic testing is significantly impacting medical care in a population of individuals with infantile- or childhood-onset epilepsy. Genetic testing should be included as part of the standard evaluation of individuals with unexplained pediatric epilepsy as a means of achieving diagnostic precision and informing clinical management, study lead author Isabel Haviland, MD, a neurologist with Boston Childrens Hospital/Harvard Medical School, said in an interview.

According to Haviland, the causes of epilepsy are unexplained in an estimated two-thirds of pediatric epilepsy cases. Increasingly, when genetic testing is available, previously unexplained cases of pediatric epilepsy are being found to have single-gene etiologies, she said. Though a genetic diagnosis in this population has implications for medical care, the direct impact on medical management in a clinical setting has not been measured. We aimed to describe the impact of genetic diagnosis on medical management in a cohort of individuals with pediatric epilepsy.

Researchers tracked 602 patients at Boston Childrens Hospital who received next-generation gene sequencing testing from 2012 to 2019. Of those, Haviland said, 152 (25%) had a positive result that indicated genetic epilepsy (46% female, median age of onset = 6 months [2-15 months]). These patients were included in the study.

We documented an impact on medical management in nearly three-fourths of participants (72%), Haviland said. A genetic diagnosis affected at least one of four categories of medical management, including care coordination (48%), treatment (45%), counseling about a change in prognosis (28%), and change in diagnosis for a few individuals who had a prior established diagnosis (1%).

As examples, she mentioned three cases:

Testing revealed that a subject has a disease-causing genetic variant in a gene called PRRT2. This gene is involved in the release of neurotransmitters in the brain, Haviland said. Thanks to his diagnosis, he was treated with the antiseizure medication oxcarbazepine, which is often effective for epilepsy caused by variants in this gene. He had excellent response to the medication and later became seizure free.

A subject had a variation in the SCN1A gene that causes types of epilepsy. At the time of his diagnosis, there was a trial for a medication called fenfluramine being offered for individuals with SCN1A variants, and his family elected to participate, she said. This medication was later approved by the [Food and Drug Administration] for SCN1A-related epilepsy.

Testing identified disease-causing variant in the GRIN2A gene in another subject. This gene is involved in brain cell communication, Haviland said. This individual was treated with memantine, which acts on the specific biological pathway affected by the gene. This treatment would not have been considered without the genetic diagnosis as it is currently only approved for Alzheimers disease.

In addition, Haviland said, researchers found that there was impact on medical management both in those with earlier age of epilepsy onset (under 2 years) and those with later age of onset, as well as both in those with developmental disorders (such as autism spectrum disorder, intellectual disability and developmental delay) and those with normal development.

As for the cost of genetic tests, Haviland pointed toa 2019 studythat she said estimated epilepsy panel testing runs from $1,500 to $7,500, and the whole exome sequencing from $4,500 to $7,000. Insurers sometimes cover testing, but not always, she said. In some cases, insurance will only cover testing if it is documented that results will directly alter medical management, which highlights the importance of our findings.

No study funding was reported. Haviland and several other authors report no disclosures. One author reports consulting fees from Takeda, Zogenix, Marinus, and FOXG1 Research Foundation. Another author reports research support from the International Foundation for CDKL5 Research.

This story originally appeared onMDedge.com, part of the Medscape Professional Network.

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How to Know What Strain of COVID-19 You Have – Do Doctors Know What Variant You Have? – Prevention.com

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The Omicron variant of COVID-19 has quickly taken over as the dominant strain of the virus in the United States. Omicron, which was responsible for just 0.7% of COVID-19 cases in the country on December 4, was responsible for a whopping 73.2% of cases on December 18and that percentage is expected to grow.

With this, Omicron has unseated the Delta variant as the dominant strain of SARS-CoV-2, the virus that causes COVID-19, in the country. If youre diagnosed with COVID-19, its more than understandable to want to know what strain of COVID you have. While doctors say this isnt easy information to obtaineven for themthere may be a way to learn what strain of COVID-19 you have. Heres what you need to know about how to know what strain of COVID you have.

When the Centers for Disease Control and Prevention (CDC) releases information on percentages of variants in the U.S., theyre not analyzing every single positive test in the country to get those numbers, explains Thomas Russo, M.D., professor and chief of infectious disease at the University at Buffalo in New York.

Instead, the CDC conducts genetic sequencing on a percentage of positive tests across the country. For example, to get the latest results, the CDC analyzed 160 test results from Alabama, 4,157 from Arizona, 18,424 from California, and so on, to get a breakdown of what percentage of those positive tests matched up with a particular strain of COVID-19.

CDC officials and lab technicians dont even know whose test results theyre analyzingfor privacy purposes, theyre de-identified before testing. Meaning, your name is taken out of the equation. As a result, the CDC couldnt call you or your doctor and say what strain of COVID-19 you had, even if they had the manpower to do it, Dr. Russo points out.

Not usually, and there are a few reasons for this. The tests that are run by doctors in offices and hospitals dont sequence and specify the variant, says infectious disease expert Amesh A. Adalja, M.D., a senior scholar at the Johns Hopkins Center for Health Security. The rapid antigen tests that are often used to get quick results instead just tell if the test result is positive or negative for COVID-19.

Even a PCR test, which is considered the gold standard of COVID-19 testing, is not going to tell youits not going to sequence the test, Dr. Adalja says. PCR testing can also take days to give you results, which is why your doctor will typically just do a rapid test in their office to help you know quickly whether you have COVID-19 or not, Dr. Russo explains.

Heres where things get a little tricky. The Omicron variant has a particular genetic sequencing that can show up differently on PCR test results that you wouldnt see with other strains of COVID-19, like Delta. Its called S-gene target failure and can show up as a band drop-out on the test results, Dr. Russo says.

This can give you a hint that its Omicron, but its not definitive, Dr. Adalja says. Right now, if you got a PCR test, the lab technician could tell you that this looks consistent with Omicron.

That said, Dr. Adalja points out that most family medicine doctors arent going to be asking about thisthey typically just want to know if you're positive or negative. Its more something that infectious disease experts and microbiologists would ask about. Still, he says, If you wanted to know and your doctor gave you a PCR test, you could ask them if there was S-gene target failure. If there is, for all intents and purposes, thats an Omicron.

Theres a slight caveat with all of this, though: Dr. Russo points out that not every case of Omicron shows up with S-gene target failure on a PCR test result. Were still trying to understand why that is, he says. So, its possible to have Omicron and not have that show up on a PCR test resultor you could simply be infected with the Delta strain.

It wont be a slam-dunk diagnosis, but there may be some indication if you have one variant or the other, depending on your COVID-19 symptoms and vaccination status, Dr. Russo says.

If youre fully vaccinated, its been at least two weeks since youve had a booster shot, and you still contract COVID-19, the odds are high that you have the Omicron variant, Dr. Russo says. Statistically speaking, youre more likely to be infected with Omicron than Delta anyway, he says. But thats particularly true if youve been boostedOmicron seems to be more resistant to vaccination.

According to a recent CDC study, those symptoms may include:

But if you havent been vaccinated against COVID-19, Omicron and Delta are likely to cause similar symptoms of COVID-19. Per the CDC, those include:

For the average-risk patient, it doesnt really matter, Dr. Russo says. At the end of the day, if youre infected, you want to go ahead and monitor for more serious symptoms like shortness of breath and present to your healthcare provider, regardless of if youre infected with Delta or Omicron, he says. For healthcare providers, symptoms and severity of illness usually drive treatment.

There is one exception, though. Certain monoclonal antibody treatments dont work against Omicron, Dr. Adalja says. He specifically cites the Eli Lilly monoclonal antibodies as being expected to be less effective against the variant, while GSKs monoclonal antibody treatment is expected to do well against Omicron. Its important from a clinical perspective for someone who is high risk to know that information, Dr. Adalja says.

Still, getting that information within the needed timeframe may be challenging unless the diagnosis was via PCR and S-gene target failure occurred and that information was readily available to the provider, Dr. Russo says. Basically, there are a lot of ifs involved. Given that Omicron is now the dominant strain of COVID-19, Dr. Adalja says that resources are likely to shift to allow for more production of GSK's monoclonal antibody treatment, just to be safe.

Overall, doctors say its not vital for you or most other COVID-19 patients to know what strain of the virus you have. However, it doesnt hurt to ask.

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Outlook on the Advanced Therapy Medicinal Products CDMO Global Market to 2028 – Rising Number of Clinical Trials for ATMP is Driving Growth -…

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DUBLIN, Dec. 21, 2021 /PRNewswire/ -- The "Global Advanced Therapy Medicinal Products CDMO Market Size, Share & Trends Analysis Report by Product (Gene Therapy, Cell Therapy, Tissue Engineered), Phase, Indication, Region, and Segment Forecasts, 2021-2028" report has been added to ResearchAndMarkets.com's offering.

The global advanced therapy medicinal products CDMO market size is expected to reach USD 12.9 billion by 2028, according to the report. It is expected to expand at a CAGR of 12.0% from 2021 to 2028.

The advanced therapy medicinal products are a group of biological products for human use that involve gene therapy products, cell therapy products, and tissue-engineered products. The growth of the market is credited to the increasing clinical trials of ATMP and the rising awareness and belief among researchers regarding the benefits of advanced therapy. The COVID-19 pandemic has significantly disrupted the cell and gene therapy industry due to the complexity in the manufacturing process.

The COVID-19 pandemic has adversely affected the overall medical industry, but the pandemic boosted the operations and development of advanced therapy due to the high requirement of the products such as mesenchymal stromal cells (MSCs) for the treatment of the virus. The regulations put forward by the FDA and government authorities have created a safe environment for the healthcare workers and allowed emergency approval for the supply of essential raw materials and faster development of the vaccines and other therapy products.

Technological advancement has been a major part of tissue engineering in the last few years. This method helps to replace or restore the injured tissues and organ function. Similarly, gene and cell therapy is attracting many patients for the treatment of rare diseases, the cases of which are augmenting globally.

Advanced Therapy Medicinal Product CDMO Market Report Highlights

Key Topics Covered:

Chapter 1 Methodology and Scope

Chapter 2 Executive Summary

Chapter 3 Advanced Therapy Medicinal Products CDMO Market: Variables, Trends, & Scope3.1 Market Segmentation and Scope3.2 Market Dynamics3.2.1 Market Driver Analysis3.2.1.1 Rising number of clinical trials for ATMP3.2.1.2 Increasing outsourcing activities3.2.1.3 Growing awareness of the treatment3.2.2 Market Restraint Analysis3.2.2.1 Stringent regulatory approvals3.2.2.2 High cost of outsourcing3.3 Penetration & Growth Prospect Mapping3.4 Advanced Therapy Medicinal Products CDMO: Market Analysis Tools3.4.1 Industry Analysis - Porter's3.4.1.1 Porter's Five Forces Analysis3.4.2 PESTEL Analysis

Chapter 4 Advanced Therapy Medicinal Products CDMO Market: Product Estimates4.1 Market Share Analysis, 2020 & 20284.2 Gene Therapy4.2.1 Gene therapy market, 2016 - 2028 (USD Billion)4.3 Cell Therapy4.3.1 Cell therapy market, 2016 - 2028 (USD Billion)4.4 Tissue Engineered4.4.1 Tissue engineered market, 2016 - 2028 (USD Billion)4.5 Others4.5.1 Market, 2016 - 2028 (USD Billion)

Chapter 5 Advanced Therapy Medicinal Products CDMO Market: Phase Estimates5.1 Market Share Analysis, 2020 & 20285.2 Phase I5.2.1 Phase I market, 2016 - 2028 (USD Billion)5.3 Phase II5.3.1 Phase II market, 2016 - 2028 (USD Billion)5.4 Phase III5.4.1 Phase III market, 2016 - 2028 (USD Billion)5.5 Phase IV5.5.1 Phase IV market, 2016 - 2028 (USD Billion)

Chapter 6 Advanced Therapy Medicinal Products CDMO Market: Indication Estimates6.1 Market Share Analysis, 2020 & 20286.2 Oncology6.2.1 Oncology market, 2016 - 2028 (USD Billion)6.3 Cardiology6.3.1 Cardiology market, 2016 - 2028 (USD Billion)6.4 Central Nervous System6.4.1 Central nervous system market, 2016 - 2028 (USD Billion)6.5 Musculoskeletal6.5.1 Musculoskeletal market, 2016 - 2028 (USD Billion)6.6 Infectious Disease6.6.1 Infectious disease market, 2016 - 2028 (USD Billion)6.7 Dermatology6.7.1 Dermatology market, 2016 - 2028 (USD Billion)6.8 Endocrine, Metabolic, Genetic6.8.1 Endocrine, metabolic, genetic market, 2016 - 2028 (USD Billion)6.9 Immunology & inflammation6.9.1 Immunology & inflammation market, 2016 - 2028 (USD Billion)6.10 Ophthalmology6.10.1 Ophthalmology market, 2016 - 2028 (USD Billion)6.11 Haematology6.11.1 Haematology market, 2016 - 2028 (USD Billion)6.12 Gastroenterology6.12.1 Gastroenterology market, 2016 - 2028 (USD Billion)6.13 Others6.13.1 Others market, 2016 - 2028 (USD Billion)

Chapter 7 Advanced Therapy Medicinal Products CDMO Market: Regional Analysis

Chapter 8 Company Profiles8.1 Strategic Framework8.2 Company Profiles8.2.1 Celonic8.2.1.1 Company Overview8.2.1.2 Financial performance8.2.1.3 Product Benchmarking8.2.1.5 Strategic Initiatives8.2.2 Bio Elpida8.2.2.1 Company Overview8.2.2.2 Financial performance8.2.2.3 Product Benchmarking8.2.2.6 Strategic Initiatives8.2.3 CGT Catapult8.2.3.1 Company Overview8.2.3.2 Financial performance8.2.3.3 Product Benchmarking8.2.3.6 Strategic Initiatives8.2.4 Rentschler Biopharma SE8.2.4.1 Company Overview8.2.4.2 Financial performance8.2.4.3 Product Benchmarking8.2.4.6 Strategic Initiatives8.2.5 AGC Biologics8.2.5.1 Company Overview8.2.5.2 Financial performance8.2.5.3 Product Benchmarking8.2.5.6 Strategic Initiatives8.2.6 Catalent8.2.6.1 Company Overview8.2.6.2 Financial performance8.2.6.3 Product Benchmarking8.2.6.6 Strategic Initiatives8.2.7 Lonza8.2.7.1 Company Overview8.2.7.2 Financial Performance8.2.7.3 Product Benchmarking8.2.7.5 Strategic Initiatives8.2.8 WuXi Advanced Therapies8.2.8.1 Company Overview8.2.8.2 Financial performance8.2.8.3 Product Benchmarking8.2.8.5 Strategic Initiatives8.2.9 BlueReg8.2.9.1 Company Overview8.2.9.2 Financial performance8.2.9.3 Product Benchmarking8.2.9.6 Strategic Initiatives8.2.10 Minaris Regenerative Medicine8.2.10.1 Company Overview8.2.10.2 Financial performance8.2.10.3 Product Benchmarking8.2.10.5 Strategic Initiatives8.2.11 Patheon8.2.11.1 Company Overview8.2.11.2 Financial performance8.2.11.3 Product Benchmarking8.2.11.5 Strategic Initiatives

For more information about this report visit https://www.researchandmarkets.com/r/rjc62f

Media Contact:

Research and Markets Laura Wood, Senior Manager [emailprotected]

For E.S.T Office Hours Call +1-917-300-0470 For U.S./CAN Toll Free Call +1-800-526-8630 For GMT Office Hours Call +353-1-416-8900

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Low expression of PLAT in Breast cancer | IJGM – Dove Medical Press

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Introduction

Breast cancer (BC) accounts for the highest incidence of tumors globally and is the leading cause of death of female cancer patients.1 In recent years, the application of precise surgery and adjuvant systemic treatments (chemotherapy, radiotherapy, endocrine therapy, and molecular targeting drugs) dramatically enhances the therapeutic effect. The prognosis of BC patients remains unsatisfactory, however. Screening and diagnosis are essential to reduce BC patients incidence rate and mortality rate in the early stage.2 Although clinical, pathological, and molecular features are commonly used to predict prognosis, the underlying pathogenesis of BC invasiveness is still poorly understood. Minimally invasive biomarkers to detect early BC and gauge treatment response are crucial in BC research.3

Tumor microenvironment (TME) plays a vital role in tumor progression and the overall efficacy of cancer treatments, such as immunotherapy, chemotherapy, and radiotherapy.4,5 The abundance of immune infiltrating cells in TME affects tumor initiation, progression, metastasis, and treatment resistance.6

Tissue type plasminogen activator (PLAT) and urokinase type plasminogen activator (PLAU), two essential proteins of the plasminplasminogen system, not only participated in the intravascular dissolution of blood clots but also played a significant role in tumor progression and metastasis.7 PLAU has been involved in different steps of cancer progression, such as tumorigenesis,8 angiogenesis,9 cell invasion, and metastasis.10 PLAT can affect the development of many tumors. BC patients with low PLAT levels often have a poor prognosis, while PLAT levels are higher in melanoma, neuroblastoma, acute myeloid leukemia, and pancreatic cancer.11,12

Our study evaluated the expression level of PLAT in BC and the relationships between PLAT expression and clinical pathological characteristics, together with prognosis, through publicly available data from The Cancer Genome Atlas (TCGA). PLAT protein expression was assessed with UALCAN databases. Moreover, the possible molecular functions of PLAT were screened by using GSEA software (version 4.1.0). Furthermore, the relationships between PLAT and immune infiltrating cells were explored using TIMER, TISIDB database, and ssGSEA algorithm. We investigated the correlation between PLAT expression level, clinicopathological characteristics, and DNA methylation with TCGA data. Our findings reveal the predictive value of PLAT in BC and show a potential correlation between PLAT and immune infiltrating cells, which will help clarify a possible mechanism for BC.

Transcriptional data of mRNA-sequencing, DNA methylation data, phenotype, and survival profiles of BC patients were accessed from UCSC Xena (https://xenabrowser.net/),13 which analyzes data from TCGA. The pre-processing steps were conducted by R (version 4.1.0) and Perl (version 5.30.2) software.

We selected 1071 primary BC samples, and 96 paired normal samples with clinicopathological profiles such as age, sex, menopausal status, histological type, TNM stage, and PAM50 subtype14 for further analysis. PAM50 algorithm using the 50-gene classifier divides BC into five intrinsic subtypes: luminal A, luminal B, HER2-enriched, basal-like, and normal-like. We explored the different expressions of PLAT in all clinicopathologic features. PLAT methylation data of 890 samples and its correlated gene expression levels were applied to calculate the methylation score of PLAT and the relationships between gene expression, DNA methylation, and clinicopathologic profiles.

Profiles of overall survival (OS) and progression-free survival (PFS) were downloaded from TCGA survival data. From this data, 1071 samples were assigned to high and low expression groups based on the median score of PLAT. R survival package was employed to generate KaplanMeier (KM) curves, while the optimal cut-off point for survival curves was generated through the res. cut function in the survminer package. Univariable and multivariable Cox regression models were established through the coxph function in the survival package, which was used to confirm whether PLAT is an independent prognostic factor of BC.

The clusterProfiler R package15 was employed to perform gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses on the basis of differentially expressed genes (DEGs_ (| log2FC | 1, FDR < 0.05) between two different expressed groups. P-values were adjusted by the BH method. We used Spearman correlation coefficient analysis to show the relationship between PLAT and co-expression genes. GSEA was conducted based on KEGG (v7.4) gene-set collections using GSEA software (v4.1.0 6)16,17 to uncover pathways in the DEGs groups. Gene sets with NOM p-value < 0.05 were considered significant.

The gsva package18 was utilized to conduct the ssGSEA,19 which can be applied to evaluate the scores of immune infiltrating cells and calculate the activity of immune-related pathways. TIMER (https://cistrome.shinyapps.io/timer/)20 contains an abundant resource for systematically exploring the immune infiltrates between various tumors. We employed TIMER 2.0 gene module to calculate the relationships between PLAT mRNA expression and the infiltration of immune cells. TISIDB database (http://cis.hku.hk/TISIDB)21 is a portal web containing a variety of tumor and immune system resources. In this study, TISIDB providers the correlations between PLAT and the immune system.

Gene expression profiles, methylation degree, and clinical characteristics were compared through Wilcoxon signed rank tests and displayed by box plot. Survival rates were assessed by applying KM curves and the log rank test. The Pearson chi-square test was employed to analyze the correlation between PLAT expression and DNA methylation level. R version 4.1.0 was used in all tests conducted. A statistically significant difference was considered when p < 0.05.

We achieved PLAT expression and BC-related clinical profiles from the TCGA database. The detailed data are summarized in Supplementary Table 1. PLAT had a lower expression in BC tissues than in normal tissues both in TCGA-BRCA all samples (Figure 1A) and paired samples (Figure 1B). The CPTAC dataset of the UALCAN database was used to analyze the PLAT protein expression. PLAT in BC tissues was significantly lower than in normal tissues, which was consistent with the gene expression level (Figure 1C). After that, PLAT expression in BC with different clinical characteristics such as gender, menopausal status, histological type, molecular subtype, N stage, and T stage displayed statistical differences. The expression level of PLAT in women was lower than that in men (Figure 1D), and it was lower in postmenopausal women than premenopausal women (Figure 1E). Invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC) are the two main histological types of BC. The expression level of PLAT in IDC was lower than in other types, including ILC. But there was no significant difference between ILC and other types (Figure 1F). Among the five PAM50 molecular subtypes of BC, luminal A, luminal B, HER2-enriched, basal-like, and normal-like, the expression level of PLAT was statistically different, in which luminal A was the highest and basal-like was the lowest (Figure 1G). The expression level was lower in the advanced stage in the T stage (Figure 1H); however, it was higher in the advanced N stage (Figure 1I).

Figure 1 Associations between PLAT expression and clinicalpathological parameters in BC. Low expression of PLAT was observed in tumor tissues both in all samples (A) and paired samples (B). Protein expression of PLAT in normal and primary tumor tissues with CPTAC samples (C). PLAT expression was analyzed in female and male (D), postmenopausal and premenopausal (E) patients, with different histological types (F), including invasive ductal carcinoma (IDC), invasive lobular carcinoma (ILC), and all other specific types, different PAM50 molecular subtypes (G), different tumor size (H) (T1 versus T2, T3, and T4), and different lymph node metastasis status (I) (N0 versus N1, N2, and N3). T1, tumor 20 mm in greatest dimension; T2, Tumor >20 mm but 50 mm in greatest dimension; T3, Tumor >50 mm in greatest dimension; T4, Tumor of any size with direct extension to the chest wall or the skin (ulceration or macroscopic nodules); invasion of the dermis alone does not qualify as T4; N0, no regional lymph node metastasis; N1, metastases in 1 to 3 axillary lymph nodes; N2, metastases in 4 to 9 axillary lymph nodes; and N3, metastases in 10 or more axillary lymph nodes. The asterisks represent the statistical p-value (ns: p > 0.05, *p 0.05, **p 0.01, ***p 0.001, ****p 0.0001).

We explored whether PLAT expression was correlated with the prognosis of BC patients. KM curves were utilized to evaluate the influence of PLAT expression on OS and DFS. The high PLAT expression group has a longer OS than low expression patients (Figure 2A) but there was no statistical significance in DFS (Figure 2B). We further investigated OS in the different molecular subtypes. Statistical significance of OS difference was found in all luminal samples, especially in luminal B subtypes (Figure 2C).

Figure 2 Prognostic value of PLAT expression in BC. (A) Low PLAT expression was associated with a poor OS in BC patients using KaplanMeier plotter. (B) DFS had no statistically significant difference in high and low PLAT expression groups. (C) Low PLAT expression was inferred as a poor OS in all luminal samples and all luminal B samples. (D) Forest plots show the association between PLAT expression and clinicopathological features using univariate and multivariate COX hazard analysis.

Univariate and multivariate regression analyses were applied to evaluate whether PLAT is an independent prognostic factor for BC. Univariate Cox hazard analysis identified that age (HR = 1.033, 95% CI:1.0201.046, p < 0.001), menopausal status (HR = 2.025, 95% CI:1.3473.045, p < 0.001), T stage (HR = 1.459, 95% CI:1.1971.779, p < 0.001), N stage (HR = 1.600, 95% CI:1.3471.901, p <0.001), M stage (HR = 4.860, 95% CI:2.9008.144, p < 0.001), Stage (HR = 2.187, 95% CI:1.7442.742, p < 0.001), and PLAT (HR = 0.886, 95% CI:0.7970.984, p = 0.024) were prognostic factors of BRCA. Multivariate analysis revealed that, after excluding other confounding factors, age (HR = 1.044, 95% CI:1.0231.067, p < 0.001), N stage (HR = 1.451, 95% CI:1.0522.000, p = 0.023), and PLAT (HR = 0.850, 95% CI:0.7420.974, p = 0.020) were still prognostic factors of BCRA (Figure 2D). The above results show that PLAT is an independent prognostic factor for BC and is a protective factor.

All TCGABRCA samples were assigned to two groups in the light of PLAT expression to gain insight into PLAT biological clues in BC. The volcano plot and heatmap show DEGs between the two groups (Figure 3A and B). PLAT and its co-expression genes are shown in Figure 3C. GO, and KEGG enrichment analyses were conducted based on 93 genes that had a positive correlation with PLAT to identify PLAT-related pathways and biological functions. The top 30 enriched GO terms are shown in Figure 3D. We can see that PLAT was mainly enriched in the pathway related to response to steroid hormone, humoral immune response, intracellular steroid hormone receptor signaling pathway, steroid hormone mediated signaling pathway, and response to progesterone. KEGG enrichment showed that PLAT was closely related to the pathways that correlate with BC and the immune response, such as the estrogen signaling pathway, apelin signaling pathway, IL-17 signaling pathway, and BC (Figure 3E).

Figure 3 DEGs and enrichment analyses of PLAT in BC. (A) Volcano plot and (B) heatmap show the DEGs in high and low PLAT expression patients. (C) Correlation of PLAT and the top 40 coexpressed genes. (D and E) GO enrichment and KEGG pathway analysis of PLAT in BC. The red box highlights the pathways correlated with BC and immune infiltrates. (F) The GSEA results showed that the terms antigen processing and presentation, natural killer cell mediated cytotoxicity, homologous recombination, and nucleotide excision repair were differentially enriched in BC samples with high PLAT.

We further used GSEA to predict PLAT-related pathways between patients with different PLAT expressions; 70 of 178 gene sets were up-regulated in the low PLAT group, and 15 pathways were enriched at NOM p < 0.05 and FDR < 0.25. The presenting figures include antigen processing and presentation, natural killer cell mediated cytotoxicity, homologous recombination, and nucleotide excision repair (Figure 3F). These results show that PLAT may affect immune cell infiltration.

Immune characteristics are closely related to tumor progression. Through the functional analyses, we evaluated the enrichment scores of 16 immune cells and the activity of 13 immune-related pathways between the two expressed groups by employing ssGSEA. The low expression subgroup of PLAT generally had higher levels of infiltration of immune cells, especially of aDCs, CD8 + T cells, DCs, iDCs, macrophages, pDCs, Tfh, Th1 cells, Th2 cells, TILs, and Treg cells. Except for the parainflammation pathway, the other 12 immune pathways performed higher activity in the low expression group than in the high expression group (Figure 4A). After that, we evaluated the relationship between the PLAT expression in BRCA and immune cell infiltration in TIMER. The finding revealed that the expression level of PLAT had a negative correlation with the infiltration of neutrophil (Rho = 0.175, p = 2.59e-08), T cell cd4+ (Rho = 0.158, p = 5.16e-07), B cell (Rho = 0.117, p = 2.12e-04) and dendritic cell (Rho = 0.098, p = 2.08e-03). Meanwhile it had a positive correlation with the infiltration level of T cell CD8+ (Rho = 0.2, p = 2.13e-10) and macrophage (Rho = 0.266, p = 1.45e-17). Not surprisingly, tumor purity was negatively correlated with PLAT expression level (Figure 4B). Then, to understand the association between PLAT and immune infiltration, TISIDB was employed to evaluate the association between PLAT expression and various immune characteristics. Figure 4C shows the relationship between PLAT and tumor-infiltrating lymphocytes (TILs) like CD4, CD8, DC, and B cell and Figure 4D the relationship between PLAT and immunostimulators like IL2RA, ICOS, TNFRSF13C, and PVR. Figure 4E shows the relationship between PLAT and immunoinhibitors like CD274, PDCD1, PDCD1LG2, and CTLA4 and Figure 4F the relationships between PLAT and MHC molecules like TAP2, HLA-DOB, TAP1, and HLA-F. Figure 4G shows the relationship between PLAT and chemokines like CXCL10, CCL8, CCL18, and CCL7. Figure 4H shows the relationship between PLAT and chemokine receptors like CCR8, CXCR6, CCR1, and CCR5. The results mentioned above indicate that PLAT widely participates in adjusting many immune molecules in BC and influences the immune infiltration in TME.

Figure 4 Associations of the PLAT expression level with tumor immune infiltration in BC. (A) Comparison of the enrichment scores of 16 immune cells and 13 immune-related pathways between low- and high-expression groups. (B) The correlation of PLAT expression with infiltration levels of neutrophil, CD4+T cell, B cell, and dendritic cell in BC is available on the TIMER 2.0 database. (C) Correlations between the abundance of tumor-infiltrating lymphocytes (TILs) and PLAT (plus the four TILs with the highest correlation) in the TISIDB database. (DF) Correlations between immunomodulators and PLAT (plus the four immunomodulators with the highest correlation, respectively) in the TISIDB database. (G and H) Correlations between chemokines (or receptors) and PLAT (plus the four chemokines (or receptors) with the highest correlation, respectively) in the TISIDB database. The asterisks represent the statistical p-value (*p 0.05, **p 0.01, ***p 0.001).

After the studies mentioned above, we continued to explore the possible reasons for the difference in PLAT expression. The box plot shows the methylation degree of each methylation site of PLAT DNA. Sites cg03960326 and cg18460120 had a higher degree of methylation and sites cg22038738 and cg04563438 had lower methylation degree (Figure 5A). Subsequently, the association between DNA methylation level and gene expression was calculated. Figure 5B shows that there is a negative association between DNA methylation and gene expression on the whole. When analyzing a single site, it was found that the methylation levels of cg13880167, cg12091331, cg04563438, cg03960326, cg00491021, and cg22038738 were negatively correlated with gene expression (Figure 5C). After that, survival analysis was further conducted according to the methylation degree of each site. It was found that, among the six DNA methylation sites of PLAT that had a negative correlation with gene expression, the methylation degree of the cg03960326 site was significantly related to OS (Figure 5D). We further assessed the methylation differences of the cg03960326 site of PLAT DNA in different clinical feature groups. We can see that there are no distinctions in methylation levels between different TNM and stages. However, there existed differences in methylation levels of cg03960326 site in people with different menopause status, tumor histological types, and PAM50 molecular types (Figure 5E). These differences are contrary to the previous differences of PLAT gene in cases with different clinical features, which also verifies the negative relationship between DNA methylation and gene expression.

Figure 5 Correlation of DNA methylation level with PLAT expression and clinical features. (A) Methylation level of 8 methylation site in PLAT. (B) Correlation of PLAT expression with gross methylation level. (C) Correlation of PLAT expression with different methylation sites (cg13880167, cg12091331, cg04563438, cg03960326, cg00491021, and cg22038738). (D) High methylation level of cg03960326 site was associated with a poor OS in BC patient. (E) Methylation level of cg03960326 site was analyzed with different menopausal status, histological types and PAM50 molecular subtypes. The asterisks represent the statistical p-value (ns: p > 0.05, **p 0.01, ***p 0.001, ****p 0.0001).

PLAT, a serine protease, mainly takes part in the intravascular dissolution of blood clots.22 Previous studies have shown that PLAT promoter hypermethylation can down-regulate the expression of nasal polyps gene, resulting in excessive fibrin deposition, which can be used as a therapeutic target of NP.23 PLAT can also promote angiogenesis by mobilizing CD11 + cells.24 It can be applied to the treatment of acute stroke25,26 and non-small cell lung cancer.27 It is also an estrogen-induced protein in the human BC cell line.11 BC is one of the highest incidence rate diseases in the world, which has a poor prognosis. Early detection and timely treatment are the most effective methods to improve the survival rate of BC patients. Traditional prognostic factors include tumor type, grade, size, and lymph node status. They can provide some course information, but they are not very accurate. Tumor immunotherapy provides a new remedy option for BC. Therefore, we assessed the role of PLAT in BRCA.

We analyzed BC cases in the context of RNA-seq data, methylation profiles, and clinical characteristics achieved from TCGA. The findings revealed that the expression level of PLAT was lower in BC patients. And patients in an advanced stage or with a more aggressive histological type may have lower expression levels in general. Consistent with that, lower expression of PLAT in TCGABRCA profiles was related to shorter overall survival, especially in the luminal B subtype. So, we deem that higher PLAT expression is related to a better prognosis of BC. After that, univariate and multivariate Cox regression analyses showed that PLAT was an independent prognostic factor affecting the prognosis of BC patients and could be used as a predictive marker.

The enrichment analysis showed that PLAT was related to the immune and tumor-associated pathway. Infiltrating immune cells are an essential component of TME.28 Recently, immunotherapy for the interaction between immune cells and BC cells has been developed as an alternative to classical anticancer therapy.29,30 PLAT has been affirmed to predict the prognosis of multiple tumor types such as colon cancer, ovarian cancer, lung cancer, and BC.31,32 There is evidence proving that tumor-infiltrating lymphocytes (TIL) that existed before the treatment of BC can predict treatment response and improve prognosis.33 TIL plays a vital role in chemotherapy response and clinical prognosis of all subtypes of BC.34 In our study, the low expression subgroup of PLAT generally had higher levels of infiltration of immune cells and higher activity of immune-related pathways. PLAT expressed level had a negative correlation with the infiltration level of neutrophil, T cell CD4+, dendritic cell, and B cell. Meanwhile, it had a positive correlation with the infiltration level of T cell CD8+ and macrophage. PLAT expression is closely related to TILs, immunomodulatory factors, and chemokines. Our results verified the association between PLAT and the prognosis and immune infiltration of BC, suggesting that PLAT can help predict treatment response and improve prognosis.

DNA methylation plays a vital role in gene-expressed regulation, mainly related to transcriptional inhibition.35 Therefore, we continue to search for the possible causes of different gene expressions. Our results showed a negative relationship between the degree of DNA methylation and gene expression level. By further analyzing the methylation level of PLAT DNA in the cg03960326 site, which is significantly related to OS, methylation differences were observed in patients with different tumor histological types, molecular subtypes, and menopause. These differences are opposite to the previous differences of the PLAT gene in other clinical feature groups. This also verified that DNA methylation was negatively related to PLAT expression, which might cause PLAT expression differences.

Immune infiltration in the TME has been shown to play a critical role in cancer progression and occurrence and to affect clinical outcomes of cancer patients.36 In triple-negative BC, tumor-associated macrophages derived from peripheral blood monocytes promote tumor growth and progression by several mechanisms that include the secretion of inhibitory cytokines, the reduction of effector functions of TIL, and the promotion of Treg cells. Besides, tumor-associated macrophages have been shown to directly and indirectly modulate PD-1/PD-L1 expression in tumor environment.37 Immunotherapy has raised significant concern in the treatment of cancer, which aims to eliminate cancer cells by enhancing natural defenses. The blockade of PD-1/ PD-L1 and CTLA4 has achieved remarkable therapeutic success in multiple kinds of cancer, including BC. An in-depth understanding of immune infiltration cells in the TME is essential to uncover the underlying molecular mechanisms and provide new strategies to improve immunotherapeutic efficacy.

Previous analysis showed that PLAT, a tumor suppressor gene, has differential expression levels and independent prognostic value and is significantly correlated with tumor-related pathways and immune infiltrating cells in TME. However, one study has shown that PLAT cannot foresee the response to systemic adjuvant therapy.11 The presented research only shows the results of online databases. To further confirm this conclusion, we will conduct PCR and IHC on our clinical samples and further analyze the different clinical characteristics and survival information. Finally, the internal molecular mechanism of PLAT and tumor immune cell infiltration will be further explored. Therefore, further research is needed to improve the proof of the biological impact of PLAT.

PLAT can be considered a prognostic factor and biomarker to provide personalized treatment, improve the survival rate, and contribute to developing immunological treatment strategies.

BC, breast cancer; TME, tumor microenvironment; PLAT, tissue-type plasminogen activator; PLAU, urokinase type plasminogen activator; TCGA, The Cancer Genome Atlas; OS, overall survival; PFS, progression-free survival; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; IDC, invasive ductal carcinoma; ILC, invasive lobular carcinoma; TIL, tumor-infiltrating lymphocytes.

This study was approved by the institutional ethical committee of the First Affiliated Hospital with Nanjing Medical University.

We would like to acknowledge the TCGA, TIMER, and TISIDB databases for free use.

This study is supported by the Natural Science Foundation of Jiangsu Province (BK20171506).

The authors report no conflicts of interest in this work.

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7. Mahmood N, Mihalcioiu C, Rabbani SA. Multifaceted role of the urokinase-type plasminogen activator (uPA) and its receptor (uPAR): diagnostic, prognostic, and therapeutic applications. Front Oncol. 2018;8:24. doi:10.3389/fonc.2018.00024

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12. Daz VM, Planaguma J, Thomson TM, Revents J, Paciucci R. Tissue plasminogen activator is required for the growth, invasion, and angiogenesis of pancreatic tumor cells. Gastroenterology. 2002;122(3):806819. doi:10.1053/gast.2002.31885

13. Cline MS, Craft B, Swatloski T, et al. Exploring TCGA pan-cancer data at the UCSC cancer genomics browser. Sci Rep. 2013;3:2652. doi:10.1038/srep02652

14. Parker JS, Mullins M, Cheang MC, et al. Supervised risk predictor of breast cancer based on intrinsic subtypes. J Clin Oncol. 2009;27(8):11601167. doi:10.1200/JCO.2008.18.1370

15. Yu G, Wang LG, Han Y, He QY. clusterProfiler: an R package for comparing biological themes among gene clusters. OMICS. 2012;16(5):284287. doi:10.1089/omi.2011.0118

16. Mootha VK, Lindgren CM, Eriksson KF, et al. PGC-1-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes. Nat Genet. 2003;34(3):267273. doi:10.1038/ng1180

17. Subramanian A, Tamayo P, Mootha VK, et al. Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc Natl Acad Sci U S A. 2005;102(43):1554515550. doi:10.1073/pnas.0506580102

18. Hnzelmann S, Castelo R, Guinney J. GSVA: gene set variation analysis for microarray and RNA-seq data. BMC Bioinform. 2013;14:7. doi:10.1186/1471-2105-14-7

19. Barbie DA, Tamayo P, Boehm JS, et al. Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1. Nature. 2009;462(7269):108112. doi:10.1038/nature08460

20. Li T, Fu J, Zeng Z, et al. TIMER2.0 for analysis of tumor-infiltrating immune cells. Nucleic Acids Res. 2020;48(W1):W509w514. doi:10.1093/nar/gkaa407

21. Ru B, Wong CN, Tong Y, et al. TISIDB: an integrated repository portal for tumor-immune system interactions. Bioinformatics. 2019;35(20):42004202. doi:10.1093/bioinformatics/btz210

22. Kruithof EK, Dunoyer-Geindre S. Human tissue-type plasminogen activator. Thromb Haemost. 2014;112(2):243254. doi:10.1160/th13-06-0517

23. Kidoguchi M, Noguchi E, Nakamura T, et al. DNA methylation of proximal PLAT promoter in chronic rhinosinusitis with nasal polyps. Am J Rhinol Allergy. 2018;32(5):374379. doi:10.1177/1945892418782236

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25. Pea-Martnez C, Durn-Laforet V, Garca-Culebras A, et al. Pharmacological modulation of neutrophil extracellular traps reverses thrombotic stroke tPA (tissue-type plasminogen activator) resistance. Stroke. 2019;50(11):32283237. doi:10.1161/strokeaha.119.026848

26. Zhu J, Wan Y, Xu H, Wu Y, Hu B, Jin H. The role of endogenous tissue-type plasminogen activator in neuronal survival after ischemic stroke: friend or foe? Cell Mol Life Sci. 2019;76(8):14891506. doi:10.1007/s00018-019-03005-8

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30. Hall M, Liu H, Malafa M, et al. Expansion of tumor-infiltrating lymphocytes (TIL) from human pancreatic tumors. J Immunother Cancer. 2016;4:61. doi:10.1186/s40425-016-0164-7

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MiNA Therapeutics Appoints Two Independent Directors With Extensive Industry Experience to Support Next Phase of Growth – BioSpace

Posted: at 1:36 am

Dec. 21, 2021 07:00 UTC

LONDON--(BUSINESS WIRE)-- MiNA Therapeutics Limited (MiNA or the Company), the pioneer in small activating RNA (RNAa) therapeutics, announces the expansion of its Board, with the appointment of Susan Clement-Davies and Professor Sir Robert Lechler as Independent Directors, effective 1 January 2022.

Susan is an experienced life sciences financier with over 25 years of capital markets and investment banking experience, including as Managing Director of Equity Capital Markets at Citigroup Global Markets Limited and Managing Director at Torreya Partners LLC. Susan is currently a Non-Executive Director of Scancell Holdings, a UK listed biotechnology company developing innovative immunotherapies, EvgenPharma plc, a UK-listed clinical stage drug development company, and Exploristics, a world-leading provider of biosimulation software and biostatistics services for clinical trials. Susan is also Corporate Finance Advisor for Theolytics, a biotechnology company developing anticancer viral therapies, and an Advisor for Oxford Sciences Innovation, the worlds largest university-partnered venture firm. In addition, Susan is a member of the Innovation Advisory Group for the Chelsea and Westminster Hospital NHS Foundation Trust.

Robert is a recognised leader in biomedical research, management and governance with over 40 years of distinguished experience in academic medicine, having started his immunology career in 1979. Since then, Robert has held various leadership roles in a range of hospitals and laboratories, including serving as Head of Imperial College Londons Division of Medicine, Vice Principal (Health) of Kings College School, and Executive Director of Kings Health Partners Academic Health Sciences Centre. He has also been at the forefront of scientific innovation, nationally, through his Presidency of the Academy of Medical Sciences, Membership of the UK Council for Science and Technology, and Chairmanship of the UK MHRA Clinical Trials Expert Advisory Group. In 2012, Robert was Knighted in the Queens Birthday Honours for his services to academic medicine, which has centred around immunology, cancer and transplantation. He is currently a Non-executive Director of Quell Therapeutics, a biopharmaceutical company specialising in addressing a range of autoimmune and inflammatory diseases through cell therapy.

Nagy Habib, Chairman and Head of R&D of MiNA Therapeutics, commented: We are thrilled to welcome Susan and Robert to MiNAs Board of Directors to support our strengthened senior leadership team as we remain focused on driving the Companys next phase of growth. Susan's expertise in finance and as a biopharma company director, combined with Roberts leadership in biomedicine will be invaluable as we continue to advance our pipeline through clinical development and expand our partnerships to scale and amplify the impact of our pioneering RNAa technology for patients.

Susan Clement-Davies, Independent Director of MiNA Therapeutics, commented: I am extremely excited to be joining MiNA. What the team has achieved, particularly in recent years, is impressive and I hope to bring my experience in the life sciences sector to further unlock MiNAs significant potential.

Professor Sir Robert Lechler, Independent Director of MiNA Therapeutics, commented: This is a fantastic opportunity to be involved with a pioneering company in such an interesting space. The Companys RNAa approach and pipeline is a truly innovative way of treating diseases and I look forward to guiding MiNA on its journey, which I believe will be highly successful.

About MiNA Therapeutics MiNA Therapeutics is the leader in small activating RNA therapeutics. Harnessing innate mechanisms of gene activation, small activating RNA therapeutics are a revolutionary new class of medicines that can restore or boost normal function in patients' cells. We are advancing a proprietary pipeline of new medicines with an initial focus on cancer and genetic diseases, while collaborating with leading pharmaceutical companies to apply our technology platform across a broad range of therapeutic areas. Based on our unique know-how in RNA activation we are expanding the possibilities of RNA-based medicine for patients. http://www.minatx.com

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Scientists Used CRISPR Gene Editing to Choose the Sex of Mouse Pups – Singularity Hub

Posted: at 1:35 am

Do you want a boy or a girl? can be an awkward question.

But in certain circles, its a question thats asked every day. Take agriculture. In a perfect world, most cows would only birth females. Chicks would grow up to be all hens. Sexing a farm animal when theyre at a young age wouldnt be a thingespecially when it means male animals, without the ability to produce milk or eggs, are often culled at a young age to preserve resources.

There might be a better way. This month, a team tapped into the power of CRISPR to control the sex of the offspring in mice. By splicing CRISPR components into the parents genome, the team was able to flip onor offa switch that nearly perfectly determined the sex of their litters.

Unlike previous attempts, the baby mice could go on to have litters of their own of both sexes. The targeted gene used for the edit is conserved across evolution, suggesting the technique could work in more animals than just mice.

But its controversial. Essentially, the technique selectively kills off embryos of a certain sex, which immediately raises ethical red flags. For now, scientists arent concerned about the technology being used in humans due to its complexity. But the study is the latest to showcase biotechs increasing ability to manipulate reproduction.

Its an impressive result and a state-of-the-art solution to producing single-sex species, said Dr. Ehud Qimron at Tel Aviv University, who was not involved in the work.

Skewing the sex of offspring is nothing new. For over a decade, scientists have gradually hijacked the mosquito genome with gene drives to rewrite evolution. The idea is that the genetic edit would override natural selection, spreading across subsequent generations into a dominant gene. Instead of a genes usual 50-50 chance of inheritance, artificial gene drives have a far higher chance of infiltrating the next generation, fundamentally changing a species genetic code. When its a gene that biases the sex of their offspring, a species could gradually only have one sex, leading to their extinction.

Its a doomsday plan with potentially massive benefits, such as curbing malaria. Because female mosquitoes are generally the carrier for the disease, a gene drive that leads to only males is a sure-fire way to reduce transmission. In one study, within a dozen generations, the genetic edit was sufficient to collapse a whole colony of mosquitoes in the lab. Similar studies have been tried in mice.

Its not a perfect solution. The gene edit is powerfulmaybe too much so. With farm animals, the goal isnt to eradicate a species, but rather to bias the sex of the animal towards one side and increase animal welfare. Animal and animal products are used globally, and ethical discussions regarding animal usage are ongoing, said the authors. Over 100,000 male calves are culled each year, and stats for other common farm animals paint a similarly uncomfortable picture.

The new study took a different approach. With CRISPR, the team skewed the sex of only the next generation in mice, allowing the same-sex litters to eventually reproduce normally.

CRISPR has two parts: an RNA guide (the bloodhound that sniffs out the target gene) and Cas9 (a scissor protein that physically cuts the gene). Usually, the two components are encoded into a single carrier, dubbed a vector, and inserted into a cell or animal. By targeting a gene that is essential for reproduction, for example, its then possible to trigger spontaneous failed pregnancies in animals.

But how does that help with sex selection? Let me explain.

The first step was to find a gene critical for embryo survivalone that when disrupted causes synthetic lethality. The team honed in on Top1, well known for its role in DNA repair. Cutting the gene triggers embryos to fail at a very early stage, when theyre just 8 to 16 cells, not yet implanted into the uterine wall and far from viable.

The team then engineered a CRISPR system that targets the start codons of Top1a chunk of DNA that acts as an on switch to activate the gene. Heres the clever part. They split the two components of CRISPR into two vectors.

One part, which carries the genetic code for a guide RNA that targets Top1, was then inserted into a female mouses X chromosome. The other vector, carrying the code for Cas9 scissors, was edited into the males Y chromosome.

When combined, the two components meet up like peanut butter and jelly, forming the full recipe to disrupt Top1. This can only happen in X/Y embryosthose that define maleand so selectively interrupt these embryos from developing. X/X, or genetically female embryos, are spared, as they only contain half of the CRISPR mechanism. The system is flexible. If Cas9 scissors were attached to the males X chromosome, all X/X embryos were eliminated before they grew to 16 cells.

The efficiency of the edit was crazy at 100 percent. Mice born from these genetically-edited parents were completely normal, with a hefty body size and in larger numbers than normally expected, suggesting the edit may cause less stress on the mother. Unlike those born using gene drives, the mice grew up to have perfectly normal litters with both male and female offspring.

The results are a long time in the making. Back in 2019, a team led by Dr. Udi Qimron at Tel Aviv University used CRISPR to produce mice in which 80 percent of the offspring were females. With the new study, the efficacy leaps to 100 percent, with the choice towards either sex. If further tested in farm animals, the technique could be a boost to both animal welfare and conservation.

Its not an entirely comfortable solution for some. To Sue Leary, president of the non-profit Alternatives Research & Development Foundation, You cant solve an ethical problem with another ethical problem, which is genetic engineering. And given the animosity towards GMOs, the new technology, regardless of efficacy, may be dead in the water.

For now, the CRISPR edits arent feasible in humans due to their complexity. Whats clear, though, is that weve begun parsing the biological machinery behind gender selection. Add in recent work on genetically-engineered embryos, or eggs and sperm from stem cells, and were on the fast track for CRISPR to completely change our current conception of reproduction.

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Report calls for broad public deliberation on releasing gene-edited species in the wild – EurekAlert

Posted: at 1:35 am

NEW YORK, December 21 -- A new report released by The Hastings Center, a leading ethics research institute, finds that the complex issues raised by releasing gene-edited species into the wild demand deep and broad public engagement. The report, Gene Editing in the Wild: Shaping Decisions Through Broad Public Deliberation, provides a path forward to move decision-making from the realm of experts to a more inclusive, values-based approach using the technique of public deliberation or deliberative democracy.

The goals of gene editing in the wild efforts are wide-ranging, and the benefits potentially transformative--such as preventing mosquitoes from spreading disease. But this work poses major trade-offs that require the publics consideration.

The reports twelve essays take up fundamental questions: how should public deliberation be designed? Who should participate? How should deliberation be linked to policy?

The introductory essay, Public Deliberation About Gene Editing in the Wild, summarizes the key design elements that can improve broad public deliberations about gene editing in the wild: Framing the question and deciding when to hold broad public deliberation, choosing participants, addressing power, and accounting for and capturing perspectives that are hard to express. The introduction was written by the special report editors: Michael K. Gusmano, Gregory E. Kaebnick, Karen J. Maschke, Carolyn P. Neuhaus, and Ben Curran Wills.

Regulating Gene Editing in the Wild: Building Regulatory Capacity to Incorporate Deliberative Democracy, by Karen J. Maschke and Michael K. Gusmano, says that there has not been enough attention to how we should connect public deliberation to the existing regulatory process. The authors argue that, while federal agencies may have capacity to undertake public deliberative activities, there may not be sufficient political support for them to do so.

Deliberative Public Consultation via Deliberative Polling: Criteria and Methods, by James S. Fishkin, makes the case that Deliberative Polling, an approach developed by the author, can be usefully employed to engage representative samples to deliberate in depth in controlled experiments so as to yield a picture of the publics considered judgments. Another it can be cost-effectively conducted online.

The Decision Phases Framework for Public Engagement: Engaging Stakeholders about Gene Editing in the Wild, by S. Kathleen Barnhill-Dilling, Adam Kokotovich, and Jason A. Delborne, puts forth a framework for shaping public engagement that tackles when and whom to engage on genetic engineering questions.

Empowering Indigenous Knowledge in Deliberations on Gene Editing in the Wild, by Riley Taitingfong and Anika Ullah, identifies Indigenous peoples as key stakeholders in decisions about gene-editing in the wild and argues that engagement activities need not only include Indigenous peoples but also should be designed, conducted, and analyzed in ways that confront longstanding power imbalances that dismiss Indigenous expertise.

The special report grew out of a Hastings Center project funded by the National Science Foundation, The complete report is available for download here.

For more information, contact:

Susan Gilbert or Mark Cardwellcommunications@thehastingscenter.org845-424-4040, ext. 244

Systematic review

Not applicable

Gene Editing in the Wild: Shaping Decisions through Broad Public Deliberation

15-Dec-2021

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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RNA and DNA Extraction Kit Market Study | Know the Post-Pandemic Scenario of the Industry – BioSpace

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RNA and DNA extraction plays a crucial role in cancer genetic studies, which involves mutation analysis, comparative genomic hybridization, and microsatellite analysis. The rising incidences of cancer globally are creating a need for the advanced RNA and DNA extraction kit and are expected to drive market growth in the coming years.

Based on the product, the market is expected to segregate into RNA extraction kit and DNA extraction kit. Of these, the DNA extraction kit segment is expected to account for the leading share in the overall RNA and DNA extraction kit market. Additionally, the applications of DNA extraction kits mainly in the genetic engineering of animals and plants in pharmaceutical manufacturing. This is expected to fuel growth of RNA and DNA extraction kit market.

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Global RNA and DNA Extraction Kit Market: Notable Developments

Some of the most prominent competitors operating in the competitive landscape of global RNA and DNA extraction kit market include

Global RNA and DNA Extraction Kit Market: Drivers and Restraints

The rise and progress in customized drug have helped social insurance experts create exact sub-atomic focused on treatment dependent on a person's hereditary cosmetics and prescient information explicit to patients. The advancement of customized medication requires genome-mapping investigations of separated cells, which can be completed with the assistance of DNA and RNA extraction kits. DNA extraction kits are utilized to recognize quality polymorphisms identified with sickness or medication digestion though RNA extraction kits are utilized to break down RNA combination in separated cells. With the expanding appropriation of customized prescription, the demand for RNA and DNA extraction kits will likewise develop.

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There is a developing rate of malignant growth over the globe. The inside and out understanding of tumor hereditary qualities given by trend-setting innovations in malignant growth research has empowered the advancement of novel treatments to battle disease-causing qualities. The virtue, amount, and nature of separated RNA assume a huge job in the accomplishment of RNA examination and examination and consequent capacity of specific quality articulation. RNA extraction likewise helps in recognizing circulating tumor cells (CTCs) and non-intrusive observing of cutting edge malignant growths.

Global RNA and DNA Extraction Kit Market: Regional Outlook

On the basis of region, the RNA and DNA extraction kit market is segmented into North America, Europe, Latin America, Asia Pacific, and the Middle East & Africa. Of these, North America is expected to dominate the global RNA and DNA extraction kit market owing to robust innovation procedures running in the region. This factor is expected to offer robust growth opportunities to key players in RNA and DNA extraction kit market. Additionally, increasing demand for the automated systems coupled with the rising need for the RNA and DNA extraction kit across the extraction kits especially in the medical diagnosis is expected to drive growth of the market in coming years.

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Opinion: Allow Golden Rice to save lives – pnas.org

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Vitamin A deficiency (VAD) has killed millions of children in less-developed countries for at least the last three decadesroughly 2 million annually in the early 1990s alone (14). Although the number is declining, it was estimated to be 266,200 (4) at the start of the millennium.

Widespread consumption of the genetically modified rice variety known as Golden Rice offers a potent and cost-effective strategy to combat vitamin A deficiency. Image credit: International Rice Research Institute; photo licensed under CC BY 2.0.

The consumption of the genetically modified rice variety known as Golden Rice (GR) offers a potent and cost-effective strategy to combat VAD. But this innovation has been cast aside owing to fear or false accusations, resulting in numerous lives needlessly lost (13). With the recent exception of the Philippines, governments have not approved the cultivation of GR (5). We believe it should be broadly approved and given the opportunity to save and improve lives.

In high-income nations where populations have access to a diversity of foods, VAD is rare. In many low-income nations, however, populations have limited access to foods rich in vitamin A or beta-carotene, a vitamin A precursor; hence, VAD rates can be dangerously high in children. There have been recent improvements: from 1991 to 2013, the VAD rate among children in low- and middle-income countries declined from 39% to 29%, with notable improvements among children in East and Southeast Asia (4). However, children in sub-Saharan Africa and South and Southeast Asia continue to disproportionately experience VAD and its associated risks: infectious and diarrheal diseases, irreversible blindness and other sensory losses, and premature death (1, 4, 6).

VAD has not been eradicated despite a variety of strategies used globally, including education on the value of dietary diversity, promotion of home gardens and maternal breastfeeding of infants, and community health programs including vitamin A supplementation with syrups or capsules (7). Principally, VAD is caused by insufficient dietary diversity, a result of poverty and agronomic and market constraints. Animal source foods and many kinds of produce are unavailable or expensive in local markets. Conversely, white rice or other cereal grains are easily available and inexpensive but primarily contain carbohydrates while lacking sufficient micronutrient levels.

GR, developed first in the 1990s and then modified in 2004 with transgenes from maize and a common soil bacterium Erwinia uredovora, could be an important public health intervention for VAD populations worldwide. This transgenic, or genetically modified, rice produces beta-carotene, a precursor to vitamin A, in the normally white endosperm (8) and has proven an effective source of vitamin A in humans (9). GR* is now awaiting final approval in Bangladesh. In July 2021, it was approved for cultivation in the Philippines. Other countries will likely follow.

A recent study has estimated that substituting conventional rice for GR could provide 89% to 113% and 57% to 99% of the recommended vitamin A requirement for preschool children in Bangladesh and the Philippines, respectively (10). Even if there were no other sources of vitamin A in the diets, this boost in dietary beta-carotene could do much to prevent diseases associated with VAD.

GR is also financially viable. In Bangladesh, the current practice of fortifying rice with vitamin A and zinc using food additives, although supported by the World Food Programme, increases the cost of rice by 5% to 6% and is applied to only about 1 million metric tonnes of rice of the roughly 25 million metric tonnes produced in Bangladesh per year (11). GR, by contrast, poses no extra cost to governments, growers, or consumers in comparison with white rice.

Meanwhile, VAD has continued to cause severe illness and death among certain populations worldwide, especially children (12). The total estimated deaths from VAD-related diarrheal diseases and measles in children under five years of age in 2013 was 94,500 and 11,200, respectively, totaling 105,700 deaths across the world (4). Had GR become a part of diets in vulnerable populations worldwide, a portion of these lives might have been saved. Hopefully, approval of the commercialization of GR in the Philippines will provide impetus for Bangladesh and other nations with high VAD rates to provide poor consumers with an option that may save lives and improve health.

Those who oppose transgenic or genetically modified organisms raised concerns that led policymakers to delay the approval of the technologies (13). One argument relates to biotechnology company profits. But because the GR technology to the public sector is available at no cost for humanitarian uses, this concern is irrelevant. There are no limitations, except export, on GR use: replanting or selling or giving away seed, or polishing for consumption or sale.

Greenpeace summarized a food security-related objection to GR in a 2012 statement (14): If introduced on a large scale, GR can exacerbate malnutrition and ultimately undermine food security. The implication: GR will worsen malnutrition because it leads to a diet based on one staple. However, the replacement of traditional rice with GR would not exclude the development of diversified diets; in the meantime, vitamin A status could improve for many in the population. And optimizing vitamin A delivery could improve public health in at-risk populations.

A reasonable objection concerns possible human or environmental health risks. The United Nations (UN) Cartagena Protocol on Biosafety (15) provides a framework for the regulation of genetically engineered crops in many countries, emphasizing the Precautionary Principle in assessing risks, and leaving out assessment of benefits. This Protocol was signed in 2000 and became effective in 2003, in the relatively early days of agricultural genetic engineering. Since then, multiple studies have reported on benefits of genetically modified organism (GMO) adoption through increased yields, reduced pesticide use, improved farmer income, reduced prices to consumers, and in some cases even improved food safety (16). Meanwhile, there have been no confirmed incidents of adverse human health or environmental effects from genetically engineered crops during nearly three decades of global use (16).

Transgenic crops are subject to many required regulatory tests before approval, including animal feeding and invitro studies for toxicity and allergenicity. Yet opponents of these crops have continued to amplify suspicion on the long-term health effects of genetically engineered crops (17). Protection against such risks can be achieved through monitoring of the performance and the impacts of technologies and intervening when setbacks occur. However, the food safety assessments for transgenic crops in many countries are more demanding than for conventionally bred varieties. In fact, often less is known about the properties of plants developed by conventional mutagenesis than those developed by transgenic methods.

Another concern is that GR genes may intermingle with those of conventionally bred rice varieties. This uncertainty, however, applies not just to GR but also to any other new rice variety. Humans have consumed rice for more than 4,000 years, including varieties that have been crossed genetically across multiple strains. Transgenic methods of introducing novel genes is not inherently of greater concern, unless those genes produce proteins with potential adverse health effectssomething that food safety tests for approval can determine. Clearly the lives saved with VAD outweigh concerns about these so-called unknown risks. In response to such criticisms, in 2016 more than 150 Nobel Laureates have signed an open letter to the UN, governments of the world, and Greenpeace, urging a more balanced approach toward genetically modified crops in general and GR in particular: Scientific and regulatory agencies around the world have repeatedly and consistently found crops and foods improved through biotechnology to be as safe as, if not safer than, those derived from any other method of production. Opposition based on emotion and dogma contradicted by data must be stopped (18).

The arguments used by organizations to delay adoption of GR often resemble the arguments of anti-vaccination groups, including those protesting vaccines to protect against COVID-19. Some of the opponents of GR and agricultural biotechnology more generally see the introduction of GR as forcing the consumption of GMOs on the population. However, for the case of GR, consumers have the option of easily avoiding consumption because GR is very easily identifiable by its color.

The tragedy of GR is that regulatory delays of approval have immense costs in terms of preventable deaths, with no apparent benefit (13). The approval of GR is even more urgent with the ongoing pandemic, which has made access to healthcare services more difficult in vulnerable populations worldwide. The World Bank has recommended that micronutrient biofortification of staple crops, including specifically GR, should be the norm and not the exception in crop breeding (19).

Golden rice can effectively control VAD. Delaying the uptake of a genetically modified product shown to have clear health benefits has and will cost numerous lives, frequently of the most vulnerable individuals. Policymakers must find ways to overcome this resistance and accelerate the introduction and adoption of Golden Rice.

Author contributions: J.W., D.Z., and A.D. designed research; F.W., J.W., C.C., and A.D. performed research; F.W., J.W., and C.C. analyzed data; and F.W., J.W., D.Z., R.R., C.C., and A.D. wrote the paper.

Competing interest statement: A.D. is a member and the Executive Secretary of the Golden Rice Humanitarian Board. He is a volunteer, unpaid and without grants. R.R. is a member of the Golden Rice Humanitarian Board. He is a volunteer, unpaid and without grants. The Golden Rice Humanitarian Board (http://www.goldenrice.org) holds the rights for humanitarian applications of the nutritional technology created by Professors Ingo Potrykus and Peter Beyer and related licensed technology. The Board is not legally incorporated in any way. It is a group of individuals who voluntarily share the objective of making Golden Rice available to resource-poor populations as a public good, delivered by the public sector in locally adapted and preferred rice varieties, at no greater cost than white rice and with no use limitations except export. All other authors declare no competing interests.

Any opinions, findings, conclusions, or recommendations expressed in this work are those of the authors and do not necessarily reflect the views of the National Academy of Sciences.

*Many transformation events were produced (8), from which event GR2E has been selected on the basis of molecular structure and insertion in the rice genome, together with agronomic performance. It is the basis of the regulatory data generated and is the only form of GR which is offered for approval and use.

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