Monthly Archives: July 2022

Patients with high-grade ovarian cancer and uterine serous cancer (USC) often respond well to surgery and chemotherapy. At first.

But these can be highly aggressive tumors that often spread into the space within the abdomen known as the peritoneal cavity. According to a recent study, one rare but aggressive type of uterine cancer is propelling an increase in deaths from the disease in the United States, particularly among Black women.

Moreover, resistance to chemotherapy often develops, and the disease recurs. This results in ovarian cancer causing more deaths than any other cancer of the female reproductive system.

For one possible treatment, clinical trials demonstrated the effectiveness of injecting a drug known as epothilone B (EB) into the abdominal cavity, targeting tumor cells that have grown resistant to standard chemotherapy medications. However, the drugs high toxicity when delivered this way causes severe side effects, preventing further use.

Now, thanks in part to research begun more than a decade ago with funding from Womens Health Research at Yale, our colleagues are closing in on a way to deploy effective cancer-fighting medication safely with the help of ultra-tiny non-toxic biodegradable objects known as nanoparticles. Developed by Dr. W. Mark Saltzman, the Goizueta Foundation Professor of Biomedical and Chemical Engineering, these nanoparticles have organic chemicals on their surface that allow them to stick to cells in the abdominal cavity so they are not cleared from the area before they can do their job.

With bioadhesive nanoparticles, we can safely entrap a drug and deliver it so it slowly releases in a high concentration, directly to our target, over a long time, Saltzman said. By localizing the delivery of the drug, we are decreasing toxicity and increasing effectiveness.

With data funded through WHRYs grant, Drs. Saltzman and Alessandro Santin, professor of obstetrics, gynecology, and reproductive sciences, secured funding from the National Institutes of Health to demonstrate the safety and efficacy of this technique in a model system, publishing their results in 2016.

Saltzman then partnered with Dr. Michael Girardi, Evans Professor of Dermatology, to develop a non-surgical treatment for skin cancer using injections of nanoparticles carrying a chemotherapy agent. In a paper published last year, they demonstrated the capacity for this method to bind to the tumors and kill a significant number of cancer cells. In addition, the treatment involves triggering an immune response to rid the body of cancer cell waste and respond against any remaining cancer cells.

Drs. Saltzman and Girardi founded a company called Stradefy Biosciences, which has licensed patents to this technology from Yale, while continuing to develop these techniques for clinical use.Dr. Nita Ahuja, William H. Carmalt Professor of Surgery and chair of surgery, serves as an advisor for abdominal cancer applications.

We are thrilled that the work we sponsored many years ago continues to produce such varied applications for serious health concerns, said WHRY Director Carolyn M. Mazure, PhD. This is the model for how investing in Yales most innovative and collaborative individuals can produce steady progress that will improve and even save lives.

Dr. Saltzman also used a WHRY grant to create a vaginal ring that provides contraception while protecting against sexually transmitted infections. Yale has filed a patent application on this unique ring design, and Saltzman continues to seek funding to further develop the product and possibly adapt it to treat endometriosis.

The type of funding WHRY provides is critical for the innovation-based work I do, Saltzman said. I could say, We are going to make these particles with this unique property. But to get substantial buy-in from a company or the NIH, you need to have the data to demonstrate that this works. Early funding, particularly for collaborative projects with unproven technologies, is critical.

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Using Particles That Are Smaller Than the Head of a Pin to Treat Cancer - Yale School of Medicine

DUBLIN--(BUSINESS WIRE)--The "Stem Cell Assays Market by Type (Viability, Proliferation, Differentiation, Apoptosis), Cell Type (Mesenchymal, iPSCs, HSCs, hESCs), Product & Service (Instrument), Application (Regenerative Medicine, Clinical Research), End User - Global Forecast to 2027" report has been added to ResearchAndMarkets.com's offering.

The stem cell assay market is projected to reach USD 4.5 Billion by 2027 from USD 1.9 Billion in 2022, at a CAGR of 17.7% during the forecast period.

The growth of the market is projected to be driven by collaborations and agreements among market players for stem cell assay products & services, the launch of new stem cell analysis systems such as flow cytometers, and increase in R&D expenditure by biopharmaceutical and biotechnology companies.

The viability/cytotoxicity assays accounted for the largest share of the type segment in the stem cell assays market in 2021

Cell viability assays help to determine the number of live and dead cells in a culture medium. The viability/cytotoxicity assays include various types such as tetrazolium reduction assays, resazurin cell viability assays, calcein-AM cell viability assays, and other viability/cytotoxicity assays. The cell viability/cytotoxicity market is likely to be driven by rising R&D spending on stem cell research, an increase in demand for stem cell assays in drug discovery, and development of new stem cell therapies..

The adult stem cells segment accounted for the largest share of the cell type segment in the stem cell assays market in 2021.

Adult stem cells account for the largest share of the stem cell assay market. The adult stem cells include mesenchymal stem cells, induced pluripotent stem cells, hematopoietic stem cells, umbilical cord stem cells, and neural stem cells. The growth of the adult stems cells segment is driven by the increasing usage of adult stem cells in regenerative medicine and the development of advanced therapies.

Asia Pacific: The fastest-growing region in the stem cell assays market

The Asia Pacific is estimated to be the fastest-growing segment of the market, owing to the rising prevalence of cancer & other diseases, increasing R&D spending on biopharmaceutical projects, and focus on developing stem cell-based therapies. In this region, China and Japan are the largest markets.

Key Topics Covered:

1 Introduction

2 Research Methodology

3 Executive Summary

4 Premium Insights

4.1 Stem Cell Assays Market Overview

4.2 North America: Stem Cell Assays Market, by Product & Service and Country (2021)

4.3 Stem Cell Assays Market Share, by Type, 2022 Vs. 2027

4.4 Stem Cell Assays Market Share, by Application, 2021

4.5 Stem Cell Assays Market: Geographic Growth Opportunities

5 Market Overview

5.1 Introduction

5.2 Market Dynamics

5.2.1 Drivers

5.2.1.1 Increasing Awareness About Therapeutic Potency of Stem Cells

5.2.1.2 Increasing Funding for Stem Cell Research

5.2.1.3 Rising Demand for Cell-Based Assays in Drug Discovery

5.2.1.4 Collaborations and Agreements Among Market Players for Stem Cell Assay Products & Services

5.2.1.5 Rising Incidence of Cancer

5.2.2 Restraints

5.2.2.1 Issues in Embryonic Stem Cell Research

5.2.2.2 High Cost of Stem Cell Analysis Instruments

5.2.3 Opportunities

5.2.3.1 Emerging Economies

5.2.3.2 Government Initiatives to Boost Stem Cell Research

5.2.4 Challenges

5.2.4.1 Lack of Infrastructure for Stem Cell Research in Emerging Economies

5.2.4.2 Dearth of Trained and Skilled Professionals

5.3 Ranges/Scenarios

5.4 Impact of COVID-19 on Stem Cell Assays Market

5.5 Trends/Disruptions Impacting Customers' Business

5.6 Pricing Analysis

5.6.1 Average Selling Prices of Products Offered by Key Players

5.6.2 Average Selling Price Trend

5.7 Technology Analysis

6 Stem Cell Assays Market, by Type

6.1 Introduction

6.2 Viability/Cytotoxicity Assays

6.3 Isolation & Purification Assays

6.4 Cell Identification Assays

6.5 Proliferation Assays

6.6 Differentiation Assays

6.7 Function Assays

6.8 Apoptosis Assays

7 Stem Cell Assays Market, by Cell Type

7.1 Introduction

7.2 Adult Stem Cells

7.3 Human Embryonic Stem Cells

8 Stem Cell Assays Market, by Product & Service

8.1 Introduction

8.2 Instruments

8.3 Kits

8.4 Services

9 Stem Cell Assays Market, by Application

9.1 Introduction

9.2 Regenerative Medicine & Therapy Development

9.3 Drug Discovery & Development

9.4 Clinical Research

10 Stem Cell Assays Market, by End-User

11 Stem Cell Assays Market, by Region

12 Competitive Landscape

13 Company Profiles

Companies Mentioned

For more information about this report visit https://www.researchandmarkets.com/r/hvgp4o

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Stem Cell Assays Market Report 2022-2027: Increasing Awareness About Therapeutic Potency of Stem Cells Driving Growth - ResearchAndMarkets.com -...

A common plant from west Africa works as a treatment for sickle cell disease, new research has found.

Scientists at Aberystwyth University isolated a chemical in the Alchornea cordifolia plant, also known as the Christmas Bush, which could help relieve the symptoms of the life-threatening and painful disease suffered by 15,000 people in the UK.

In sufferers of sickle cell anaemia, red blood cells change from their usual soft disc shape to a curved "sickle" shape and also become sticky and hard, which means they don't move properly around the body.

Blood is blocked from flowing, particularly to joints, the chest and abdomen, leading to severe pain, swelling of hands and feet, delayed growth and problems with eyesight, among other symptoms. It can lead to stillbirth and is also fatal in some cases.

A genetic disease, it is more common among people of African, Mediterranean and Middle Eastern descent, with over 20m people around the world affected.

In Nigeria around 150,000 children are born with sickle cell anaemia each year. Half of them are likely to die before their 10th birthday.

Juice from the plant, which grows widely across the tropical regions of Africa, has been used in a "blood tonic" as a traditional remedy for generations, but it has never been scientifically proven to work until now.

Dr Olayemi Adeniyi, a researcher at the university who suffers from the condition herself, interviewed traditional healers from south western Nigeria, who said the plant had been used for years as a treatment.

Leaves are crushed manually or blended, and can also be brewed into a tea.

Dr Adeniyi said the research had shown that quercitrin, the active ingredient in the plant, could both prevent and reverse the "sickling" caused by the disease.

She said: "Until now there has been no scientific proof of the plants effectiveness.

The research is particularly important because so many people affected by sickle cell disease live below the poverty line and have no access to medicine. The plant grows in bushes and is relatively easy to grow on fertile land - all you need are seeds.

Its crucial that people in the countries affected, Africa in particular, hear that this plants benefits have now been scientifically proven. Our findings show that this is a treatment that has firm scientific foundations, not just psychological ones.

Existing treatments are expensive, and some involve blood transfusions. It can only be cured with a stem cell or bone marrow transplant, but this is rarely done because of the risks involved.

The finding "could inform efforts directed to the development of an anti-sickling drug", the paper concluded.

The study formed part of an Aberystwyth University project looking at the scientific effectiveness of traditional and herbal remedies, which has also focused on developing new antibiotics to counter the growing problem of antimicrobial resistance.

Professor Luis Mur, who led the research, said: "We're running out of drug leads. There is a recognition, especially with diseases, that they are evolving, and they're evolving through misuse of antimicrobials for example, and so we need to look at new sources.

"So let's go back to where traditional practices have actually given a hint that this particular plant or fungus has some efficacy."

The results were published in the Journal of Clinical Medicine.

See the article here:
Sickle cell disease could be treated with common plant, study finds - The Telegraph

From left, Vincent Cryns, Mo Chen and Richard A. Anderson. Photo by Tianmu Wen

Two of the most common genetic changes that cause cells to become cancerous, which were previously thought to be separate and regulated by different cellular signals, are working in concert, according to new research from the University of WisconsinMadison.

To date, researchers have focused on finding drugs that block one or the other to treat cancer. Understanding their cooperative effects may lead to more effective treatments.

Cells muster a protein, called p53, which acts inside the cell nucleus to respond to stress, but mutations of the gene that produces p53 are the most frequent genetic abnormalities in cancer. Mutations activating a cellular pathway called PI3K/Akt, located on the surface of cells, are also often implicated in runaway cell growth in cancer.

Outlined in green, this nucleus of a cancerous cell contains DNA in blue and red blobs marking the cells p53 protein binding with parts of the Akt cellular signaling pathway, a partnership that will prevent the cancerous cell from dying as it should and instead prolong its life and lead it to divide into more cancer cells. Image by Mo Chen

Cellular signaling pathways allow cells to accomplish important communications tasks that maintain healthy cell functions. The process is a bit like sending mail, which requires a specific series of steps and appropriate stamps and marks on the envelope to deliver a letter to the correct address.

A team led by UWMadison cancer researchers Richard A. Anderson and Vincent Cryns has discovered a direct link between the p53 and PI3K/Akt pathways. The findings, published today in the journal Nature Cell Biology, identified links in the pathways that make promising targets for new cancer treatments.

We have known for some time that lipid messenger molecules that activate the PI3K/Akt pathway found in membranes are also present in the nucleus of cells, says Anderson, a professor at the UW School of Medicine and Public Health. But what they were doing in the nucleus separate from membranes was a mystery.

Mo Chen, an associate scientist and first author of the new study, used chemotherapy drugs to stress cancer cells and damage their DNA as they were replicating, or creating new copies of themselves (which cancer cells do often). She discovered that proteins called enzymes that are part of the PI3K/Akt pathway bind to the mutated p53 protein in the nucleus of the cell and attach lipid messengers to p53, showing the two are directly linked.

Instead of entering apoptosis the proactive process of cell suicide which removes damaged cells the cancer cells repaired their chemotherapy-damaged DNA and went on growing and dividing, promoting cancer growth.

These results also have critical implications for cancer treatment,

Vincent Cryns

Our finding that the PI3K/Akt pathway is anchored on p53 in the nucleus was entirely unexpected, says Cryns, a physician-scientist and professor at UW School of Medicine and Public Health.

The PI3K/Akt pathway was thought to be confined to membranes.

These results also have critical implications for cancer treatment, Cryns says. Current treatments that target PI3K may not work because they operate on a different enzyme than the one in the pathway the research team discovered.

The enzyme in the new pathway is called IPMK and rendering it inactive keeps p53 proteins from binding with and activating the Akt pathway, like correcting the address on an envelope so it doesnt go to the wrong place. This prevents the pathway from benefitting cancer cells, making IPMK a promising new drug target.

The researchers, whose work is supported by the National Institutes of Health, the Department of Defense and the Breast Cancer Research Foundation, have also identified another enzyme, called PIPKIa, that is a key regulator of both p53 and Akt activation in the cell nucleus.

The team had previously shown that PIPKIa stabilizes the p53 protein, allowing it to be active. When PIPKIa was turned off, p53 levels inside the cell fell sharply. In the new study, the team showed that blocking PIPKIa by genetic approaches or a drug triggered cancer cell death by preventing p53 from activating Akt in the cell nucleus.

What this means is that drug inhibitors of PIPKIa will reduce mutant p53 levels and block Akt activation in the nucleus, potentially a very powerful one-two punch against cancer cells, Cryns says. Their team is actively searching for better PIPKIa drug inhibitors that could be used to treat cancers with p53 mutations or abnormally active PI3K/Akt pathway.

In addition to searching for drugs to block the newly discovered cancer pathway, the scientists are investigating whether other proteins in the cell nucleus are targets of the PI3K/Akt pathway.

We know other nuclear proteins are modified by lipid messengers like p53, but we have no idea how broad the landscape is, Anderson says.

However, the evidence suggests that this could be a feature shared among many kinds of cancers, a mechanism we are calling a third messenger pathway, he adds.

This research was supported in part by grants from the National Institutes of Health (R35GM114386), the Department of Defense (W81XWH-17-1-0258, W81XWH-17-1-0259, W81XWH-21-1-0129) and the Breast Cancer Research Foundation.

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Unexpected link between most common cancer drivers may yield more effective drugs - University of Wisconsin-Madison

With no current treatments for hepatitis A, UNC School of Medicine scientists led by Stanley M. Lemon, MD, discovered how a protein and enzymes interact to allow hepatitis A virus to replicate, and they used a known drug to stop viral replication in an animal model.

CHAPEL HILL, NC The viral replication cycle is crucial for a virus to spread inside the body and cause disease. Focusing on that cycle in the hepatitis A virus (HAV), UNC School of Medicine scientists discovered that replication requires specific interactions between the human protein ZCCHC14 and a group of enzymes called TENT4 poly(A) polymerases. They also found that the oral compound RG7834 stopped replication at a key step, making it impossible for the virus to infect liver cells.

These findings, published in the Proceedings of the National Academy of Sciences, are the first to demonstrate an effective drug treatment against HAV in an animal model of the disease.

Our research demonstrates that targeting this protein complex with an orally delivered, small-molecule therapeutic halts viral replication and reverses liver inflammation in a mouse model of hepatitis A, providing proof-of-principle for antiviral therapy and the means to stop the spread of hepatitis A in outbreak settings, said senior author Stanley M. Lemon, MD, professor in the UNC Department of Medicine and UNC Department of Microbiology & Immunology, and member of the UNC Institute for Global Health and Infectious Diseases.

Lemon, who in the 1970s and 80s was part of a Walter Reed Army Medical Center research team that developed the first inactivated HAV vaccine administered to humans, said research on HAV tapered off after the vaccine became widely available in the mid-1990s. Cases plummeted in the 2000s as vaccination rates skyrocketed. Researchers turned their attention to hepatitis B and C viruses, both of which are very different from HAV and cause chronic disease. Its like comparing apples to turnips, Lemon said. The only similarity is that they all cause inflammation of the liver. HAV is not even part of the same virus family as hepatitis B and C viruses.

Hepatitis A outbreaks have been on the rise since 2016, even though the HAV vaccine is very effective. Not everyone gets vaccinated, Lemon pointed out, and HAV can exist for long periods of time in the environment such as on our hands and in food and water resulting in more than 44,000 cases, 27,000 hospitalizations and 400 deaths in the United States since 2016, according to the CDC.

Several outbreaks have occurred over the past several years, including in San Diego in 2017 driven largely by homelessness and illicit drug use, causing severe illness in about 600 people and killing 20. In 2022, there was a small outbreak linked to organic strawberries in multiple states, leading to about a dozen hospitalizations. Another outbreak in 2019 was linked to fresh blackberries. Globally, tens of millions of HAV infections occur each year. Symptoms include fever, abdominal pain, jaundice, nausea, and loss of appetite and sense of taste. Once sick, there is no treatment.

In 2013, Lemon and colleagues discovered that the hepatitis A virus changes dramatically inside the human liver. The virus hijacks bits of cell membrane as it leaves liver cells, cloaking itself from antibodies that would have otherwise quarantined the virus before it spread widely through the blood stream. This work was published in Nature and provided insight into how much researchers had yet to learn about this virus that was discovered 50 years ago and has likely caused disease dating back to ancient times.

A few years ago, researchers found that hepatitis B virus required TENT4A/B for its replication. Meanwhile, Lemons lab led experiments to search for human proteins that HAV needs in order to replicate, and they found ZCCHC14 a particular protein that interacts with zinc and binds to RNA.

This was the tipping point for this current study, Lemon said. We found ZCCHC14 binds very specifically to a certain part of HAVs RNA, the molecule that contains the viruss genetic information. And as a result of that binding, the virus is able to recruit TENT4 from the human cell.

In normal human biology, TENT4 is part of an RNA-modification process during cell growth. Essentially, HAV hijacks TENT4 and uses it to replicate its own genome.

This work suggested that stopping TENT4 recruitment could stop viral replication and limit disease. Lemons lab then tested the compound RG7834, which had previously been shown to actively block Hepatitis B virus by targeting TENT4. In the PNAS paper, the researchers detailed the precise effects of oral RG7834 on HAV in liver and feces and how the viruss ability to cause liver injury is dramatically diminished in mice that had been genetically modified to develop HAV infection and disease. The research suggests the compound was safe at the dose used in this research and the acute timeframe of the study.

This compound is a long way from human use, Lemon said, But it points the path to an effective way to treat a disease for which we have no treatment at all.

The pharmaceutical company Hoffmann-La Roche developed RG7834 for use against chronic hepatitis B infections and tested it in humans in a phase 1 trial, but animal studies suggested it may be too toxic for use over long periods of time.

The treatment for Hepatitis A would be short term, Lemon said, and, more importantly, our group and others are working on compounds that would hit the same target without toxic effects.

This research was a collaboration between the Lemon lab and the lab of Jason Whitmire, professor of genetics at the UNC School of Medicine. Lemon and Whitmire are members of the UNC Lineberger Comprehensive Cancer Center.

First authors of the PNAS paper are You Li and Ichiro Misumi. Other authors, all at UNC, are Tomoyuki Shiota, Lu Sun, Erik Lenarcic, Hyejeong Kim, Takayoshi Shirasaki, Adriana Hertel-Wulff, Taylor Tibbs, Joseph Mitchell, Kevin McKnight, Craig Cameron, Nathaniel Moorman, David McGivern, John Cullen, Jason K. Whitmire, and Stanley M. Lemon.

This work was supported by grants from the National Institute of Allergy and Infectious Diseases (R01-AI131685), (R01-AI103083), (R01-AI150095), (R21-AI163606), (R01-AI143894), (R01-AI138337). The UNC Pathology Services Core and UNC High-Throughput Sequencing Facility were supported in part by a National Cancer Institute Center Core Support Grant (P30CA016086) to the UNC Lineberger Comprehensive Cancer Center.

Media contact: Mark Derewicz, 919-923-0959

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Scientists Discover Key to Hepatitis A Virus Replication, Show Drug Effectiveness | Newsroom - UNC Health and UNC School of Medicine

The research showed that chemotherapy combined with the erectile dysfunction drugs known as PDE5i shrunk the tumors more than chemotherapy alone.

According to a recent study supported by Cancer Research UK and the Medical Research Council, a category of drugs often used to treat erectile dysfunction may be able to improve the effectiveness of chemotherapy in treating esophageal cancer.

The study, which was recently published in Cell Reports Medicine, discovered that PDE5 inhibitors, which are drugs that target cells called cancer-associated fibroblasts (CAFs) in the vicinity of the tumor, may reverse chemotherapy resistance.

Even though it is still early in the research process, PDE5 inhibitors with chemotherapy may be able to shrink certain esophageal tumors more effectively than chemotherapy alone, conquering chemotherapy resistance, one of the biggest obstacles to treating esophageal cancer.

Although it is a relatively uncommon condition, the UK has one of the highest rates in the world, with 9,300 new instances of esophageal cancer diagnosed there each year. Esophageal cancer affects the food pipe that links your mouth to your stomach.

Currently, this illness has substantially worse outcomes and treatment choices than other cancers, with just around 1 in 10 patients living for 10 years or more. Part of the reason for this is that it can be resistant to chemotherapy in many circumstances, with roughly 80% of patients not responding.

Resistance to chemotherapy in esophageal cancer is influenced by the tumor microenvironment, the area that sounds the tumor. This is made up of molecules, blood vessels, and cells such as cancer-associated fibroblasts (CAFs), which are important for tumor growth. It feeds the tumor and can act as a protective cloak, preventing treatments like chemotherapy from having an effect.

The team of researchers led by Professor Tim Underwood at the University of Southampton wanted to identify the cells in the tumor microenvironment which protect the tumor from treatment so they could target them.

The researchers found that levels of PDE5, an enzyme originally found in the wall of blood vessels are higher in esophageal adenocarcinoma compared with healthy esophageal tissue. High levels of PDE5 were found in CAFs within the tumor microenvironment. They also found that high expression of PDE5 is associated with worse overall survival, suggesting that PDE5 would be an effective target for treatment.

Following this, the researchers tested a PDE5 inhibitor, PDE5i, on CAFs from esophageal tumors. They found that PDE5i were able to suppress CAF activity and make them look more like normal fibroblasts.

Next, collaborating researchers at the University of Nottingham took samples of tumor cells from 15 tissue biopsies from eight patients and used them to create lab-grown artificial tumors. They tested a combination of PDE5i and standard chemotherapy on the tumors. Of the 12 samples from patients whose tumors developed a poor response to chemotherapy in the clinic, 9 were made sensitive to standard chemotherapy by targeting CAFs with PDE5i.

The researchers also tested the treatment on mice implanted with chemotherapy-resistant esophageal tumors and found that there were no adverse side effects to the treatment and that chemotherapy combined with PDE5i shrunk the tumors more than chemotherapy alone.

An added benefit of using PDE5 inhibitors is that they are already proven to be a safe and well-tolerated class of drug thats given to patients worldwide, even in the high doses that would be required for this treatment. The researchers also say that giving PDE5 inhibitors to people with esophageal cancer would be extremely unlikely to cause erections without the appropriate stimulation.

Professor Tim Underwood, the lead author of the study and a professor of gastrointestinal surgery at the University of Southampton, said, The chemotherapy-resistant properties of esophageal tumors mean that many patients undergo intensive chemotherapy that wont work for them. Finding a drug, which is already safely prescribed to people every day, could be a great step forward in tackling this hard-to-treat disease.

With the proven safety of these drugs and the positive results from this research, the researchers next step is a phase I/II clinical trial testing a PDE5 inhibitor in combination with chemotherapy in patients with advanced esophageal cancer.

If successful, this treatment could be helping a significant proportion of the around 9300 people a year diagnosed with esophageal cancer within the next 5 to 10 years. The study could pave the way for the use of PDE5 inhibitors in other cancer types.

Michelle Mitchell, chief executive of Cancer Research UK, said: Developing new drugs for cancer is incredibly important, but doing so from scratch is a challenging process, and many fail along the way. Weve also been keen to explore whether existing drugs, licensed for other diseases, can be effective in treating cancer. If these turn out to be successful treatments, they will also prove to be more affordable and become available to patients quicker.

Progress in treatment for esophageal cancer over the last 40 years has seen only limited improvement, which is why weve made it a research priority. Were looking forward to seeing how the combined treatment of PDE5 inhibitors with chemotherapy performs in clinical trials.

Nicola Packer, an HR manager from Basingstoke, was diagnosed with esophageal cancer at age 53. She was being monitored due to her diagnosis of a condition called Barretts esophagus, which can be a risk factor for esophageal cancer They found my tumor last February. They caught it at stage 2, which is unusual for esophageal tumors as they often go undetected for a long time and are mostly diagnosed at stage 3 or 4.

Chemo generally doesnt work that well on my kind of esophageal tumor so I knew it couldnt get rid of the tumor completely, that it could only shrink it with the hopes of making surgery more effective. The chemo was draining and each week they would tell me it was shrinking my tumor, but slowly. The anxiety you feel after going through chemotherapy and then having to wait through the weeks of recovery before you can have surgery, knowing that the chemo could only do so much is overwhelming.

Research like this that could mean people like me can have a better response to chemotherapy is incredibly important.

The study was funded by Cancer Research UK and the University Hospital Southampton NHS Foundation Trust.

Reference: Phosphodiesterase type 5 inhibitors enhance chemotherapy in preclinical models of esophageal adenocarcinoma by targeting cancer-associated fibroblast by Benjamin P. Sharpe, Annette Hayden, Antigoni Manousopoulou, Andrew Cowie, Robert C. Walker, Jack Harrington, Fereshteh Izadi, Stella P. Breininger, Jane Gibson, Oliver Pickering, Eleanor Jaynes, Ewan Kyle, John H. Saunders, Simon L. Parsons, Alison A. Ritchie, Philip A. Clarke, Pamela Collier, Nigel P. Mongan, David O. Bates, Kiren Yacqub-Usman, Spiros D. Garbis, Zo Walters, Matthew Rose-Zerilli, Anna M. Grabowska and Timothy J. Underwood, 21 June 2022, Cell Reports Medicine.DOI: 10.1016/j.xcrm.2022.100541

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How Erectile Dysfunction Drugs Can Help Treat Cancer and Save Thousands of Lives - SciTechDaily

Dr Mohan R Wani has been appointed as the director of Pune-based National Centre for Cell Science (NCCS), a premier research institute under the Department of Biotechnology, Ministry of Science and Technology, Government of India.

The NCCS has been carrying out cutting-edge research in various domains such as cell and cancer biology, infectious diseases and immunology, stem cell and regenerative medicine, structural biology and bioinformatics, said Dr Wani.

Notably, Dr Wani has made significant research contribution in understanding the regulation of cellular and molecular pathophysiology of important skeletal and autoimmune diseases, including osteoporosis, osteoarthritis, and rheumatoid arthritis. His group has also contributed to the field of stem cell biology and regenerative medicine.

Dr Wani said the NCCS will continue to address research questions pertaining to human health and diseases by further strengthening basic and translational research through a multidisciplinary approach, along with national and international collaborations.

Dr Wani completed his post-graduation in Veterinary Surgery from Nagpur Veterinary College. Thereafter, he obtained his PhD in Human Medicine from St Georges Hospital Medical School, University of London, England. He is also a fellow of prestigious science academies like the Indian National Science Academy (INSA), National Academy of Sciences India (NASI), National Academy of Veterinary Sciences (NAVS) and National Academy of Medical Sciences (NAMS).

His research work is published in several high impact peer-reviewed international journals and he has mentored scores of PhD, medical and veterinary students, and postdoctoral fellows. He is a recipient of several prestigious awards including the Commonwealth Fellowship, BM Birla Science Prize, and National Bioscience Award, among others.

The rest is here:
Pune: Dr Mohan Wani appointed as director of National Centre for Cell Science - The Indian Express