CAMBRIDGE, England--(BUSINESS WIRE)--Divide & Conquer (D&C), a biotechnology company formed in 2018 with a 10 million (approximately $13.1 million) Series A financing from Medicxi. has left stealth mode to mark the publication of another paper in Nature co-authored by one of its founders, Prof. Frank Winkler of Heidelberg University.

Leveraging Prof. Winklers ground-breaking research published in Nature in 2015 and again this month, Divide & Conquer aims to open a new front in the war on cancer by disrupting the cell-to-cell communication mechanisms of solid tumour cells. The new research shows that the ability of cancer cells to form social networks makes them almost invincible, which is why current drugs fail to cure many patients.

The companys initial focus is on glioblastoma, a lethal form of brain cancer, where cancer cells have been shown to communicate with each other via structures called tumour microtubes.

Co-Founder David Grainger, PhD commented, There is mounting evidence, accumulated over decades, and now taken to the next level in Prof. Winklers papers in Nature, that solid tumours can leverage this network effect to evade all attempts to kill them. We now have compelling evidence that it can be disrupted, with the potential to render the most lethal tumour types curable.

Professor Miroslav Radman, the third co-founder of Divide & Conquer, was one of the first academic scientists to propose that mutation-riddled tumours must share materials between themselves, and with healthy cells, in order to survive and propagate. Bringing together his expertise with that of Prof. Winkler has allowed Divide & Conquer to discover a new class of cancer therapeutics that focus on disrupting these networks.

There is no shortage of biotech start-ups targeting cancer, but this research from Professors Radman and Winkler represents some of the most exciting work in the area that Ive seen, said Moncef Slaoui, PhD, a Director at Divide & Conquer. Glioblastoma is a devastating disease and one of the greatest unmet medical needs. The evidence is now compelling that these networks lie at the heart of this cancers resistance to treatment. At Divide & Conquer we aim to develop new medicines that disrupt such communication between cancer cells and bring these to clinical trials in patients.

Nature is publishing Prof Winklers latest research concurrently with an article on a related topic by a team at Stanford Medicine led by Michelle Monje, MD, PhD, Associate Professor of Neurology and Neuro-Oncology, emphasising the growing body of research in this area.

Dr. Slaoui concluded, Beyond glioblastoma, we envision expanding to other solid tumours such as brain metastasis, the hardest to treat form of breast cancer (so-called triple negative), pancreatic cancer and others. Indeed, we predict that the drugs we develop may be most effective in tumours that are currently the most difficult to treat.

Links

About the Divide & Conquer Founding Team

About Cellular Parabiosis

Cellular parabiosis refers to the ability of individual cells in a tissue to share and exchange contents: ions, small molecules, ribonucleic acid (RNA), proteins, and even whole cell organelles. This cellular solidarity is established via extensions such as tunnelling nanotubes (TNTs) and tumour microtubes (TMs), and transport vehicles such as exosomes, and pores such as gap junctions. Cellular parabiosis allows mutation-riddled tumours to survive and thrive, and even share their toolkit of resistance mechanisms. More information on Cellular Parabiosis is here.

About Divide & Conquer

Divide & Conquer is a biotechnology company focused on discovery and development of a new class of oncology therapeutics aimed at disrupting communication and complementation between cancer cells, also known as cellular parabiosis. The company was founded by David Grainger, PhD, Prof. Miroslav Radman, and Prof. Frank Winkler, and received A-round funding from Medicxi.

Please see conquer.bio for more information, and connect with the company on Twitter and LinkedIn.

About Medicxi

Medicxi is an international investment firm with the mission to create and invest in companies across the full healthcare continuum. Medicxi was established by the former Index Ventures life sciences team and invests in both early stage and late stage therapeutics with a product vision that can fulfill a clear unmet medical need. GlaxoSmithKline, Johnson & Johnson Innovation JJDC, Inc., Novartis and Verily (an Alphabet company) are investors in Medicxi funds.

Medicxis team has been investing in life sciences for over 20 years. Globally, it has invested in 89 innovative biopharma companies and achieved 32 exits through IPO and M&A, including Genmab (NASDAQ Copenhagen: GEN), PanGenetics (sold to AbbVie), Cellzome (sold to GSK), Micromet (sold to Amgen), Molecular Partners (SWX: MOLN), XO1 (sold to Janssen Pharmaceuticals, Inc.), Minerva Neurosciences (NASDAQ: NERV), Padlock Therapeutics (sold to Bristol-Myers Squibb), Gadeta (structured transaction with Gilead), Impact Biomedicines (sold to Celgene), and Adaptive Biotechnologies (NASDAQ: ADPT).

Please see http://www.medicxi.com for more information.

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About one in three diabetic patients develops diabetic retinopathy (DR), which can impair vision and lead to blindness. A newstudyinThe American Journal of Pathology, published by Elsevier, provides clear evidence that high glucose increases the levels of enzymatic precursor--lysyl oxidase propeptide (LOX-PP)--that promotes cell death, which was verified in an animal model of diabetes. These findings may help develop novel DR treatments by targeting LOX-PP or its metabolites.

"We found that hyperglycemic and diabetic conditions increased LOX-PP levels," explained lead investigator Sayon Roy, PhD, of the Departments of Medicine and Ophthalmology at Boston University School of Medicine, Boston, MA, USA. "LOX-PP may induce cell death by compromising a cell survival pathway, and in retinas of diabetic rats, increased LOX-PP contributed to retinal vascular cell death associated with DR. Administration of recombinant LOX-PP alone was sufficient to induce cell death. This report shows novel functionality of LOX-PP in mediating cell death under high glucose condition in retinal endothelial cells as well as in diabetic animals."

Studies in pancreatic and breast cancer cells suggest that LOX-PP overexpression may trigger cell death. The researchers therefore studied the role of LOX-PP in the retinal tissue. The retinal blood vessels of normal and diabetic rats and normal rats administered artificially synthesized LOX-PP (recombinant LOX-PP, rLOX-PP) directly into the eye, were examined. Changes associated with DR such as swelling, blood vessel leakage, blockage or thickening of vascular walls, and histologic indicators such as acellular capillaries (AC) and pericyte loss (PL) were studied.

More AC and PL were observed in the retinas of diabetic rats compared to controls. In non-diabetic rats, injection of rLOX-PP directly into the eye also increased the number of ACs and PLs compared to rats receiving a control injection.

The effect of high glucose on retinal endothelial cells grown in culture was also studied. Adding glucose to the cell cultures up-regulated LOX-PP expression and reduced AKT (protein kinase B) activation. Cells exposed to rLOX-PP alone exhibited increased cell death along with decreased AKT phosphorylation. The present study provides clear evidence that high glucose increases LOX-PP levels, which in turn promotes cell death. Furthermore, LOX-PP appears to induce cell death by compromising a pathway involved in cell survival.

"DR is the leading cause of blindness in the working age population," noted Dr. Roy. "Unfortunately, there is no cure for this devastating ocular complication. Our findings suggest a novel mechanism for high glucose-induced cell death involving LOX-PP, which may be a therapeutic target in preventing retinal vascular cell loss associated with DR."

LOX is an extracellular enzyme responsible for cross-linking collagen and elastin molecules to form a stable extracellular matrix. The role of the LOX propeptide, LOX-PP, is less understood, although it may play a role in keeping LOX in an inactive state.

Reference: Kim, et al. (2019) Effects of High GlucoseInduced Lysyl Oxidase Propeptide on Retinal Endothelial Cell Survival: Implications for Diabetic Retinopathy.The American Journal of PathologyDOI:https://doi.org/10.1016/j.ajpath.2019.06.004

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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A Potential Drug Target for Diabetic Retinopathy - Technology Networks

Scientists have discovered a compound could help slow down pancreatic cancer by targeting proteins that promote metastatic cells.

Researchers at Johns Hopkins Medicine found that the compound, 4-HAP, reduced tumors in mice and could improve survival for pancreatic cancer patients.

According to the National Cancer Institute, 73,554 people in the U.S. have pancreatic cancer and only 9.3 percent of those diagnosed survive five or more years.

The study, published in the journal Cancer Research, examined two types of proteins, mechanoresponsive proteins and non-mechanoresponsive proteins.

Scientists looked at a total of seven proteins, including nonmuscle myosin IIA, IIB and IIC; alpha-actinin 1 and 4; and filamin A and B. The mechanoresponsive proteins IIA, IIC, active actinin 4 and filamin B increased cancer tissue in the pancreas by over-producing the cancer cells.

Scientists found that even though the protein nonmuscle myosin IIC was found to be low in the cancer cells it had a profound impact on the cell's overall function. When they exposed these proteins to 4-HAP, it increased the cells' overall structure and stiffened the cells.

The group then tested 4-HAP as a treatment for pancreatic cancer by using a mouse model that had human pancreatic tissue implanted in the mouse's liver. They found that the tumors reduced by 50 percent.Researchers believe that treating the cells with the compound will allow scientists to target cancerous cells while protecting the healthy cells in the pancreas.

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A compound may improve pancreatic cancer survival rate, scientists find - PhillyVoice.com

As of Sept. 1, Kara Sawarynski, Ph.D., has been continuing to tap the problem-solving/critical thinking skills she developed as an academic throughout her education and career, but in a new capacity as the vice chair of Foundational Medical Studies at Oakland University William Beaumont School of Medicine.

As vice chair, her primary responsibilities are to support the departments ongoing development of research programs, assist the chair in promoting faculty development and collaborations, and serve as a sounding board for faculty ideas and issues. She hopes to use her substantial connections at both Oakland University and Beaumont Health, to help foster Foundational Medical Studies strategic mission and goals.

Sawarynski said shes excited about the opportunity and plans to begin by learning more about her colleagues what their respective strengths are, and what their goals are with respect to careers and research.

I really hope to offer assistance and help build connections between shared interests that might be undiscovered, so that I can help others succeed, she said.

Sawarynski joined the Department of Foundational Medical Studies as a full-time faculty member in 2012. Sawarynski, a recently tenured associate professor, will continue teaching cell biology in the basic science courses, as well as co-directing the Embark research program.

Sawarynski received her bachelor of science degree in Biomedical Sciences from the Lee Honors College of Western Michigan University. She completed her doctoral work in cancer biology at Wayne State University School of Medicine and the Barbara Ann Karmanos Cancer Institute.

When Sawarynski completed her work at Karmanos, she started working as a research associate at William Beaumont Hospital in Royal Oak, in the infectious disease lab of Matt Sims, M.D., director of Infections Disease Research, Beaumont Health, and OUWB professor.

While still at Beaumont, Sawarynski became an adjunct assistant professor in the Department of Biomedical Sciences (since changed to the Department of Foundational Medical Studies) and was involved with helping to plan the basic science curriculum. She also taught some of the schools first sessions to its charter class in 2011.

Finding her passion as an educatorSawarynski said it didnt take her long to realize how much she liked being an educator. After the inaugural OUWB class completed its first year, Sawarynski made the move to OUWB on a full-time basis as a tenure-track assistant professor.

I love research and I love everything that comes with it, she said, noting her research career has included molecular and cellular biology, cancer biology, infectious diseases (and now medical education techniques).

But the bacteria youre working with (in research) doesnt talk back to you, Sawarynski said. Being a people person, I realized its a lot more fun engaging with students. I also came to realize how fulfilling it can be.

Thats why she also finds it rewarding to be co-director of OUWBs Embark research program an OUWB required scholarly concentration that provides a mentored introduction to research and scholarship. The four-year longitudinal curriculum consists of structured coursework in research design and implementation, compliance training, research communication, and scholarly presentation, with protected time to develop mentored projects in a wide-range of community and health-related settings.

Sawarynskis responsibilities include development and implementation of the longitudinal research design courses, directing of the first year through fourth year medical students in the conception and execution of their required independent research projects, and oversight on Embark program events.

Its so energizing to not necessarily be a specific expert in all of the fields students are trying to research, but help them look at specific problems and analyze them, Sawarynski said. I enjoy helping them realize that while there can be frustrating aspects of what theyre doing, they gain from every experience.

With regard to her work as a department vice chair, Sawarynski said she plans to begin by learning more about her colleagues what their respective strengths are, and what their goals are with respect to careers and research.

Sawarynski said that its an exciting time at the school as it moves into its next phase.

Someone says You know, I have this idea and I start brainstorming. I think about all the different ways that we could think about the idea, or how to attack different goals, she said We can really start to look for ways to involve the mission of the school, our own experiences and expertise, and look for ways to work together to do some pretty cool things.

For more information, contact Andrew Dietderich, marketing writer, OUWB, atadietderich@oakland.edu.

Follow OUWB on Facebook, Twitter, and Instagram.

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New vice chair named for OUWB Department of Foundational Medical Studies - News at OU

In a recent review, scientists highlight the potential of gene editing technologies like CRISPR/Cas9 to not only understand the molecular mechanisms behind Parkinsons disease, but also identify new targets for treatment.

The review study, Interrogating Parkinsons disease associated redox targets: Potential application of CRISPR editing, was published in the journal Free Radical Biology and Medicine.

One of the hallmarks of PD is the loss of dopamine-producing neurons in the substantia nigra a brain region involved in the control of voluntary movements, and one of the most affected in PD. This occurs due to the clustering of a protein called alpha-synuclein in structures commonly known as Lewy bodies inside neurons.

Parkinsons is complex and multifactorial disease, with both genetic and environmental factors playing a role in either triggering or exacerbating the disease.

Genetic causes can explain 10% of all cases of PD called familial PD , meaning that in the majority of the cases (sporadic PD) there is an interplay between genetics and environmental risk factors.

Researchers atSechenov Universityin Russia and theUniversity of Pittsburgh reviewed the role of metabolic pathways, especially problems with mitochondria cells powerhouses and iron accumulation, as well as mechanisms in cell death (called apoptosis and ferroptosis) in the development and progression of Parkinsons disease.

These processes were discussed in the context of genome editing technologies, namely CRISPR/Cas9 a technique that allows scientists to edit genomes, inserting or deleting DNA sequences, with precision, efficiency and flexibility.

CRISPR is a promising technology, a strategy to find new effective treatments to neurodegenerative diseases, Margarita Artyukhova, a student at the Institute for Regenerative Medicineat Sechenov and the study first author, said in a press release.

Mitochondria dont work as they should in people withPD, resulting in shortages of cellular energy that cause neurons to fail and ultimately die, particularlydopamine-producing neurons. Faulty mitochondria are also linked to the abnormal production of reactive oxygen species, leading to oxidative stressan imbalance between the production of free radicals and the ability of cells to detoxify them that also damages cells over time.

Because mitochondrial dysfunction is harmful, damaged mitochondria are usually eliminated (literally, consumed and expelled) in a process called mitophagy an important cleansing process in which two genes, called PINK1 and PRKN, play crucialroles. Harmful changes in mitophagy regulation is linked with neurodegeneration in Parkinsons.

Previous studies with animal models carrying mutations in the PINK1and PRKNgenes showed that these animals developed typical features of PD mitochondrial dysfunction, muscle degeneration, and a marked loss of dopamine-producing neurons.

PINK1codes for an enzyme that protects brain cells against oxidative stress, whilePRKNcodes for a protein called parkin. Both are essential for proper mitochondrial function and recycling by mitophagy. Mutations in both the PINK1 and PRKNgene have been linked with early-onset PD.

However, new research suggests that the role of PINK1 and PRKNin Parkinsons could be more complex and involve other genes likePARK7(DJ-1), SNCA (alpha-synuclein) andFBXO7 as well as a fat molecule called cardiolipin.

CRISPR/Cas9 genome editing technology may be used to help assess the role of different genetic players in Parkinsons disease, and to look for unknown genes associated with disease progression and development. Moreover, this technology can help generate animal and cellular models that might help scientists decipher the role of certain proteins in Parkinsons and discover potential new treatment targets.

Iron is another important metabolic cue in Parkinsons. While its essential for normal physiological functions, excessive levels of iron can be toxic and lead to the death of dopamine-producing neurons in the substantia nigra.

Iron may also interact with dopamine, promoting the production of toxic molecules that damage mitochondria and cause alpha-synuclein buildup within neurons.

CRISPR/Cas9 technology can be used to help dissect the role of proteins involved in iron transport inside neurons, which in turn may aid in designing therapies to restore iron levels to normal in the context of Parkinsons disease.

Finally, researchers summarized evidence related to the role of two cell death pathways ferroptosis and apoptosis in PD. Ferroptosis is an iron-dependent cell death mechanism by which iron changes fat (lipid) molecules, turning them toxic to neurons. This process has been implicated in cell death associated with degenerative diseases like Parkinsons, and drugs that work to inhibit ferroptosis have shown an ability to halt neurodegeneration in animal models of the disease.

Apoptosis refers to a programmed cell death mechanism, as opposed to cell death caused by injury. Both apoptosis and ferroptosis speed the death of dopaminergic neurons.

CRISPR/Cas9 may help to pinpoint the key players in cell death that promote the loss of dopaminergic neurons in Parkinsons disease, while understanding the array of proteins that are involved in these processes.

These insights into the mechanisms of PD pathology [disease mechanisms] may be used for the identification of new targets for therapeutic interventions and innovative approaches to genome editing, including CRISPR/Cas9, the researchers wrote.

Genome editing technology is currently being used in clinical trials to treat patients with late-stage cancers and inherited blood disorders, Artyukhova notes in the release.

These studies allow us to see vast potential of genome editing as a therapeutic strategy. Its hard not to be thrilled and excited when you understand that progress of genome editing technologies can completely change our understanding of treatment of Parkinsons disease and other neurodegenerative disorders, she adds.

Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.

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CRISPR/Cas9 Potential in Advancing Parkinson's Understanding and Treatment Focus of Review Study - Parkinson's News Today

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JOHANNESBURG - After the establishment of the new constitution of the US, Benjamin Franklin wrote a letter in 1789 stating that nothing in this world is certain, except death and taxes. But now it seems that some scientists are not that sure about death anymore.

For a long time people have strived to live longer with the result that one of the important medical frontiers today is to extend the human lifespan. In June 2018, the World Health Organisation published the 11th edition of its International classification of diseases, which contained a seemingly insignificant new addition, namely, Code MG2A: Old age.

However, this minute inscription could be one of the most important inclusions in human history and could potentially lead to the development of new drugs designed to treat one of the worlds most universal ailments ageing, which has been known as a major contributing cause to most other age related illnesses.

Although regulatory changes will be necessary, this new approach to ageing would make it possible for medical doctors to eventually prescribe medicines to slow the condition of ageing and ultimately death.

Notwithstanding the absence of the necessary regulatory environment, bio-medical research has been making considerable progress over the past few years. Since Clive McCay discovered in 1934 that the restriction of caloric intake through limited diets extended the live of rats, Michael Rose from the University of California, Irvine, in 1981 bred a strain of fruit fly that can live four times longer than normal.

In 1993 Cynthia Kenyon and her team from the University of San Francisco discovered the daf-2 mutation, which doubled the life span of roundworms (nematodes).

In addition to numerous genetic studies, it was inevitable that drugs would be developed to slow ageing and extend human life. In 2006 Matt Kaeberlein from the University of Washington, demonstrated that rapamycin a drug isolated from soil bacteria on Easter Island could increase the life span of yeast cells. It was later proven that rapamycin increases the life span of mice by 24percent.

In 2016 Nir Barzilai, director of the Institute for Ageing Research at the Albert Einstein College of Medicine discovered that metformin, could prolong the life span of silkworms. Metformin (marketed under the trade name Glucophage) is a well-known and effective first-line medication used by millions of people with type 2 diabetes.

Over the last five years researchers discovered that this now inexpensive generic and widely available drug influences several metabolic and cellular processes closely associated with the development of age-related conditions. Except for metformins lowering of glucose levels, it also has an effect on inflammation, ameliorates DNA and cellular damage, improves muscle tissue health, preserve cognitive function, and reduce mortality.

The reduction of chronic damage resulting from inflammation eventually could have positive benefits for ageing, cardiovascular disease, Alzheimers disease and cancer.

Numerous animal studies have proved that metformin may delay the ageing process and have a neuroprotective role. Therefore Barzilai and his team are taking their research one step further to demonstrate metformins ability in humans to delay the onset of comorbidities related to ageing, thereby reducing the period of morbidity at the end of life and increasing the health span of people.

Dr Tze Pin Ng and colleagues from the National University of Singapore published their research in The Journal of Alzheimer disease, indicating that metformin was inversely associated with cognitive impairment.

After reviewing thousands of medical records, Dr Scherrer form Saint Louis University in June 2019 published an article showing that African Americans older than 50 years and treated with metformin had a much lower risk for dementia. It is thus becoming clear that metformin could play an important role in deferring the onset of Alzheimers disease and dementia.

In an observational study Dr Bannister from Cardiff University found patients with type 2 diabetes treated with metformin monotherapy lived significantly longer than patients treated with alternative medicine or even a large control group without diabetes or medication. This research implies that metformin may have benefits even for non-diabetes.

However, despite all the benefits of metformin, we are still years away from being able to state with absolute confidence that metformin prevents ageing.

Numerous new start-ups are currently searching for life extending drugs, such as the biopharmaceutical company resTORbio that is researching a drug known to enhance immunity against age-related viral infections. The same drug may in fact also prevent numerous other manifestations of ageing.

Calico (an acronym for California Life Company) is a secretive biotech company in the USA that is a division of Alphabet (the Google parent company). Although the company states that they focus on health and wellbeing and the challenge of ageing, it is well known that according to Art Levinson, the chief executive, the mission of the company is in fact to achieve human immortality. The company therefore researches therapies for age-related illnesses in an attempt to extend human life span.

In November last year Calico hired Dr Garret FitzGerald, an Irish professor, who is an expert on molecular clocks or the idea that genes operate on 24-hour cycles, which could be altered to slow down cell damage and delay Alzheimers.

The California start-up Unity Biotechnology is researching drugs that could remove the zombie-like cells that accumulate with age, while CohBar is attempting to harness the power of mitochondria-based therapeutics aimed at slowing ageings effects.

A research team from Mayo, Wake Forest and the University of Texas, San Antonio, recently announced promising results from early human trials with senolytics agents that selectively destroy senescent cells or induce cell death.

The researchers claimed that they were able to stop Alzheimers disease in it tracks.

Without doubt, anti-ageing medicines are now amongst the top ten disruptive innovations. Contrary to popular belief, there is no biological law that determines that people must age. Ageing is currently the biggest risk factor behind most of the age-related diseases. Quite often when one disease in older people is addressed through treatment and it improves, another disease will often replace it, unless ageing itself is targeted.

Ageing research is therefore focusing not only on extending human life, but the eradication of disease itself.

Although the processes for extending life are complicated, the metformin research has shown that sometimes it may be as simple as repurposing medications that are already available and affordable.

If we ask a person to point out persons who are 70 years old it is quite easy, since we all know the biology of ageing. But to think that it is normal and that we cannot do anything about it, is an error.

Research shows that we can intervene in ageing, even in the later phases. People 50 years or older most probably have a brighter future since it is possible that they would not be ageing as fast or poorly as their parents.

Over the years cosmetic companies have through clever marketing convinced women to buy moisturisers and other anti-ageing cosmetics. Most pharmacies would have at least fifty or more products that falsely claim to be anti-ageing.

Unfortunately most creams achieve very little and the vitamins only give users expensive urine. Currently this market is worth hundreds of billions of rand per year. Just imagine how much a pill that could really slow ageing or stop death could be worth. In the era of the fourth industrial revolution nothing seems to be impossible everything could be hacked, including the human body.

Although some people might frown on the possibility of a tablet extending human life, the situation is not unfamiliar. Before Louis Pasteur enlightened the world with his germ theory in the 1880s, people believed death by disease was inevitable.

The discovery of penicillin in 1928 totally changed this believe. So why not envisage a time in the future when scientists could stop ageing and age-related illnesses and offer a better quality of life? Economically it would bring welcome relieve to overextended healthcare services and the ill-planned National Health Insurance of South Africa.

The technologies being developed now would not only give us extra years of life, but also extra years of youth.

In the years to come we will begin to understand that ageing is something that can be reversed.

Whether we will live long enough to benefit from innovation in this sector or be the last generation to live a relatively short life depends on current innovation, human trials and regulatory changes to make it possible.

Perhaps, it is indeed time that we start treating age as a disease.

Professor Louis C H Fourie is a futurist and technology strategist.

BUSINESS REPORT

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OPINION: Bid to stop ageing - research continues - IOL

DUBLIN, Sept. 20, 2019 /PRNewswire/ -- The "Global Stem Cell Therapy Market: Focus on Treatment Type, Cell Source, Indication,11 Countries' Data, and Competitive Landscape - Analysis and Forecast, 2019-2029" report has been added to ResearchAndMarkets.com's offering.

Key Questions Answered in this Report:

The Global Stem Cell Therapy Industry Analysis projects the market to grow at a significant CAGR of 27.99% during the forecast period, 2019-2029.

The global stem cell therapy market growth has been primarily attributed to the major drivers in this market such as the increasing prevalence of chronic diseases, rising number of clinical trials for cell-based therapy, steady investment, and consolidation in the regenerative medicine market, and favorable regulatory environment.

The market is expected to grow at a significant growth rate due to the opportunities that lie within its domain, which include product approvals, declining product price, and increasing adoption rate.

However, there are significant challenges which are restraining the market growth. High treatment cost, the exorbitant cost required for set up, and ethical considerations related to the use of embryonic stem cells are the challenges faced by the market.

Key Topics Covered:

Executive Summary

1 Product Definition

2 Scope of the Work2.1 Overview: Report Scope2.2 Segmentation of the Global Stem Cell Therapy Market2.3 Assumptions and Limitations2.4 Key Questions Answered in the Report2.5 Base Year and Forecast Period

3 Research Methodology3.1 Overview: Report Methodology

4 Global Stem Cell Therapy Market4.1 Market Overview4.2 Introduction of Stem Cell Therapy4.3 Application of Stem Cells in Different Therapeutic Areas4.4 Market Dynamics4.5 Global Market Scenario4.6 Assumptions and Limitations

5 Competitive Landscape5.1 Overview5.2 Key Developments and Strategies5.2.1 Collaborations, and Partnerships5.2.2 Approvals and Clinical Studies5.2.3 Funding5.2.4 Business Expansions5.2.5 Product Launches and Developments5.2.6 Mergers and Acquisitions5.2.7 Others5.3 Market Share Analysis

6 Industry Insights6.1 Regulatory Scenario6.2 Regulatory Designations6.3 Expedited Designation Vs. Traditional Approval Timelines:6.4 Regulatory Challenges:

7 Global Stem Cell Therapy Market (by Treatment Type)7.1 Overview7.2 Key Trends of the Global Stem Cell Therapy Market (by Treatment Type)7.3 Autologous Treatment7.4 Allogenic Treatment

8 Global Stem Cell Therapy Market (by Cell Source)8.1 Overview8.2 Key Trends of the Global Stem Cell Therapy Market (by Cell Source)8.3 Bone Marrow and Peripheral Blood8.4 Adipose Tissue8.5 Placenta and Umbilical Cord8.6 Embryo8.7 Others

9 Global Stem Cell Therapy Market (by Indication)9.1 Overview9.2 Key Trends of the Global Stem Cell Therapy Market (by Indication)9.3 Orthopaedic and Dental9.4 Wounds and Injuries9.5 Cardiology and Neurology9.6 Immunology and Inflammatory9.7 Oncology and Metabolism9.8 Others

10 Global Stem Cell Therapy Market (by Region)10.1 Overview10.2 North America10.2.1 Overview10.2.2 U.S.10.2.3 Canada10.3 Europe10.3.1 Overview10.3.2 Germany10.3.3 U.K.10.3.4 France10.3.5 Italy10.3.6 Rest-of-Europe10.4 Asia-Pacific10.4.1 Overview10.4.2 Japan10.4.3 Australia10.4.4 China10.4.5 South Korea10.4.6 India10.4.7 Rest-of-Asia-Pacific10.5 Rest-of-the-World10.5.1 Overview10.5.2 Middle East and Africa10.5.3 Latin America

11 Company Profiles

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Cannibalism among cancer cells is one of the major causes of chemotherapy resistance.

Resistance, which occurs when cancers that have been responding to chemo suddenly begin to grow, is normally associated with the massive production by cancer cells of p-glycoprotein pumps, gene amplification and the repair of DNA breaks caused by some anti-cancer drugs such as doxorubicin, among others.

But cannibalism does exist and while uncommon, adds to the burden of curing or mitigating cancer via chemotherapy.

A new study from Tulane University suggests some cancer cells survive chemotherapy by devouring their neighboring tumor cells in a ruthless bid to withstand chemotherapy. This cellular cannibalism is thought to give predatory cancer cells the energy they need to stay alive. It also allows them to begin tumor relapse after the chemotherapy treatment is completed.

Chemotherapy drugs, among them doxorubicin, kill cancer cells by damaging their DNA. Unfortunately, cancer cells that survive the initial treatment give rise to relapsed tumors.

This is an especially thorny problem in breast cancers that retain a normal copy of a gene called TP53. This protein acts as a tumor suppressor. This means it regulates cell division by keeping cells from growing and proliferating too fast or in an uncontrolled way.

Some cancer cells generally stop proliferating and enter a dormant but metabolically active state known as senescence, instead of dying due to chemotherapy-induced DNA damage. Senescent cancer cells also produce large amounts of inflammatory molecules and other factors that can promote the tumors regrowth.

Chemotherapy-treated breast cancer patients with normal TP53 genes become prone to relapse and have poor survival rates.

Understanding the properties of these senescent cancer cells that allow their survival after chemotherapy treatment is extremely important, Crystal A. Tonnessen-Murray, a postdoctoral research fellow at James G. Jacksons laboratory at the Tulane University School of Medicine, who led the research team, said.

Her team also discovered that senescent breast cancer cells frequently engulf neighboring cancer cells following exposure to doxorubicin or other chemotherapy drugs. Researchers observed this surprising behavior in cancer cells grown in the lab and also in tumors growing in mice.

They also found that lung and bone cancer cells are also capable of engulfing their neighbors after becoming senescent.

Tonnessen-Murray and her colleagues found that senescent cancer cells activate a group of genes, which are normally active in white blood cells, that engulf invading microbes or cellular debris. They saw that after eating their neighboring cancer cells, senescent cancer cells digested them by delivering them to lysosomes, which are acidic cellular structures highly active in senescent cells.

But the most important finding was that this process helps senescent cancer cells stay alive. Senescent cancer cells that engulfed neighboring cells survived in culture for longer than senescent cancer cells that didnt.

The blood test could rapidly confirm whether breast cancer is responding to the drug palbociclib. Miguel . Padrin/Pexels

Continued here:
Cancer Cells Devise Way To Survive Chemotherapy - Medical Daily

Breast cancer is very heterogeneous. For many years researchers have recognized different subtypes of breast cancer, for instance, estrogen receptor positive (ER+), ER- and triple negative, and these categories can be further divided into subcategories.

Adding to the complexity of the tumor microenvironment, in recent years it has been increasingly appreciated that immune cells contribute to tumor progression and, importantly, to the tumors response to therapy.

To tumor cell heterogeneity, we now have to add the diversity of the immune cell component in the tumor microenvironment, said Dr. Xiang Shawn Zhang, professor at the Lester and Sue Smith Breast Center and member of the Dan L Duncan Comprehensive Cancer Centerat Baylor College of Medicine.

One of the interests of the Zhang lab is to better understand the role immune cells within tumors play in tumor growth and in response to therapy. In this study, Zhang and his colleagues conducted a series of analyses to profile the immune cell composition of tumor microenvironments in eight murine models and in clinical datasets of triple negative breast cancers.

We focused on two types of immune cells, neutrophils and macrophages, to investigate whether different tumors had the same immune cell composition and whether seemingly similar immune components played the same role in tumor growth. Importantly, we wanted to find out whether differences in immune cell composition contributed to the tumors responses to immunotherapy, said Zhang, a McNair Scholar at Baylor.

The researchers found large diversity in the frequency of neutrophils and macrophages among the tumor samples, including some tumors that preferentially attracted macrophages, and others that attracted more neutrophils. The predominance of one cell type over the other can be explained in part by the type of molecules produced by the tumor. As Zhang explained, some tumors secrete molecules that attract macrophages, while other tumors produce other molecules that lure neutrophils to the tumor site.

Interestingly, macrophages and neutrophils tended to exclude each other.

Once one type of cell starts accumulating in the tumor, the other will tend to stay away, Zhang said. What supports one type of cell, does not seem to support the other.

Exploring the roles macrophages and neutrophils play in tumor growth revealed that in some tumors macrophages favored tumor growth, while in others they helped control it. Neutrophils, on the other hand, tended to promote tumor growth.

These findings are just the beginning. They highlight the need to investigate these two cellular types deeper. Under the name macrophages there are many different cellular subtypes and the same stands for neutrophils, Zhang said.

We need to identify at single cell level which immune cell subtypes favor and which ones disrupt tumor growth taking also into consideration tumor heterogeneity as both are relevant to therapy.

The report appears in the journal Nature Cell Biology.

Other contributors to this work include first author Ik Sun Kim, Yang Gao, Thomas Welte, Hai Wang, Jun Liu, Mahnaz Janghorban, Kuanwei Sheng, Yichi Niu, Amit Goldstein, Na Zhao, Igor Bado, Hin-Ching Lo, Michael J. Toneff, Tuan Nguyen, Wen Bu, Weiyu Jiang, James Arnold, Franklin Gu, Jian He, Deborah Jebakumar, Kimberly Walker, Yi Li, Qianxing Mo, Thomas F. Westbrook, Chenghang Zong, Arundhati Rao, Arun Sreekumar and Jeffrey M. Rosen. Find the complete list of author affiliations here.

Financial support was provided by the Breast Cancer Research Foundation NCI CA151293 and NCI-CA16303, U.S. Department of Defense DAMD W81XWH-16-1-0073 and W81XWH-18-1-0574, Susan G. Komen CCR14298445 and McNair Medical Institute. The National Institutes of Health (grants P30 AI036211, P30 CA125123 and S10 RR024574) supported the Cytometry and Cell Sorting Core at Baylor College of Medicine.

By Ana Mara Rodrguez, Ph.D.

Read more here:
What to expect within the tumor microenvironment - Baylor College of Medicine News

Malignant skin cancer is one of the most dangerous types of cancer. 5000 people are diagnosed with it every year in Austria. The number of cases has risen sharply in recent decades. Thirty years ago, there were only five hundred people suffering from malignant melanomas.

In contrast, mortality rates have risen by only a slight margin. If detected early, the chances for recovery are good. But as soon as metastases start to form, the chances for a cure drop rapidly. This is also due to the fact that there are hardly any long-term effective treatment options (source: Austrian Society for Dermatology (GDV).

The Institute for Pharmaceutical Sciences at the University of Graz has been conducting research for many years into natural substances that can be used for the treatment of cancer. The team has now achieved a breakthrough which might also make it possible to cure advanced stages of malignant skin cancer. An active substance from the roots of theOnosma paniculata plant, a subspecies of the borage plant (also known as forget-me-not), has been successfully tested on cancer cells and on mice. The researchers also succeeded in modifying the active ingredient and further improving its effect.

The project was carried out in collaboration with the Technical University of Munich and the Helmholtz Institute Munich (the German Research Center for Environmental Health). The group was led by Rudolf Bauer from the Institute of Pharmaceutical Sciences (Pharmacognosy) at the University of Graz. He has been researching medicinal plants that are used in traditional medicine for fifteen years with the aim of identifying bioactive ingredients and discovering new key substances.

The main purpose of the research was to identify the plants that are used in traditional Chinese medicine (TCM) as cures for cancer-related diseases. Cancer-related, because the definition of cancer in TCM differs from that in Western medicine, Nadine Kretschmer explains. She has worked with the project and is a biologist at the Heidelberg University of Medicine. Another goal was to test their suitability as an active substance for a particular medicine. Approximately eighty percent of all Chemotherapeutic drugs are derived from nature, especially from plants. This figure is as high as seventy percent just for cancer therapies. The active substances on the market are usually synthetically modified even more so that they have an optimal effect. The active substances are then usually produced synthetically or biotechnologically for commercial purposes, Kretschmer says.

The contribution made by the University of Graz to the project was based on a database of several hundred medicinal plants used in traditional medicine which have been accumulated over several years. This project focused on plants from traditional Chinese medicine (TCM). Part of the contribution made by the German partners was the implementation of RNA (ribonucleic acid) sequencing and preliminary evaluations. RNA sequencing serves as a means of determining the nucleotide sequence in the RNA and provides information on how the genetic information of a gene is expressed.

The project included seventy-six of the most promising specimens from the database. These were dried, processed into 253 extracts and tested on various cancer cells. In the end, it was the Onosma Paniculata Bureau & Franch, a type of borage shrub, that offered prospects for further studies. The potent substance --Dimethylacrylshikonin (DMAS) is found in the root of the plant.

During the experiments, the substance was tested on cells of malignant melanomas. The substance destroyed the cells thereby confirming their efficacy. In order to test the substance for side effects, the initial in vivo tests were carried out on mice that were afflicted with skin cancer. - dimethylacrylshikonin was injected directly into the tumor which caused it to change and die off. Two types of cell death were observed:

There were no side effects.

Subsequent trials were conducted expressly with the aim of modifying the substance in order to improve its efficacy. A specific shikonin derivative proved to be especially effective. This demonstrated that the substance is well suited for the development of pharmaceuticals. In the meantime, two more follow-up projects have been planned. More extensive studies are required and the method of application is still an open question, Kretschmer states.

Kretschmer emphasizes that TCM was purely an inspiration for the active substance. It is still not clear how this works within TCM. Normally no singular plants are used in TCM, instead plant mixtures are used. These are prepared like tea. In an attempt to unravel the effect of TCM, the team cooked up the dried plant according to the TCM method and used it in cell cultivation experiments. However, no anti-tumor effect was observed. Kretschmer sees more potential in an oil-based preparation method that is applied to the affected areas of the skin. This is because shikonins are found in higher concentrations in the oil.

Over the course of the project, the identity of the borage plant species sold as TCM remedies was also tested. There are roots that look very similar to the plant we are studying and we have found that the species is often sold under fake names in China. This is problematic because some of the plants that are marketed contain substances that are potentially harmful.

Kretschmer and the research team found a technical solution to the problem: a method which uses thin-layer chromatography for the identification of plants. This innovation is based on a CAMAG system and is simple enough for use in pharmacies.

Thin-layer chromatography (TLC) is a physicochemical separation process that is used to examine the composition of specimens.

The core project was funded by the Austrian Science Fund FWF and was completed in early 2019.

Publications:

Kretschmer, N.; Deutsch, A.; Durchschein, C.; Rinner, B.; Stallinger, A.; Higareda-Almaraz, J.C.; Scheideler, M.; Lohberger, B.; Bauer, R.: Comparative Gene Expression Analysis in WM164 Melanoma Cells Revealed That --Dimethylacrylshikonin Leads to ROS Generation, Loss of Mitochondrial Membrane Potential, and Autophagy Induction, in: Molecules 2018, 23

Durchschein, C.; Hufner, A.; Rinner, B.; Stallinger, A.; Deutsch, A.; Lohberger, B.; Bauer, R.; Kretschmer, N.: Synthesis of Novel Shikonin Derivatives and Pharmacological Effects of Cyclopropylacetylshikonin on Melanoma Cells, in: Molecules 2018, 23

Jahanafrooz, Z; Stallinger, A; Anders, I; Kleinegger, F; Lohberger, B; Durchschein, C; Bauer, R; Deutsch, A; Rinner, B; Kretschmer, N.: Influence of silibinin and --dimethylacrylshikonin on chordoma cells, in: Phytomedicine 2018, 49

Also of interest:

Dual Therapy to Reduce the Relapse Rate in Cancers

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Plant used in traditional Chinese medicine is effective against malignant skin cancer - Innovation Origins