'Virtual biopsy' device to detect skin tumors

Using sound vibrations and pulses of near-infrared light, a Rutgers University scientist has developed a new "virtual biopsy" device that can quickly determine a skin lesion's depth and potential malignancy without using a scalpel.

The ability to analyze a skin tumor non-invasively could make biopsies much less risky and distressing to patients, according to a report in Wiley Online Library. Currently, physicians who perform surgical biopsies often don't know the extent of a lesion and whether it will be necessary to refer the patient to a specialist for extensive tissue removal or plastic surgery until surgery has already begun.

The first-of-its-kind experimental procedure, called vibrational optical coherence tomography (VOCT), creates a 3-D map of the legion's width and depth under the skin with a tiny laser diode. It also uses soundwaves to test the lesion's density and stiffness since cancer cells are stiffer than healthy cells. An inch-long speaker applies audible soundwaves against the skin to measure the skin's vibrations and determine whether the lesion is malignant.

"This procedure can be completed in 15 minutes with no discomfort to the patient, who feels no sensation from the light or the nearly inaudible sound. It's a significant improvement over surgical biopsies, which are invasive, expensive and time consuming," said Frederick Silver, a professor of pathology and laboratory at Rutgers Robert Wood Johnson Medical School.

The study found that a prototype VOCT device, which awaits FDA approval for large-scale testing, is able to accurately distinguish between healthy skin and different types of skin lesions and carcinomas. The researchers tested the device over six months on four skin excisions and on eight volunteers without skin lesions. Further studies are needed to fine-tune the device's ability to identify a lesion's borders and areas of greatest density and stiffness, which would allow physicians to remove tumors with minimally invasive surgery.

An important announcement regarding our upcoming conference 12^th World Congress on Cell & Tissue Science (Cell Tissue Science 2019) scheduled on September 13-14,2019 in Singapore. You can also present your latest research at the different topics such as Cancer Cell Biology, Stem Cell & its applications and many more along with other distinguished professors, doctors and researchers from all over the world.

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Source: https://www.sciencedaily.com/releases/2019/06/190613103129.htm

How prostate cancer cells mimic bone when they metastasize

Prostate cancer often becomes lethal as it spreads to the bones, and the process behind this deadly feature could potentially be turned against it as a target for bone-targeting radiation and potential new therapies.

Study published online in the journal PLOS ONE, Duke Cancer Institute researchers describe how prostate cancer cells develop the ability to mimic bone-forming cells called osteoblasts, enabling them to proliferate in the bone microenvironment.

Attacking these cells with radium-233, a radioactive isotope that selectively targets cells in these bone metastases, has been shown to prolong patients' lives. But a better understanding of how radium works in the bone was needed.

The mapping of this mimicking process could lead to a more effective use of radium-233 and to the development of new therapies to treat or prevent the spread of prostate cancer to bone.

"Given that most men who die of prostate cancer have bone metastases, this work is critical to helping understand this process," said lead author Andrew Armstrong, Director of Research at the Duke Cancer Institute Center for Prostate and Urologic Cancers.

The research team enrolled a small study group of 20 men with symptomatic bone-metastatic prostate cancer. When analyzing the circulating tumor cells from study participants, they found that bone-forming enzymes appeared to be expressed commonly, and that genetic alterations in bone forming pathways were also common in these prostate cancer cells.

They validated these new genetic findings in a separate multicenter trial involving a larger group of more than 40 men with prostate cancer and bone metastases.

Following treatment with radium-223, the researchers found that the radioactive isotope was concentrated in bone metastases, but tumor cells still circulated and cancer progressed within six months of therapy. The researchers found a range of complex genetic alterations in these tumor cells that likely enabled them to persist and develop resistance to the radiation over time.

"Osteomimicry may contribute in part to how prostate cancer spreads to bone, but also to the uptake of radium-223 within bone metastases and may thereby enhance the therapeutic benefit of this bone targeting radiotherapy," Armstrong said.

He said by mapping this lethal pathway of prostate cancer bone metastasis, the study points to new targets and thus critical areas of research into designing better tumor-targeting therapies.

An important announcement regarding our upcoming conference 12^th World Congress on Cell & Tissue Science (Cell Tissue Science 2019) scheduled on September 13-14,2019 in Singapore. You can also present your latest research at the different topics such as Cancer Cell Biology, Stem Cell & its applications and many more along with other distinguished professors, doctors and researchers from all over the world.

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Energizing the immune system to eat cancer

Immune cells called macrophages are supposed to serve and protect, but cancer has found ways to put them to sleep. Now researchers at the Abramson Cancer Center of the University of Pennsylvania say they've identified how to fuel macrophages with the energy needed to attack and eat cancer cells. It is well established that macrophages can either support cancer cell growth and spread or hinder it. But most tumors also express a signal called CD47, which can lull macrophages into a deep sleep and prevent them from eating. Researchers have found that rewiring macrophage metabolism can overcome this signal and act like an alarm clock to rouse and prepare macrophages to go to work. Their findings were published in Nature Immunology today.

Macrophages are immune cells just like T and B cells, but differ in that they can eat cells that are not supposed to be in the body. In fact, they are the most prominent immune cell found in cancer, but unfortunately, most are often convinced to help cancer grow and spread. Cancer cells frequently stop macrophages from attacking them by expressing CD47, a "don't eat me" signal. Researchers now say that merely blocking inhibitory signals like CD47 is not always sufficient to convince macrophages to attack cancer. Instead, two signals are required. First, they need a signal to activate them -- such as a toll-like receptor agonist. After that, a second signal -- such as a CD47 inhibitor -- can lower the threshold needed to wage battle on the cancer.

"It turns out macrophages need to be primed before they can go to work, which explains why solid tumors may resist treatment with CD47 inhibitors alone," said the study's senior author Gregory L. Beatty, Assistant Professor of Hematology-Oncology at Penn's Perelman School of Medicine. 

The team used this approach by activating macrophages with CpG, a toll-like receptor agonist that sends the first signal, and found that it rapidly induced shrinkage of tumors and prolonged survival of mice even without the requirement of T cells. Unexpectedly, they also found that the activated macrophages were able to eat cancer cells even in the presence of high levels of CD47.

To understand the molecular basis of this phenomenon, the team traced the metabolic activity of macrophages and determined that activated macrophages began to utilize both glutamine and glucose as fuel to support the energy requirements needed for them to eat cancer cells. This rewiring of the macrophages metabolism was necessary for CpG to be effective, and the researchers say these findings point to the importance of macrophage metabolism in determining the outcome of an immune response.

"Cancer does not shrink without the help of macrophages and macrophages need the right fuel to eat cancer cells and shrink tumors," Liu said. "To do this, a shift in metabolism is needed to steer the energy in the right direction. It is the metabolism that ultimately allows macrophages to override signals telling them not to do their job."

Beatty points out that patients with diabetes, cardiovascular disease, and other conditions are routinely treated with drugs that could affect macrophage metabolism, but virtually nothing is known about how these drugs might impact immunotherapy responses in cancer, meaning the team's discovery has implications even for existing treatments.

Researchers from different part of the world are invited to submit abstract on their unpublished latest research at our upcoming conference Cell Tissue Science 2019 which is focused on the complications and consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology,Technical Advancements in cancer treatment and many more. We as committee members of the conference welcome you to be a part of the conference “ 12th World Congress on Cell & Tissue Science” in Singapore on March 11-12, 2019. 

You can submit your abstract on Session or Track : 08. Advancement in Cancer Treatments

New nanoparticle targets tumor-infiltrating immune cells, flips switch

Immunotherapy's promise in the fight against cancer drew international attention after two scientists won a Nobel Prize this year for unleashing the ability of the immune system to eliminate tumor cells.

But their approach, which keeps cancer cells from shutting off the immune system's powerful T-cells before they can fight tumors, is just one way to use the body's natural defenses against deadly disease. A team of Vanderbilt University bioengineers today announced a major breakthrough in another: penetrating tumor-infiltrating immune cells and flipping on a switch that tells them to start fighting. The team designed a nanoscale particle to do that and found early success using it on human melanoma tissue.

"Tumors are pretty conniving and have evolved many ways to evade detection from our immune system," said John T. Wilson, Assistant Professor of Chemical and Biomolecular Engineering and Biomedical Engineering. "Our goal is to rearm the immune system with the tools it needs to destroy cancer cells.Checkpoint blockade has been a major breakthrough, but despite the huge impact it continues to have, we also know that there are a lot of patients who don't respond to these therapies. We've developed a nanoparticle to find tumors and deliver a specific type of molecule that's produced naturally by our bodies to fight off cancer."

That molecule is called cGAMP, and it's the primary way to switch on what's known as the stimulator of interferon genes (STING) pathway: a natural mechanism the body uses to mount an immune response that can fight viruses or bacteria or clear out malignant cells. Wilson said his team's nanoparticle delivers cGAMP in a way that jump-starts the immune response inside the tumor, resulting in the generation of T-cells that can destroy the tumor from the inside and also improve responses to checkpoint blockade.

While the Vanderbilt team's research focused on melanoma, their work also indicates that this could impact treatment of many cancers, Wilson said, including breast, kidney, head and neck, neuroblastoma, colorectal and lung cancer.

His findings appear today in a paper titled "Endosomolytic Polymersomes Increase the Activity of Cyclic Dinucleotide STING Agonists to Enhance Cancer Immunotherapy" in the journal Nature Nanotechnology.

Daniel Shae, a Ph.D. student on Wilson's team and first author of the manuscript, said the process began with developing the right nanoparticle, built using "smart" polymers that respond to changes in pH that he engineered to enhance the potency of cGAMP. After 20 or so iterations, the team found one that could deliver cGAMP and activate STING efficiently in mouse immune cells, then mouse tumors and eventually human tissue samples.

"That's really exciting because it demonstrates that, one day, this technology may have success in patients," Shae said.

Researchers from different part of the world are invited to submit abstract on their unpublished latest research at our upcoming conference Cell Tissue Science 2019 which is focused on the complications and consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology,Technical Advancements in cancer treatment and many more. We as committee members of the conference welcome you to be a part of the conference “ 12th World Congress on Cell & Tissue Science” in Singapore on March 11-12, 2019. 

You can submit your abstract on Session or Track : 08. Advancement in Cancer Treatments

Mathematical model can improve our knowledge on cancer

Researchers have developed a new mathematical tool, which can improve our understanding of what happens when cells lose their polarity (direction) in diseases such as cancer. The result is advancing our understanding of how the fertilized egg cell develops into a complete organism. Biological shapes, like individual organs or an entire body, can be reproduced or maintained with great accuracy, just like in the embryonic development or during the adult stage.

It remains unknown how cells "know" which structures to form in order to repair tissue damage:

Multicellular organisms can develop highly complex structures that make up their tissue or organs and are capable of regenerating perfect reproductions of these structures after injury. This involves folding of sheets, formed by groups of dividing and interacting cells. Yet, although much is understood about some of the intermediate steps that occur during development and tissue repair, exactly how thousands of cells together work out what shapes they need to form remains unknown.

Building the mathematical model:

"In this study, we wanted to see how cells organize into folded sheets and tubes, and how this process can be so precisely reproduced as is seen during development," says lead author Silas Boye Nissen, PhD student at the Center for Stem Cell Decision Making, StemPhys, University of Copenhagen, Denmark. "To answer this question, we built a mathematical tool that can model two types of cell polarities and simulated how many cells organize themselves into folded sheets and organs."

The researchers found that by changing one of two polarities in the model, they were able to simulate a rich diversity of shapes. The differences in the shapes were dictated by two factors: The initial arrangement of the cells and external boundaries -- such as the shape of an egg influencing the development of the embryo inside.

By exploring a multitude of theoretical scenarios in which the polarities were altered, the model was able to narrow down the focus to a few theories to be tested experimentally. In miniaturized versions of organs grown in the lab (called organoids), the model predicted that rapid, off-balance growth of cells will cause the growing organoid to develop lots of shallow folds, while external pressure caused by the medium on the organoids will cause fewer, deeper and longer folds. This means the model can improve our understanding of how folded organs like the brain or the pancreas are formed.

Few, simple rules apply for the formation of biological shapes:

"Our findings advance our understanding of how properties of individual cells lead to differences in shapes formed by thousands of cells," says senior author Professor Kim Sneppen, Director of the Center for Models of Life, CMOL, University of Copenhagen, and senior coauthor Ala Trusina concludes: "Our work suggests that body parts may not need detailed instructions to form, but instead can emerge as cells follow a few simple rules. We can now explore what happens if cells gain or lose their polarities at the wrong time or place, as often happens in cancer."

Researchers from different part of the world are invited to submit abstract on their unpublished latest research at our upcoming conference Cell Tissue Science 2019 which is focused on the complications and consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology,Technical Advancements in cancer treatment and many more. We as committee members of the conference welcome you to be a part of the conference “ 12th World Congress on Cell & Tissue Science” in Singapore on March 11-12, 2019. 

You can submit your abstract on Session or Track : 08. Advancement in Cancer Treatments

Study of mutation order may change understanding of how tumors develop

Cancers most commonly arise because of a series of two to five mutations in different genes that combine to cause a tumor. Evidence from a growing number of experiments focused on truncal mutations the first mutations in a given suggests a new direction in understanding the origins of cancer.

This study was published in Cancer Cell by authors from Institute for Advanced Study and The University of Texas MD Anderson Cancer Center, present a new perspective of these data, highlighting two important variables: 1) the sequence of mutations that leads to the formation of a cancer, and 2) the cell type in which this occurs, providing a new meaningful insight into the growth, properties, and outcomes of these tumors.

The concepts developed in this paper suggest new avenues for future experimentation, help to explain previously unclear observations, and recommend new methods to impede cancer development, including blocking the defined sequence that is required to produce a tumor.

Arnold J. Levine of the Institute for Advanced Study explains, "This paper does not publish any new experiments. Rather, it outlines a new way to understand and interpret existing results, and in so doing helps to explain previously confusing facts, outlining the differences in developing cancers at young or older ages, and emphasizing the important role of inherited predispositions to developing cancers. The publication suggests entirely new paths to studying the origins of cancers over a lifetime."

The study collects numerous examples of how the order of mutations affects the outcome of the tumor and its response to therapy. This highlights of this paper is an opportunity for researchers to look at hundreds of these evolutionary trees with different orders of mutations that will perhaps provide a fingerprinting method that could reveal information about a cancer's type, growth, and potential to invade surrounding tissues at the time of diagnosis so that treatments can be planned. With an understanding of these complex mutational chains, pharmaceutical and biotechnology firms could begin to consider interventions to inhibit particular links within a mutational sequence that could block the further development of a cancer. Drugs directed against the first and second mutational outcomes may completely prevent the third and fourth mutations from ever being selected for in a clone of cells. The focus in this paper is thus on cancer prevention, not treatment.

Many different kinds of cancers arise by the random accumulation of mutations (mistakes in the information in a gene) over a lifetime. For instance, past research has shown that colorectal cancer is associated with mutations in the following four distinct genes: APC, RAS, TGF-beta, and p53, each of which contributes an error in different functions being carried out by the cells in one's colon.

Copeland and Jenkins have demonstrated that colon cancer develops most rapidly when the APC gene is mutated first, the RAS gene second, the TGF-beta gene third, and the p53 gene last. Mutations in the first three genes produce benign tumors. Only when all four genes are mutated is there a malignant tumor. But mutations occur randomly over a lifetime. The order is imposed by Darwinian selection. An APC mutation permits a clone of cells to grow (forming a benign polyp). When an RAS mutation occurs in this clone of cells the polyp enlarges, increasing the number of cells with these two mutations and, therefore, the probability that a cancer may arise. Thus, the ordering of these random mutations is selected for by the viability and replication of cells with this order of mutations. The Levine laboratory showed the same need for an order of mutations in five different genes to produce a different cancer: T-cell lymphomas. It was these two papers, published approximately three years ago, that started Copeland, Jenkins, and Levine exploring whether this was the pathway in the development of all cancers; "Order of Mutations and Cell Type Matters."

The trio's new Cancer Cell paper provides scientists and innovators with a new set of questions to ask about tumor development that could move the field of cancer research in a new and exciting direction.

Researchers from different part of the world are invited to submit abstract on their unpublished latest research at our upcoming conference Cell Tissue Science 2019 which is focused on the complications and consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology,Technical Advancements in cancer treatment and many more. We as committee members of the conference welcome you to be a part of the conference “ 12th World Congress on Cell & Tissue Science” in Singapore on March 11-12, 2019. 

You can submit your abstract on Session or Track : 07. Cancer Cell Biology

New mechanism to 'activate' the immune system against cancer

According to a study published this week in the journal Nature, A new mechanism for activating the immune system against cancer cells allows immune cells to detect and destroy cancer cells better than before,

The focus of the study is a mechanism that routinely serves the cell by marking human virus-like genes in order to avoid identifying them as viruses. Now, Prof. Levanon, together with the Harvard team, has discovered that when inhibiting this mechanism, the immune system can be harnessed to fight cancer cells in a particularly efficient manner, and most effectively in lung cancer and melanoma.

"We found that if the mechanism is blocked, the immune system is much more sensitive. When the mechanism is deactivated, the immune system becomes much more aggressive against the tumor cells," said Prof. Erez Levanon, doctoral student Ilana Buchumansky of the Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University

In recent years, a new generation of cancer drugs has been developed which blocks proteins that inhibit immune activity against malignant tumors. These drugs have shown remarkable success in several tumor types. This year's Nobel Prize in Medicine was awarded to James Allison and Tasuku Honjo, who discovered the key genes of this mechanism. Despite this achievement, the current generation of drugs helps only a small number of patients, while most of the drugs fail to cause the immune system to attack the tumor. It is hoped that the new discovery will allow enhanced activity of the immune system to attack cancer cells. A number of companies have already begun research to screen for drugs that will operate on the basis of this discovery.

Researchers from different part of the world are invited to submit abstract on their unpublished latest research at our upcoming conference Cell Tissue Science 2019 which is focused on the complications and consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology,Technical Advancements in cancer treatment and many more. We as committee members of the conference welcome you to be a part of the conference “ 12th World Congress on Cell & Tissue Science” in Singapore on March 11-12, 2019. 

You can submit your abstract on Session or Track : 08. Advancement in Cancer Treatments

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AI predicts cancer patients' symptoms

Doctors could get a head start treating cancer thanks to new AI developed at the University of Surrey that is able to predict symptoms and their severity throughout the course of a patient's treatment.

The study was first of its kind published in the PLOS One journal. Researchers from the Centre for Vision, Speech and Signal Processing (CVSSP) at the University of Surrey shared the detail how they created two machine learning models that are both able to accurately predict the severity of three common symptoms faced by cancer patients  are depression, anxiety and sleep disturbance. All three symptoms are associated with severe reduction in cancer patients' quality of life.

Researchers analysed existing data of the symptoms experienced by cancer patients during the course of computed tomography x-ray treatment. The team used different time periods during this data to test whether the machine learning algorithms are able to accurately predict when and if symptoms surfaced.

The results found that the actual reported symptoms were very close to those predicted by the machine learning methods.

This work has been a collaboration between the University of Surrey and the University of California in San Francisco (UCSF). The UCSF research in this joint collaboration is led by Professor Christine Miaskowski.

Payam Barnaghi, Professor of Machine Intelligence at the University of Surrey, said: "These exciting results show that there is an opportunity for machine learning techniques to make a real difference in the lives of people living with cancer. They can help clinicians identify high-risk patients, help and support their symptom experience and pre-emptively plan a way to manage those symptoms and improve quality of life."

Nikos Papachristou, who worked on designing the machine learning algorithms for this project, said: "I am very excited to see how machine learning and AI can be used to create solutions that have a positive impact on the quality of life and well-being of patients."

Researchers from different part of the world are invited to submit abstract on their unpublished latest research at our upcoming conference Cell Tissue Science 2019 which is focused on the complications and consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology,Technical Advancements in cancer treatment and many more. We as committee members of the conference welcome you to be a part of the conference “ 12th World Congress on Cell & Tissue Science” in Singapore on March 11-12, 2019. 

You can submit your abstract on Session or Track : 07. Cancer Cell Biology

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How breast cancer avoids immune system detection

Recent breakthroughs in immunotherapy are making a huge difference in treating some forms of cancer, especially metastatic cancer. But breast cancer has proven a tricky foe for this new therapy, and an interdisciplinary team of FSU researchers is now a little bit closer to figuring out why.

The team analyzed data from more than 1,000 breast cancer patients and found that breast cancer behaves differently than other cancers that are currently treated with immunotherapy.

"We've been trying to understand why breast cancer patients do not respond well to the current immunotherapy and cannot benefit from this major breakthrough," Sang said,Professor of Chemistry and Biochemistry, Florida State University

Immunotherapy is a course of treatment where drugs unleash the body's own immune system to fight cancer. When cancer invades the body, the immune system often fails to recognize it as abnormal. Immunotherapy drugs inactivate the mechanisms cancer cells have that allow them to hide from the immune system. And then, the immune system attacks the cancer.

However, while immunotherapy has been an effective treatment for some forms of cancer such as melanoma, breakthroughs for breast cancer patients have proven more elusive.

Researchers said the problem lies in the many different mechanisms breast cancer uses to hide from the immune system.

The team broke the data down into different groups and identified seven clusters of breast cancer patients based on the immune evasion mechanisms that breast cancer uses to avoid detection. Some of the types even used a combination of ways to hide from the immune system.

Knowing more about breast cancer tumors and how they work will give oncologists more tools to treat patients, whether it is with yet-to-be developed immunotherapy drugs or the traditional combination of chemotherapy and radiation, researchers said. It may also help researchers design clinical trials for potential drugs.

"Cancer treatment isn't as personalized as it should be," Burjas Bou Dargham, Graduate Students, Florida State University said. "We've been trying to understand what's really going on with these tumors and how they operate. That way doctors can ultimately better treat their patients."

Zhang, with the help of Liu, analyzed reams of data from the National Institutes of Health's Cancer Genome Atlas to see where patterns existed among cancer patients. He and Sang have previously collaborated on other research related to genetic biomarkers in cancer that could help dictate what type of chemotherapy might be most effective for a patient.

"There's so much data available to understand problems in cancer,"  Jinfeng Zhang, Associate Professor of Statistics, Florida State University, said. "Immunotherapy is a big breakthrough, but still we don't understand why some patients respond and others don't."

The team plans to follow up on this work by delving into data about an aggressive subtype of breast cancer called triple-negative breast cancer.

This work was funded by internal grants from Florida State University and the National Institutes of Health.

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

You can submit your abstract on Session or Track : 8.Advancement in Cancer Treatment

Healthy blood stem cells have as many DNA mutations as leukemic cells

Researchers from the Princess Máxima Center for Pediatric Oncology have shown that the number of mutations in healthy and leukemic blood stem cells does not differ. Rather the location of the mutations in the DNA is relevant. Using the mutation patterns in the hematopoietic stem and progenitor cells (HSPCs) the team was able to trace the developmental lineage tree of the cells.

Mutational load

"Blood stem cells divide about once every 40 weeks," says Van Boxtel, "and we saw that eleven mutations occur during one division." The older the test subject, the more mutations the researchers found because the mutations accumulate over the years. Yet, these people were fit as a fiddle.Nevertheless, mutations in blood stem cells may also lead to leukemia. "We thought that people with leukemia would have more mutations than healthy people," says Van Boxtel, "but this is not the case." The HSPCs of patients with acute myeloid leukemia (AML) contain as many mutations as those from healthy people. The researchers published their results in the open access journal Cell Reports.

Developmental lineage tree

The researchers also describe how they were able to trace the developmental lineage tree of hematopoiesis using the mutation pattern of HSPCs. "If you study the pattern of mutations of a cancer cell, you can figure out which cell it comes from," explains Van Boxtel. "We have shown this for HSPCs now, but especially for solid tumors the origin of the cancer cell is very relevant for selecting the most effective treatment strategy." The technique has a lot of potential according to the authors. The next step for Van Boxtel and his team will be to study the origin of causative mutations in second cancers in survivors of pediatric cancer.

"So far, we assumed that new mutations occur as a result of intensive treatment during childhood and cause second cancers later in life. We can now test whether these mutations are indeed new or already existed and contributed to both incidences of cancer. This is relevant knowledge when making a treatment plan for children with cancer."

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

You can submit your abstract on Session or Track : 9.Stem Cells and its Applications

New blood test developed for early diagnosis of ovarian cancer

Research on a bacterial toxin first discovered in Adelaide has led to the development a new blood test for the early diagnosis of ovarian cancer - a disease which kills over 1000 Australian women and 150,000 globally each year.

The new blood test has the potential to dramatically improve early detection of the disease, although it will require further testing before it is available for clinicians.

A research team from the University of Adelaide and Griffith University have been studying the interactions between the toxin and an abnormal glycan (sugar) expressed on the surface of human cancer cells and released into the blood.

The team has now engineered a harmless portion of the toxin to enhance its specificity for the cancer glycan and used this to detect it in blood samples from women with ovarian cancer.

A paper published this month in Biochemical and Biophysical Research Communications has shown that the new test detected significant levels of the cancer glycan in blood samples from over 90% of women with stage 1 ovarian cancer and in 100% of samples from later stages of the disease, but not in any of the samples from healthy controls.

"Ovarian cancer is notoriously difficult to detect in its early stages, when there are more options for treatment and survival rates are better. Our new test is therefore a potential game changer," says Professor James Paton, Director of the University of Adelaide's Research Centre for Infectious Diseases.

Professor Michael Jennings, Deputy Director of the Institute for Glycomics at Griffith University, said: "Detection of this tumor marker may also play a role in a simple liquid biopsy to monitor disease stage and treatment."

The team is currently seeking scientific and commercial partners to further test the technology with larger numbers of patient samples and to adapt it for mass screening.

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

You can submit your abstract on Session or Track : 8.Advancement in Cancer Treatment

Realizing the potential of gene therapy for neurological disorders

Promising findings from preclinical animal studies show the potential of gene therapy for treating incurable neurological disorders. In new research presented today, scientists successfully used gene therapy to slow the progression and improve symptoms of disorders such as amyotrophic lateral sclerosis and Parkinson's disease.

Gene therapy typically employs an inactivated virus to carry new genetic cargo into cells, altering specific genes to treat or prevent a disease. Researchers might replace a mutated gene with a healthy copy of the gene, turn off a disease-causing gene, or add a new gene to the body to help fight a disease.

Although gene therapy is a promising treatment option for a limited number of conditions, including certain cancers, the technique is still experimental for most diseases, with ongoing research to ensure they will be safe and effective in human patients. Animal studies are a key part of the process by which an experimental gene therapy treatment goes to clinical trial.

Research new findings show that:

• A new technique allows gene therapy to be delivered to the entire spinal cord in mice (M. Bravo Hernandez, abstract 208.10).
• Gene therapy safely and effectively extends life and improves motor function in a mouse model of ALS (Gretchen Thomsen, abstract 208.16).
• Gene therapy slows the progression of neuronal loss in a mouse model of inherited Parkinson's disease (Jose L. Lanciego, abstract 292.01).
• Gene therapy shows promise in a mouse model of Batten disease, a childhood neurodegenerative disease (Shibi Likhite, abstract 355.01).

"Gene therapy holds the promise to transform the lives of patients with incurable neurological diseases," said Fredric Manfredsson, PhD, of Michigan State University. "The research presented today represents important and exciting steps toward being able to prevent and treat disorders that currently have no cure, such as Parkinson's disease and Alzheimer's disease."

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatmentand many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

You can submit your abstract on Session or Track :2.Cellular and Gene Therapy

Secrets of engineered protein receptor, CAR

Cancer remains the second-leading cause of death in the United States. This year, an estimated 1.7 million new cases will be diagnosed, with nearly 610,000 people expected to die from the disease, according to the National Cancer Institute.

Fortunately, several recent cancer treatments show considerable promise. Among them is Chimeric Antigen Receptor (CAR) T cell therapy, which the American Society of Clinical Oncology recently named the "2018 Advance of the Year." Three USC Viterbi School of Engineering researchers, Assistant Professor Stacey Finley, Professor Pin Wang and Assistant Professor Nick Graham have just published a paper in "Biophysical Journal" that sheds light on how this new treatment works, information that could one day result in better cancer therapies with fewer side effects.

"We're trying to dig into the molecular mechanisms," said Graham,Chemical Engineering and Materials Science. "By understanding how the CAR T cells work, we could try to design better ones."

When the immune system functions normally, immune cells move around the body and look for pathogens that don't belong and kill them. However, cancer cells can mask themselves, making it harder for the good cells, such as T cells, to kill them.

With CAR T cell therapy, a person's T cells are removed, genetically engineered with proteins, and then injected back into the patient. The resulting CAR T cells are much better at fighting cancer cells. That's because these modified CAR T cells have an engineered protein receptor, the CAR, that can bind to cancer cells. When this occurs, a signal from the CAR tells the T cell to begin destroying the cancer by secreting the chemicals perforin and granzyme.

CAR T cell therapies

Earlier this year, the U.S. Food and Drug Administration approved the first CAR T cell therapy for the treatment of some people with advanced leukemia and a form of lymphoma, both blood cancers. Early results have shown great promise. However, in early tests, the CAR-T cell therapies have so far proven much less effective against breast, lung, prostate and other solid-tumor cancers. Additionally, some people undergoing CAR T cell therapy have experienced significant side effects; a few have even died.

The trio of USC researchers hope their work will greatly improve CAR T cell therapies by uncovering the complicated process by which CARs activate cancer fighting cells. Specifically, they are examining a process called phosphorylation, which is a chemical reaction that occurs when the CAR receptor bumps up against a cancer cell and sends a signal to the T cell to attack the bad cells.

"I think what's most exciting is that we're really adding to the field an understanding of which sites on the CAR are becoming phosphorylated, how quickly that happens and the amount of phosphorylation of each site," said Finley, the Gordon S. Marshall Early Career Chair.

Through their research, Finley, Wang and Graham have learned when and how much phosphorylation occurs on the CAR's six sites, which, in an imperfect analogy, could be imagined as "docking hubs," in Graham's words.

Additionally, they have found that no "gatekeeper" exists, meaning that no single CAR site must be phosphorylated before the others. Until now, scholars only had a general idea about the phosphorylation process, making it difficult to bioengineer CAR T cells that could successfully fight against complex and complicated breast, lung and other solid-tumor cancers.

Better cancer-fighting CARs

Going forward, Finley, Wang and Graham hope to leverage their findings into engineering more effective cancer-fighting CARs with fewer side effects. This could mean having phosphorylation take place quicker and more intensely at certain CAR sites, depending on the complexity of the targeted cancer cells. Alternately, the USC researchers might engineer CARs to phosphorylate less, thereby preventing the cancer-fighting T- and other cells from becoming too aggressive and killing healthy cells -- a problem that has cropped up with early CAR T cell cancer treatments.

Already, Finley has built quantitative models that holds great promise.

"Once we have these tools and quantitative models, we should be able to apply them to a variety of different designs of CARs," said Finley."Maybe you could use a model, before you do an experiment, to see if this new design would work. Instead of having to do as many tedious experiments in the lab, you could build a predictive mathematical model to screen the best design."

Added Wang, the Zohrab A. Kaprielian Fellow in Engineering and professor of chemical engineering and materials science, and biomedical engineering: "If you want to make the T cells more potent, the question is how best to design the CAR. That's our research's goal, I think."

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

For more info visit :Cell Tissue Science 2019

Breast cancer cells become invasive by changing their identity

Researchers from Karolinska Institutet in Sweden have identified a protein that determines the identity and invasive properties of breast cancer cells. The finding could lead to the development of new therapeutic and diagnostic strategies to target breast cancer invasion and metastasis. The study is published in the scientific journal Cancer Research.

Cancer cell invasion of the surrounding tissue is the first step in metastasis, the major cause of death in cancer. Our knowledge of how cancer cells acquire invasive and metastatic properties is incomplete and, consequently, there is a lack of treatment for cancer patients with metastatic disease. The current study sheds new light on this area.

"In recent years, it has become evident that a change in a cancer cell's identity may contribute to its invasive and metastatic behaviour," says Jonas Fuxe, Associate Professor, Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet.

For a long time, it was believed that a cell's identity, which is created during embryonic development, is a permanent feature. Thus, once a cell has been instructed to become, for example, a muscle cell, a nerve cell or a skin cell, it will remain this type of cell, no matter what.

Today, however, we know that a cell's identity is not as solid and can change under pathological conditions such as cancer. Cancer cells mostly originate from a cell type called epithelial cells that form the skin, the inner surfaces of our tubular organs, and glands, for example in the breast. Recent studies show that breast cancer cells may lose their epithelial identity and acquire invasive and metastatic properties through a process termed epithelial-mesenchymal transition (EMT).

"Induction of EMT may be described as a process resembling how boats in a harbour being unhitched from their anchoring points become ready to move out," says Dr. Fuxe. "This is where a protein called CXADR, or CAR, comes in."CAR was originally identified as a virus receptor, but its normal function has not been understood. CAR is often lost during cancer progression towards invasive and metastatic disease, but the implications of this have not been clear. Dr. Fuxe Continues by saying "What we show in this study is that CAR is an important anchoring point for breast cancer cells, preventing them from losing their epithelial cell identity and becoming invasive." 

What was also interesting was that, when CAR was reintroduced into breast cancer cells with low CAR levels, it was possible to change cells back to a more epithelial (normal) identity and thereby repress their invasive properties. The results may open up the way to target CAR as a new strategy for inhibiting breast cancer invasion and metastasis.

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in Cancer Treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” .

For more info visit :Cell Tissue Science 2019