'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.

If interested kindly proceed with submitting your abstract and latest biography along with a photography to our online abstract submission page given below: Link for submission: Click Here

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

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

A compound being developed to treat eye disease also kills leukemia cells

An active ingredient in eye drops that were being developed for the treatment of a form of eye disease has shown promise for treating an aggressive form of blood cancer. Scientists at the Wellcome Sanger Institute, University of Cambridge, University of Nottingham and their collaborators have found that this compound, which targets an essential cancer gene, could kill leukemia cells without harming non-leukemic blood cells.

The results was published in Nature Communications reveal a potential new treatment approach for an aggressive blood cancer with a poor prognosis.

Acute myeloid leukemia (AML) is a form of blood cancer that affects people of all ages, often requiring months of intensive chemotherapy and prolonged hospital admissions. It develops in cells in the bone marrow crowding out the healthy cells, in turn leading to life-threatening infections and bleeding.

Mainstream AML treatments have remained unchanged for over thirty years, with the current treatment being chemotherapy, and the majority of people's cancer cannot be cured. A subtype of AML, driven by rearrangements in the MLL gene has a particularly bad prognosis.

In a previous study, researchers at the Sanger Institute developed an approach, based on CRISPR gene editing technology, which helped them identify more than 400 genes as possible therapeutic targets for different subtypes of AML. One of the genes, SRPK1, was found to be essential for the growth of MLL-rearranged AML. SRPK1 is involved in a process called RNA splicing, which prepares RNA for translation into proteins, the molecules that conduct the majority of normal cellular processes, including growth and proliferation.

In a new study, Sanger Institute researchers and their collaborators set out to work out how inhibition of SRPK1 can kill AML cells and whether it has therapeutic potential in this disease. They first showed that genetic disruption of SRPK1 stopped the growth of MLL-rearranged AML cells and then went on to study the compound SPHINX31, an inhibitor of SRPK1, which was being used to develop an eye drop treatment for retinal neovascular disease -- the growth of new blood vessels on the retinal surface that bleed spontaneously and cause vision loss.

The team found that the compound strongly inhibited the growth of several MLL-rearranged AML cell lines, but did not inhibit the growth of normal blood stem cells. They then transplanted patient-derived human AML cells into immunocompromised mice and treated them with the compound. Strikingly, the growth of AML cells was strongly inhibited and the mice did not show any noticeable side effects.

Dr George Vassiliou, Wellcome Sanger Institute and the Wellcome-MRC Cambridge Stem Cell Institute, said: "We have discovered that inhibiting a key gene with a compound being developed for an eye condition can stop the growth of an aggressive form of acute myeloid leukemia without harming healthy cells. This shows promise as a potential approach for treating this aggressive leukemia in humans."

SRPK1 controls the splicing* of RNA in the production of new proteins. An example of a gene that is affected when SRPK1 is blocked is BRD4, a well-known gene that maintains AML. Inhibiting SRPK1 causes the main form of BRD4 to switch to another form, a change that is detrimental to AML growth.

Dr Konstantinos Tzelepis, the Wellcome Sanger Institute and University of Cambridge, said: "Our study describes a novel mechanism required for leukemia cell survival and highlights the therapeutic potential of SRPK1 inhibition in an aggressive type of AML. Targeting this mechanism may be effective in other cancers where BRD4 and SRPK1 play a role, such as metastatic breast cancer."

Professor David Bates, University of Nottingham and co-founder of biotech company Exonate, which develops eye drops for retinal diseases, said: "When Dr Vassiliou told me that SRPK1 was required for the survival of a form of AML, I immediately wanted to work with him to find out if our inhibitors could actually stop the leukemia cells growing. The fact that the compound worked so effectively bodes well for its potential development as a new therapy for leukemia. It will take some time, but there is real promise for a new treatment on the horizon for patients with this aggressive 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 : 09. Stem Cells and its Applications

Depression, anxiety may take same toll on health as smoking and obesity

An annual physical typically involves a weight check and questions about unhealthy habits like smoking, but a new study from UC San Francisco suggests health care providers may be overlooking a critical question: Are you depressed or anxious?

Anxiety and depression may be leading predictors of conditions ranging from heart disease and high blood pressure to arthritis, headaches, back pain and stomach upset, having similar effects as long-established risk factors like smoking and obesity, according to the new research.

In the study looked at the health data of more than 15,000 older adults over a four-year period.

They found that 16 percent (2,225) suffered from high levels of anxiety and depression, 31 percent (4,737) were obese and 14 percent (2,125) were current smokers, according to their study published in the journal Health Psychology on Dec. 17, 2018.

Participants with high levels of anxiety and depression were found to face 65 percent increased odds for a heart condition, 64 percent for stroke, 50 percent for high blood pressure and 87 for arthritis, compared to those without anxiety and depression.

"These increased odds are similar to those of participants who are smokers or are obese," said O'Donovan, who, with Niles, also is affiliated with UCSF Weill Institute for Neurosciences. "However, for arthritis, high anxiety and depression seem to confer higher risks than smoking and obesity."

Cancer an Exception to Conditions Impacted by Depression and Anxiety

Unlike the other conditions investigated, the authors found that high levels of depression and anxiety were not associated with cancer incidence. This confirms results from previous studies, but contradicts a prevailing idea shared by many patients.

"Our findings are in line with a lot of other studies showing that psychological distress is not a strong predictor of many types of cancer," O'Donovan said. "On top of highlighting that mental health matters for a whole host of medical illnesses, it is important that we promote these null findings. We need to stop attributing cancer diagnoses to histories of stress, depression and anxiety."

Niles and O'Donovan discovered that symptoms such as headache, stomach upset, back pain and shortness of breath increased exponentially in association with high stress and depression. Odds for headache, for example, were 161 percent higher in this group, compared with no increase among the participants who were obese and smokers.

Treating Mental Health Can Cut Health Care Costs

"Anxiety and depression symptoms are strongly linked to poor physical health, yet these conditions continue to receive limited attention in primary care settings, compared to smoking and obesity," Niles said. "To our knowledge this is the first study that directly compared anxiety and depression to obesity and smoking as prospective risk factors for disease onset in long-term studies."

The results of the study underscore the "long-term costs of untreated depression and anxiety," said O'Donovan. "They serve as a reminder that treating mental health conditions can save money for health systems."

The two authors evaluated health data from a government study of 15,418 retirees, whose average age was 68. Depression and anxiety symptoms were assessed using data from participant interviews. Participants were questioned about their current smoking status, while weight was self-reported or measured during in-person visits. Medical diagnoses and somatic symptoms were reported by participants.

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 : 08.Cancer Cell Biology

The source of stem cells points to two proteins

New MSU research published in the journal eLife has pinpointed two proteins that are the keys to stem cell creation.

Credit: Courtesy of MSU

Mammalian embryos are unlike those of any other organism as they must grow within the mother's body. While other animal embryos grow outside the mother, their embryonic cells can get right to work accepting assignments, such as head, tail or vital organ. By contrast, mammalian embryos must first choose between forming the placenta or creating the baby.

New research at Michigan State University and published in the journal eLife has pinpointed two proteins that are the keys to this decision making. The process of assigning cells to placenta or baby is important because that is when pluripotent cells are made. These adaptable pluripotent cells are critical to stem cell research, and these two proteins could be the key to deciphering how pluripotent cells are born, said Amy Ralston, MSU's inaugural James K. Billman Jr., M.D. endowed professor and the study's senior author.

"Pluripotent cells are the progenitors of embryonic stem cells, and they are famous because they can become any part of the body," she said. "We have discovered a process that regulates the balance between pluripotent and placenta, and it works by changing the physical location of cells within the embryo's ball of cells."

To form this wondrous ball, the mother packages two closely related proteins into her eggs, which help oversee this decision-making process. The scientific team used genetic tools to eliminate the proteins YAP1 and WWTR1 from mouse eggs and embryos. The team discovered that these two proteins first position these cells into distinct inside and outside locations, which then decides their fate: placenta or pluripotent.

Each phase of Ralston's research peels back a layer into the creation of stem cells, a process that nature performs with 100 percent efficiency. On the other end of the spectrum, lab-created stem cells are created with 1 percent efficiency.

"Obviously, our understanding of how nature creates stem cells is incomplete," said Tristan Frum, MSU biochemist and molecular biologist"We've suspected these proteins were involved in creating stem cells, but our work reveals that they do so in a surprising way."

Cells of the early embryo express proteins that make them "stick" to the outside of the embryo.

"We've identified a way that cells evade this stickiness, crawl inside the embryo and acquire the properties that make stem cells so interesting and useful," Frum said. "When we make stem cells in the lab, they must acquire a unique cell membrane. Our work shows how nature does this and provides clues that can guide us to control stem cells more efficiently for use in medicine".

For example, the team's discoveries could lead to advances in stem cell technologies using organoids, which are stem cell-derived mini organs. Organoidsare an exciting new paradigm in stem cell and regenerative medicine, The similarities between embryos and organoids are remarkable. Therefore, by studying how the mouse embryo builds itself, we may one day build organs from human stem cells." says Ralston.

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 : 09. Stem Cells and its Applications