A newly discovered process to trigger the death of cancer cells could be more effective than current methods such as chemotherapy, scientists have said.

The new method of killing cancer cells, called Caspase Independent Cell Death (CICD), led to the complete eradication of tumours in experimental models.

Most current anti-cancer therapies (chemotherapy, radiation and immunotherapy) work by killing cancer cells through a process called apoptosis, which activates proteins called caspases, leading to cell death.

However in apoptosis, therapies often fail to kill all cancer cells, leading to disease recurrence, and can also have unwanted side effects that may even promote cancer.

Cancer Research's new ad is a live colonoscopy

Scientists from the University of Glasgow wanted to develop a way to improve therapy that induces cancer cell killing while also mitigating unwanted toxicity.

"Our research found that triggering Caspase-Independent Cell Death (CICD), but not apoptosis, often led to complete tumour regression.

"Especially under conditions of partial therapeutic response, as our experiments mimic, our data suggests that triggering tumour-specific CICD, rather than apoptosis, may be a more effective way to treat cancer," Dr Stephen Tait, Cancer Research UK Beatson Institute, from the Institute of Cancer Sciences, said.

Unlike apoptosis, which is a silent form of cell death, when cancer cells die through CICD, they alert the immune system through the release of inflammatory proteins.

The immune system can then attack the remaining tumour cells that evaded initial therapy-induced death.

In research published in Nature Cell Biology, the researchers used lab-grown colorectal cancer cells to show the advantage of killing cancer cells via CICD, however, these benefits may be applicable to a wide-range of cancer types.

Dr Tait added: "In essence, this mechanism has the potential to dramatically improve the effectiveness of anti-cancer therapy and reduce unwanted toxicity.

"Taking into consideration our findings, we propose that engaging CICD as a means of anti-cancer therapy warrants further investigation."

The paper was majority funded by Cancer Research UK.

Dr Justine Alford, Cancer Research UK's senior science information officer, said: "Although many cancer treatments work by triggering apoptosis, that method sometimes fails to finish the job and instead may lead to the tumour becoming harder to treat.

"This new research suggests there could be a better way to kill cancer cells which, as an added bonus, also activates the immune system. Now scientists need to investigate this idea further and, if further studies confirm it is effective, develop ways to trigger this particular route of cell death in humans."

Additional reporting by PA

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New cancer treatment may be more effective than chemotherapy - The Independent

Researchers can activate fluorescent genes in zebrafish to cause certain tissues to glow, an indication their gene editing techniques are working as planned. ISU scientists hope to find genes in zebrafish that can lead to new treatments for diseases in humans. Image courtesy of Wesley Wierson. Larger image.

Ames, Iowa Iowa State University researchers have received a grant to further develop innovative technology that allows them to scour the genome of zebrafish for genes that might lead to advances in human health.

The researchers will use the latest gene editing techniques to create precise mutations in zebrafish. The project, supported by a four-year, $2.98 million grant from the National Institutes of Health, aims to identify genes connected to some of the most serious ailments humans and animals face, including cancer, vascular disease and neurological disorders.

By identifying particular genes related to disease and then switching them off and on again, the researchers hope their findings could lead to new treatments for various diseases.

We need to determine if a gene is curative, said Jeff Essner, a professor of genetics, development and cell biology and research team member. Were hoping to develop a toolbox that will allow us to identify genes in zebrafish, and ultimately in humans, that can be targeted with therapy to cure various ailments.

Many of the genes that lead to disease in humans are present in the zebrafish genome as well, said Maura McGrail, an assistant professor of genetics, development and cell biology and a member of the research team.

If we identify a gene in a zebrafish that affects disease, theres a good chance those results carry over to humans and agriculturally important animals as well, McGrail said. The genomes are about the same size and complexity. There are differences, but its a great starting point.

The Essner and McGrail laboratories boast scores of tanks that contain zebrafish, a small freshwater species that grow only a few centimeters in length. Zebrafish make good model organisms for this kind of genetics work because their embryos are fertilized outside the body of the mother and are transparent, making them easy for scientists to collect and target with the gene-editing technology.

The researchers can even activate fluorescent genes in the zebrafish to cause certain tissues to glow. Essner said doing so offers a direct way to confirm the gene-editing technology is working as intended. It also makes for a striking image.

The ISU team also includes Drena Dobbs, a University Professor of genetics, development and cell biology. The team will collaborate with Karl Clark and Stephen Ekker at the Mayo Clinic in Rochester, Minnesota, who are conducting similar gene editing research in cultured human cells.

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New grant will help Iowa State University scientists search zebrafish genome to promote human health - Iowa State University News Service

The force gravity and physical activity put on our bones causes tiny tears in the membranes of the tiny cells that enable us to make or break down bone, scientists say. Pictured are Drs. Meghan E. McGee-Lawrence and Paul McNeil. Credit: Phil Jones, Senior Photographer, Augusta University

The force gravity and physical activity put on our bones causes tiny tears in the membranes of the tiny cells that enable us to make or break down bone, scientists say.

While that may sound bad, it's actually a key piece of how the force we put on our bones helps keep them strong, they report in the Journal of Orthopaedic Research.

"The bone has to constantly adapt and make sure that is has the right design to withstand the loads you are going to put it through," says Dr. Meghan E. McGee-Lawrence, biomedical engineer in the Department of Cellular Biology and Anatomy at the Medical College of Georgia at Augusta University.

Osteocytes manage the osteoblasts that make bone as well as the osteoclasts that break bone down and were known to sense mechanical loading, but just how they sensed load was unknown.

McGee-Lawrence and MCG cell biologist Dr. Paul McNeil are the first to find the small tears in response to force exacted by walking up the stairs or lifting weights.

Not only do the cells experience membrane tears but it's the highest number McNeil, an expert in cell membrane repair, has seen in a variety of cell types. "It's remarkable," says the study coauthor. And, the heavier the mechanical load, the more tears; for example the mice walking on a treadmill versus just moving about in their cage.

Better understanding the specific mechanism by which these cells sense then respond to mechanical load should enable identification of logical targets for improving the strength and health of aging bones as well as bones challenged by diseases like diabetes, says McGee-Lawrence the study's corresponding author.

Osteocytes are plentiful in bone and each has hundreds of tiny processes reaching out in every direction that help secure them to the bone matrix. McGee-Lawrence likens their look to a sweetgum ball. She and McNeil have early evidence the diminutive cells and their projections are both very vulnerable to tearing and that vulnerability appears to make them a natural for responding to mechanical load.

Once tears happen to cell membranes, more calcium rushes inside the cells. This mineral closely associated with bone health and present outside the cell at concentrations 10,000 times higher than inside the cell, was known to be an initiating signal, McNeil says. His work has shown how in many cell types including now osteocytes, the load causes the tears which allows calcium to rush in to both rapidly heal tears and to set in motion inside a host of actions that, in this case, remodels bone.

In cell cultures, they watched as increased calcium levels inside osteocytes triggered an increase in the production of the protein c-fos. The protein also is well-studied and known to be involved in the signaling pathways that lead to stronger bones in response to exercise, but c-fos' connection with membrane tearing was another unknown.

Osteocytes use their micron-thin tentacles to communicate with each other and the scientists also learned that when one osteocyte gets tears, it appears to communicate its load to neighboring osteocytes so the calcium level goes up in those as well even without a tear. The message the torn osteocyte shares it to tell osteoblasts to make the bones stronger and the osteoclasts to quit breaking bone down.

The idea of further shoring up bone is likely to be better prepared for whatever mechanical load comes next, McGee-Lawrence says.

Conversely, the lack of loading and subsequent tearing may be why astronauts' bone and muscle weaken in zero gravity, McNeil says.

McGee-Lawrence is principal investigator on a new $450,000 National Science Foundation grant that will help them further parse this important puzzle and the potential for enabling better bone health with age and disease.

"We are wondering if bone loss with aging is due to osteocytes becoming more fragile or less able to repair as we age," say McNeil, co-investigator on the ongoing studies. "If they do, you would lose them over time and, in fact, we know you do lose them."

Part of what they are doing with the new grant includes looking at mice with a genetic deficiency in cell membrane repair. They want to see if the 50-year-old drug poloxamer 188, which was designed to reduce the thickness of blood, is found in products like toothpaste and has been shown to repair other cell membranes, might help osteocytes remain proficient at responding to mechanical load. Like many of our senses that dull with age, aging osteocytes don't sense critical mechanical loads as well.

"It's a way you can influence membrane repair rates so if we speed up how fast that tear repairs, is that going to influence the osteocytes?" McGee-Lawrence says. They'll also look at the impact of slowing repair down.

No drug on the market for osteoporosis is known to enhance osteocyte sensitivity.

"We are starting to understand why calcium signaling gets initiated in wounded cells and then that gives us a mechanism we can target to try to influence how well bone detects mechanical loading," McGee-Lawrence says.

Disease may also complicate the common action of cell membrane tear and repair. For example, McNeil has shown diabetes, which is associated with bone loss, can lead to problems with membrane repair of other cell types. Now the MCG scientists are looking at whether it similarly affects osteocytes.

Bone and muscle health are inextricably connected and McNeil has done pioneering work that shows one way we keep our muscles strong and even increase their size is through this process of tear and repair in the membrane of muscle cells.

"If you go to the gym and exercise your muscles, they are going to get bigger and stronger and at the same time if you sit around all day your muscles are going to get weaker," McGee-Lawrence says. "Bone does the same thing." McNeil notes the difference between the right and left hands and arms of a right-handed tennis player.

"This bone is full of cells. Some are building new bone, some are breaking down bone and it is constantly being remodeled," McNeil adds, holding up a large muskox bone.

People hit their peak bone mass in the late 20s or early 30s. After that, the percentage of osteoblasts to osteoclasts starts to shift so that you are slowly losing rather than building bones. Active youth, they note, tend to build a better bone mass that should comfortably see them into old age, particularly if they remain active.

Failure of rapid membrane repair is associated with weaker muscles even muscle disease, they note, and the scientists expect the same also holds true in bone. Future studies include exploring whether repair failure contributes to common problems like osteoporosis.

Explore further: Research identifies how master regulator, bone-building protein can be used for therapy

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Tears in tiny bone cells called osteocytes appear an important step to better bones - Medical Xpress

A researcher pulls a frozen vial of human embryonic stem cells at the University of Michigan Center for Human Embryonic Stem Cell Research Laboratory in Ann Arbor, Mich., in this Oct. 22, 2008 file photo. The face of science, writes Kristin Baetz, should be changing, and here's how to do it. Paul Sancya, THE ASSOCIATED PRESSPaul Sancya / THE ASSOCIATED PRESS

At science meetings, women need to grab the mic and not let go.

As the director of the Ottawa Institute of Systems Biology at uOttawa and as past-president of the Canadian Society for Molecular Biosciences, I get a lot of emails asking me to attend or help advertise science conferences.

Most of these emails end up in my delete file.

Why? I am no longer going to promote, sponsor or attend meetings that do not have a significant number of female speakers.

If accomplished female scientists are not asked to present at meetings, by default it suggests their research is not as exciting or as good as that of their male colleagues.

This matters both financially and professionally your speaking portfolio contributes to the success of grant applications and whether one receives tenure or becomes a full professor.

Canada needs equity in science, technology, engineering and mathematics (STEM). As Imogen Coe, dean of science at Ryerson University and a leading expert in the barriers of women in STEMs, states, If we are to solve or even address the complex problems that we face, we need all hands on deck, we need everyone at the table, we need to leverage all the human potential and intellectual capacity that is available to us.

With women comprising more than 50 per cent of trainees and early-career researchers in biomedical fields, how is it that that the problem of #YAMMM (yet another mostly-male meeting) still exists?

The answer is this: Scientists let it happen.

Consider how science conferences are run. For a number of reasons, largely mid- or late-career scientists organize meetings, and they are often men. Only established researchers, who are no longer struggling to build their research programs, build new courses or possibly to raise young families, have the time to organize meetings.

Its only human that when they solicit speakers, its colleagues they know, or want to collaborate with. If you are an early-career researcher, especially female, many meeting organizers might not have you on their radar.

This will change when organizers of meetings including scientific societies and funders start demanding that equity is a fundamental requirement of meetings.

Coe recently challenged me to ensure that the speakers at our 2017 Canadian Society for Molecular Biosciences meeting reflected our attendees. I am both proud and ashamed to announce that at our 60th annual science meeting, 50 per cent of our speakers were female.

I insisted that our organizers seek out exceptional female speakers to give plenary talks.

While this was embraced by many of my colleagues, it was strongly resisted by others. Some refused to even consider equity issues when selecting speakers. Why? One often-made excuse is that there are no excellent females in a field to invite.

Jodi Nunnari, president-elect of the American Society for Cell Biology, calls this a poor excuse, which justifies the same old status quo. To counter this argument, her society established a speaker referral list to identify outstanding women scientists across the field of cell biology.

Heres what happened at our meeting. Many back-handed comments were made about how different the speaker lineup was. I got upset emails over not being asked to give a talk. One said, I guess I didnt tick-off the right boxes.

These reactions consistently originated from mid- and late-career male scientists.

However, for every negative comment, I received tenfold more positive comments from across the research spectrum, from trainees to retired professors, both male and female.

While I am hopeful that our government will one day tackle the equity issues in STEM by directly tying it to funding, scientists cannot just wait. As individuals and as institutions we have the ability to literally change the face of conferences and success in Canadian science.

Lets commit to ending the #YAMMM.

Kristin Baetz is the director of the Ottawa Institute of Systems Biology and professor at uOttawa.

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Baetz: Standing up for female scientists and researchers - Ottawa Citizen

ByTaylor Jade Powell

Oscar, Cristian, Luis, and Lorenzo were never expected to amount to much. Born in Mexico and growing up in Arizona, the four undocumented teenagers were poor and attending an underfunded high school in the desert.

Though the students had never seen the ocean, two science teachers inspired them to build an underwater robot and compete in a marine robotics competition at the University of California, Santa Barbara.

Spare Parts: Four Undocumented Teenagers, One Ugly Robot, and the Battle for the American Dream tells the stories of young men with insurmountable odds stacked against themdeportation, prejudice, and a robotics team with 10 times more funding.

The book by Joshua Davis addresses the issue of immigration and challenges students to consider alternate ways of learning, said Tiffany Sanchez, Johns Hopkins University's interim dean of student life. That's why the Common Read Committee chose it as this year's assignment for the Class of 2021.

New students will discuss the book in small groups led by faculty, staff, resident assistants, and first-year mentors today as part of orientation.

"We hope this makes Hopkins feel a bit more like home and introduces new students to people and ideas that they might not normally come in contact with," Sanchez said.

Tiffany Sanchez

Interim dean of student life

The Common Read program started in 2007 with a mission to bring together first-year class members and new transfer students, while encouraging critical thinking and intellectual discussion. Each year a committee made up of JHU staff and faculty chooses a book that students receive via mail.

Over the summer, students had the opportunity to submit essays or short videos in response to the book, and this year there were more than 70 contest entries. Winners will be honored at the Common Read Keynote on Sept. 7, where protagonists Fredi Lajvardi and Oscar Vazquez will talk about their experiences depicted in the novel.

"It's such a great way to get to know our new students, and I enjoy learning about their lives," Sanchez said. "Each response reminded me that there are over 1,300 new individuals in our community and each of them comes with their own experiences, values, and ideas about the world."

One of three winners is Kelechi Nwankwoala, an incoming Writing Seminars and molecular cell biology double-major. In his contest submission, Nwankwoala said he considered his parents' immigration to America and his own fears of being treated differently because of his race as part of his response to the book.

"I tried to use narrative to express how racial prejudice and fear can become a constant weight on the psyche," he said. "It is my belief that constant fear does something to people; it effects the way you interact with the world. I wanted to illustrate how my own fears have changed over the years and how I have become more and more aware of the weight I shoulder."

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Something in common: New JHU students discuss shared summer reading assignment, 'Spare Parts' - The Hub at Johns Hopkins