Health24.com | 5 reasons why you might suddenly start wetting yourself

Ever laughed or sneezed so hard that a little bit of urine trickled out? Or had such a big need to go that you couldn’t keep it in?

There are a number of causes of urinary incontinence – for example pressure on the bladder, damage to the pelvic floor muscles, or an overfull bladder – and it’s a much more common condition than one might think.

It’s important that you disclose it to your doctor if it starts happening suddenly, or frequently enough to affect the quality of your life.

Here are the main underlying causes that may cause sudden urinary incontinence:

1. Neurological disorders

Nerve signals from the bladder to the brain are vital in controlling the urge to urinate. When these signals are compromised, it can cause sudden urinary incontinence. Conditions that may affect the nerves include neurological disorders such as multiple sclerosis, Parkinson’s disease, a stroke, injury of the spine or a brain injury.

neurological signals

2. Blockage of the urinary tract

Any obstruction of the urinary tract may interfere with the normal flow of urine, causing the bladder to overflow. Obstructions of the urinary tract, like urinary or kidney stones, can develop over time. When the flow of urine is disturbed, infections can occur. You will usually experience other symptoms such as a dull ache near your kidney area, but it’s possible that you may not feel anything for some time.

urinary tract illustration

3. Prostate cancer

If you are a man and you suddenly develop urinary incontinence, you should visit your doctor or urologist as soon as possible.

When men experience stress incontinence (pressure on the bladder), or urge incontinence (a sudden, more frequent urge to urinate), it could signal untreated prostate cancer. Incontinence is, however, more likely to develop as a result of the treatment of prostate cancer through surgery or radiation.

illustration of prostate cancer

4. An enlarged prostate gland

Older men are often affected by a condition called benign prostatic hyperplasia (BPH) or enlarged prostate, a non-cancerous enlargement of the prostate gland.

The enlargement of the prostate distorts the urethra, obstructing the flow of urine from the bladder and leading to symptoms of an obstructive or irritative nature, including urinal incontinence. Even though an enlarged prostate may not be cancerous, you need to visit your doctor as a matter of urgency if you experience sudden urinary incontinence. Left untreated, it may lead to kidney failure, kidney stones and other urinary obstructions.

Man discussing enlarged prostate with doctor

5. The use of certain medications

If there is no other reasonable explanation for a sudden onset of urinary incontinence, check your medicine cabinet for any recent medical prescriptions. Some medications such as alpha-blockers, commonly used for treatment of high blood pressure; diuretics, used for kidney conditions; and, very rarely, some sleeping pills and anti-depressants, can suddenly cause an overactive bladder.

a variety of pills

Image credits: iStock

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‘Baby Grady’ gives fertility hope to boys with cancer

A new approach could preserve fertility for boys having cancer treatment – thanks to a baby monkey.

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Kicking neural network automation into high gear

A new area in artificial intelligence involves using algorithms to automatically design machine-learning systems known as neural networks, which are more accurate and efficient than those developed by human engineers. But this so-called neural architecture search (NAS) technique is computationally expensive.

One of the state-of-the-art NAS algorithms recently developed by Google took 48,000 hours of work by a squad of graphical processing units (GPUs) to produce a single convolutional neural network, used for image classification and identification tasks. Google has the wherewithal to run hundreds of GPUs and other specialized circuits in parallel, but that’s out of reach for many others.

In a paper being presented at the International Conference on Learning Representations in May, MIT researchers describe an NAS algorithm that can directly learn specialized convolutional neural networks (CNNs) for target hardware platforms — when run on a massive image dataset — in only 200 GPU hours, which could enable far broader use of these types of algorithms.

Resource-strapped researchers and companies could benefit from the time- and cost-saving algorithm, the researchers say. The broad goal is “to democratize AI,” says co-author Song Han, an assistant professor of electrical engineering and computer science and a researcher in the Microsystems Technology Laboratories at MIT. “We want to enable both AI experts and nonexperts to efficiently design neural network architectures with a push-button solution that runs fast on a specific hardware.”

Han adds that such NAS algorithms will never replace human engineers. “The aim is to offload the repetitive and tedious work that comes with designing and refining neural network architectures,” says Han, who is joined on the paper by two researchers in his group, Han Cai and Ligeng Zhu.

“Path-level” binarization and pruning

In their work, the researchers developed ways to delete unnecessary neural network design components, to cut computing times and use only a fraction of hardware memory to run a NAS algorithm. An additional innovation ensures each outputted CNN runs more efficiently on specific hardware platforms — CPUs, GPUs, and mobile devices — than those designed by traditional approaches. In tests, the researchers’ CNNs were 1.8 times faster measured on a mobile phone than traditional gold-standard models with similar accuracy.

A CNN’s architecture consists of layers of computation with adjustable parameters, called “filters,” and the possible connections between those filters. Filters process image pixels in grids of squares — such as 3×3, 5×5, or 7×7 — with each filter covering one square. The filters essentially move across the image and combine all the colors of their covered grid of pixels into a single pixel. Different layers may have different-sized filters, and connect to share data in different ways. The output is a condensed image — from the combined information from all the filters — that can be more easily analyzed by a computer.

Because the number of possible architectures to choose from — called the “search space” — is so large, applying NAS to create a neural network on massive image datasets is computationally prohibitive. Engineers typically run NAS on smaller proxy datasets and transfer their learned CNN architectures to the target task. This generalization method reduces the model’s accuracy, however. Moreover, the same outputted architecture also is applied to all hardware platforms, which leads to efficiency issues.

The researchers trained and tested their new NAS algorithm on an image classification task in the ImageNet dataset, which contains millions of images in a thousand classes. They first created a search space that contains all possible candidate CNN “paths” — meaning how the layers and filters connect to process the data. This gives the NAS algorithm free reign to find an optimal architecture.

This would typically mean all possible paths must be stored in memory, which would exceed GPU memory limits. To address this, the researchers leverage a technique called “path-level binarization,” which stores only one sampled path at a time and saves an order of magnitude in memory consumption. They combine this binarization with “path-level pruning,” a technique that traditionally learns which “neurons” in a neural network can be deleted without affecting the output. Instead of discarding neurons, however, the researchers’ NAS algorithm prunes entire paths, which completely changes the neural network’s architecture.

In training, all paths are initially given the same probability for selection. The algorithm then traces the paths — storing only one at a time — to note the accuracy and loss (a numerical penalty assigned for incorrect predictions) of their outputs. It then adjusts the probabilities of the paths to optimize both accuracy and efficiency. In the end, the algorithm prunes away all the low-probability paths and keeps only the path with the highest probability — which is the final CNN architecture.

Hardware-aware

Another key innovation was making the NAS algorithm “hardware aware,” Han says, meaning it uses the latency on each hardware platform as a feedback signal to optimize the architecture. To measure this latency on mobile devices, for instance, big companies such as Google will employ a “farm” of mobile devices, which is very expensive. The researchers instead built a model that predicts the latency using only a single mobile phone.

For each chosen layer of the network, the algorithm samples the architecture on that latency-prediction model. It then uses that information to design an architecture that runs as quickly as possible, while achieving high accuracy. In experiments, the researchers’ CNN ran nearly twice as fast as a gold-standard model on mobile devices.

One interesting result, Han says, was that their NAS algorithm designed CNN architectures that were long dismissed as being too inefficient — but, in the researchers’ tests, they were actually optimized for certain hardware. For instance, engineers have essentially stopped using 7×7 filters, because they’re computationally more expensive than multiple, smaller filters. Yet, the researchers’ NAS algorithm found architectures with some layers of 7×7 filters ran optimally on GPUs. That’s because GPUs have high parallelization — meaning they compute many calculations simultaneously — so can process a single large filter at once more efficiently than processing multiple small filters one at a time.

“This goes against previous human thinking,” Han says. “The larger the search space, the more unknown things you can find. You don’t know if something will be better than the past human experience. Let the AI figure it out.”

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Research elucidates why protons are at the heart of atoms spin

A major new finding about the fundamental structure of all matter has just been published by a group of researchers that includes a Temple University physicist and two former Temple graduate students. Appearing March 14 as a rapid communication in the journal Physical Review D, the research stems from an analysis of data produced by an experiment conducted at the Brookhaven National Laboratory’s Relativistic Heavy-Ion Collider (RHIC) on Long Island in polarized proton-proton collisions.

The new data is derived from the STAR (Solenoidal Tracker At RHIC) experiment that added detail — and complexity — to an intriguing puzzle that scientists have been pondering: How the building blocks that make up a proton effect its spin (both protons and neutrons form the center of each atom). The spinning is as essential to a particle’s identity as its electric charge and mass. Because particles have spin, they can act like tiny magnets with a particular polarity. For example, aligning and flipping the polarity of proton spin is the basis for technologies such as magnetic resonance imaging (MRI), an indispensable medical diagnostic tool.

Understanding how this proton spin arises from each proton’s inner building blocks — which include quarks, gluons and what is called a sea of quark-antiquark pairs — may help scientists better understand the nuclear structure of atoms.

“After multiple years of experimental work at RHIC, this exciting new result provides a substantially deeper understanding of fundamental quantum physics questions regarding how quantum fluctuations affect the dynamics of quarks inside the proton,” says Professor Bernd Surrow, vice chair of the Temple Physics Department. “It contributes to our exploration of the structure and dynamics of the visible world around us, including the human body, a table or a car, and what gives them mass in terms of their atomic structures.”

In a field dominated by males, Surrow notes that two women who formerly were graduate students in his laboratory — Amani Kraishan and Devika Gunarathne — were two of the three graduate students who analyzed the data that led to the publication of the research, and continue in the field. Kraishan is currently an adjunct professor both in Temple’s Physics Department and at Al-Hussein Bin Talal University in Jordan. She continues to collaborate with the Temple group under the leadership of Professor Surrow, focusing on the ongoing research program at Brookhaven National Laboratory and a future U.S. Electron-Ion Collider facility.

The third student involved, Jinlong Zhang of Shandong University, subsequently was a postdoctoral fellow at the Lawrence Berkeley National Laboratory and is now at Stony Brook University.

The research was funded by an ongoing grant from the U.S. Department of Energy (DOE). Future goals of the study include more precise measurements of the quarks and antiquarks, and the gluons which “glue” or bind the quarks and antiquarks together to form both protons and neutrons.

Story Source:

Materials provided by Temple University College of Science and Technology. Note: Content may be edited for style and length.

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Health24.com | Could invasive lung cancer biopsies be replaced by blood tests?

A blood test may one day replace invasive tissue biopsies as a pain-free way to confirm lung cancer and guide treatment, new research suggests.

According to investigators, the test is as effective as a tissue biopsy in diagnosing advanced non-small cell lung cancer, by far the leading form of the leading cancer killer.

A convincing argument

The so-called “liquid biopsy” can also quickly identify tumour gene mutations that match targeted drug therapies — potentially boosting patient survival.

The new findings present “a convincing argument for use of the liquid biopsy as a first option for molecular testing in advanced non-small cell lung cancer,” said lead researcher Dr Vassiliki Papadimitrakopoulou. She’s professor of thoracic head and neck medical oncology at the University of Texas MD Anderson Cancer Center.

As the Houston team explained, if a CT scan suggests lung cancer, patients are typically asked to undergo a surgical tissue biopsy. It’s an expensive, invasive procedure that comes with risks and inconvenience to patients.

Seeking a way around these procedures, numerous companies have been developing blood-based diagnostic tests for lung cancer. The new study focuses on one such test, called Guardant360, developed by Guardant Health, the company that funded the new study.

Blood tests like Guardant360 rely on traces of tumour DNA in blood for clues to the presence of lung cancer and the best way to treat it.

In addition to the higher accuracy found in the new study, the researchers reported that the results of the blood test can be turned around sooner than those of a tissue biopsy.

Higher response rates

While results for a standard biopsy took 15 days to process, results of the liquid biopsy took just nine days, on average, the study found.

That means treatment could begin sooner, with potentially better outcomes, the researchers said.

Speedier genetic analysis of the tumour is crucial, the investigators explained, because 30% of lung cancers can now be successfully treated with new gene-targeted medicines. These drugs tend to have higher response rates than standard chemotherapy.

For the study, Papadimitrakopoulou and her colleagues used Guardant360 to identify mutant genes in the blood of nearly 300 patients.

Specifically, the tests were focused on seven “biomarkers” in blood samples — tumour-specific gene mutations that can help identify subtypes of lung cancer.

The Guardant360 test also looked for one biomarker — called KRAS — that helps predict a cancer patient’s prognosis, the research team said.

The blood test seemed to outperform standard tissue biopsy. While the standard surgical biopsy found at least one marker predictive of lung cancer in 60 patients, the blood test spotted it in 89 patients, the findings showed.

Study limitations

Drugs that target many of these lung tumour gene mutations are already approved by the US Food and Drug Administration, the researchers noted.

Among the more than 190 patients who did not show the presence of one of the seven genetic tumour biomarkers, testing was often still able to spot the KRAS prognostic biomarker, the study team said.

Again, the blood test beat tissue biopsy in this regard: The Guardant360 test spotted the KRAS biomarker in 92 patients, compared with 24 patients who underwent standard biopsy.

Still, the new study was limited in two ways. First, Guardant360 results weren’t compared to the results of the very latest gene-based surgical biopsy analyses. And secondly, the results apply only to the Guardant360 test — not to other liquid biopsies already out there.

One lung cancer specialist was still heartened by the results, however.

“For years, we have been doing surgical biopsies, but over the last few years there’s been a recognition that this is more a ‘molecular disease’, governed by [gene] mutations,” said Dr Richard Lazzaro, chief of thoracic surgery at Lenox Hill Hospital in New York City.

It’s also been known that cancer cells can shed their DNA into the blood, he said.

A better therapeutical paradigm

“If you can make diagnosis and treating decisions and save time, that’s outstanding for patient care,” Lazzaro said.

Effective treatment, delivered sooner after diagnosis, should improve survival, he added.

Already, liquid biopsies are often being used in tandem with surgical biopsies, Lazzaro noted.

However, “perhaps one day they will replace a surgical biopsy and may become a better therapeutical paradigm,” he said.

The results of the study are to be presented at the American Association for Cancer Research meeting, in Atlanta. Findings presented at medical meetings are typically considered preliminary until published in a peer-reviewed journal.

According to the American Cancer Society, lung cancer remains the number one cancer killer in the United States, with nearly 143 000 deaths expected in 2019.

Image credit: iStock

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High-fructose corn syrup boosts intestinal tumor growth in mice

Does sugar directly feed cancers, boosting their growth? The answer seems to be ‘Yes’ at least in mice according to a study led by researchers at Baylor College of Medicine and Weill Cornell Medicine. Their study, published in Science, showed that consuming a daily modest amount of high-fructose corn syrup — the equivalent of people drinking about 12 ounces of a sugar-sweetened beverage daily — accelerates the growth of intestinal tumors in mouse models of the disease, independently of obesity. The team also discovered the mechanism by which the consumption of sugary drinks can directly feed cancer growth, suggesting potential novel therapeutic strategies.

“An increasing number of observational studies have raised awareness of the association between consuming sugary drinks, obesity and the risk of colorectal cancer,” said co-corresponding author Dr. Jihye Yun, assistant professor of molecular and human genetics at Baylor. “The current thought is that sugar is harmful to our health mainly because consuming too much can lead to obesity. We know that obesity increases the risk of many types of cancer including colorectal cancer; however, we were uncertain whether a direct and causal link existed between sugar consumption and cancer. Therefore, I decided to address this important question when I was a postdoc in the Dr. Lewis Cantley lab at Weill Cornell Medicine.”

First, Yun and her colleagues generated a mouse model of early-stage colon cancer where APC gene is deleted. “APC is a gatekeeper in colorectal cancer. Deleting this protein is like removing the breaks of a car. Without it, normal intestinal cells neither stop growing nor die, forming early stage tumors called polyps. More than 90 percent of colorectal cancer patients have this type of APC mutation,” Yun said.

Using this mouse model of the disease, the team tested the effect of consuming sugar-sweetened water on tumor development. The sweetened water was 25 percent high-fructose corn syrup, which is the main sweetener of sugary drinks people consume. High-fructose corn syrup consists of glucose and fructose at a 45:55 ratio.

When the researchers provided the sugary drink in the water bottle for the APC-model mice to drink at their will, mice rapidly gained weight in a month. To prevent the mice from being obese and mimic humans’ daily consumption of one can of soda, the researchers gave the mice a moderate amount of sugary water orally with a special syringe once a day. After two months, the APC-model mice receiving sugary water did not become obese, but developed tumors that were larger and of higher-grade than those in model mice treated with regular water.

“These results suggest that when the animals have early stage of tumors in the intestines — which can occur in many young adult humans by chance and without notice — consuming even modest amounts of high-fructose corn syrup in liquid form can boost tumor growth and progression independently of obesity,” Yun said. “Further research is needed to translate these discovery to people; however, our findings in animal models suggest that chronic consumption of sugary drinks can shorten the time it takes cancer to develop. In humans, it usually takes 20 to 30 years for colorectal cancer to grow from early stage benign tumors to aggressive cancers.”

“This observation in animal models might explain why increased consumption of sweet drinks and other foods with high sugar content over the past 30 years is correlating with an increase in colorectal cancers in 25 to 50-year-olds in the United States,” said Cantley, co-corresponding author, former mentor of Yun and professor of cancer biology in medicine and director of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine.

The team then investigated the mechanism by which this sugar promoted tumor growth. They discovered that the APC-model mice receiving modest high-fructose corn syrup had high amounts of fructose in their colons. “We observed that sugary drinks increased the levels of fructose and glucose in the colon and blood, respectively and that tumors could efficiently take up both fructose and glucose via different routes.”

Using cutting-edge technologies to trace the fate of glucose and fructose in tumor tissues, the team showed that fructose was first chemically changed and this process then enabled it to efficiently promote the production of fatty acids, which ultimately contribute to tumor growth.

“Most previous studies used either glucose or fructose alone to study the effect of sugar in animals or cell lines. We thought that this approach did not reflect how people actually consume sugary drinks because neither drinks nor foods have only glucose or fructose. They have both glucose and fructose together in similar amounts,” Yun said. “Our findings suggest that the role of fructose in tumors is to enhance glucose’s role of directing fatty acids synthesis. The resulting abundance of fatty acids can be potentially used by cancer cells to form cellular membranes and signaling molecules, to grow or to influence inflammation.”

To determine whether fructose metabolism or increased fatty acid production was responsible for sugar-induced tumor growth, the researchers modified APC-model mice to lack genes coding for enzymes involved in either fructose metabolism or fatty acid synthesis. One group of APC-model mice lacked an enzyme KHK, which is involved in fructose metabolism, and another group lacked enzyme FASN, which participates in fatty acid synthesis. They found that mice lacking either of these genes did not develop larger tumors, unlike APC-model mice, when fed the same modest amounts of high-fructose corn syrup.

“This study revealed the surprising result that colorectal cancers utilize high-fructose corn syrup, the major ingredient in most sugary sodas and many other processed foods, as a fuel to increase rates of tumor growth,” Cantley said. “While many studies have correlated increased rates of colorectal cancer with diet, this study shows a direct molecular mechanism for the correlation between consumption of sugar and colorectal cancer.”

“Our findings also open new possibilities for treatment,” Yun said. “Unlike glucose, fructose is not essential for the survival and growth of normal cells, which suggests that therapies targeting fructose metabolism are worth exploring. Alternatively, avoiding consuming sugary drinks as much as possible instead of relying on drugs would significantly reduce the availability of sugar in the colon.”

While further studies in humans are necessary, Yun and colleagues hope this research will help to raise public awareness about the potentially harmful consequences consuming sugary drinks has on human health and contribute to reducing the risk and mortality of colorectal cancer worldwide.

Other contributors to this work include Drs. Sukjin Yang, Yumei Wang and Justin Van Riper with Baylor, Marcus Goncalves (lead author), Changyuan Lu, Jordan Trautner, Travis Hartman, Seo-Kyoung Hwang, Charles Murphy, Roxanne Morris, Sam Taylor, Quiying Chen, Steven Gross and Kyu Rhee, all with Weill Cornell Medicine, Chantal Pauli with the University Hospital Zurich, Kaitlyn Bosch with the Icahn School of Medicine at Mount Sinai, H Carl Lekaye with Memorial Sloan Kettering Cancer Center, Jatin Roper with Duke University and Young Kim with Chonnam National University.

This study was supported by the National Institutes of Health, Stand Up 2 Cancer, the Cancer Prevention and Research Institute of Texas and the National Cancer Institute.

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Cervical screening: DIY smear test could be ‘game-changer’

Women who miss cervical screening appointments will be given home-testing kits in a pilot scheme.

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IVF ethics pioneer Mary Warnock dies

The philosopher Baroness Mary Warnock has died at the age of 94.

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Assisted dying: Doctors’ group adopts neutral position

The Royal College of Physicians votes to adopt a neutral position on helping terminally ill patients die.

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Health24.com | New techniques let scientists zero in on individual cells

Did you hear what happened when Bill Gates walked into a bar? Everybody there immediately became millionaires – on average.

That joke about a very rich man is an old one among statisticians. So why did Peter Smibert use it to explain a revolution in biology?

‘Mushed-up average’

Because it shows averages can be misleading. And Smibert, of the New York Genome Center, says that includes when scientists are trying to understand the basic unit of life, the cell.

Until recently, trying to study key traits of cells from people and other animals often meant analysing bulk samples of tissue, producing a mushed-up average of results from many cell types. It was like trying to learn about a banana by studying a strawberry-blueberry-orange-banana smoothie.

In recent years, however, scientists have developed techniques that let them directly study the DNA codes, the activity of genes and other traits of individual cells. The approach has become widely adopted, revealing details about the body that couldn’t be shown before. And it has opened the door to pursuing an audacious goal: listing every cell type in the human body.

“Single-cell analysis is crucial for a comprehensive understanding of our biology and health,” Dr Francis Collins, the director of the National Institutes of Health, declared recently.

In fact, the journal Science named the techniques that allow single-cell tracking of gene activity over time in developing organisms and organs as its “breakthrough of the year” for 2018. Its announcement declared, “The single-cell revolution is just starting.”

Even complicated animals like us are really just massive communities of cells, each taking on a particular role and working with its neighbours. An average adult human has 37 trillion or so of them, and they’re surprisingly varied: the inner lining of the colon, for example, has more than 50 kinds of cells.

A slew of discoveries

It was just five years ago that methods for decoding of DNA and its chemical cousin RNA from individual cells became broadly accessible, according to the journal Nature Methods. New techniques are still being developed to pry more and more secrets out of individual cells.

The single-cell approach is leading to a slew of discoveries. In just the past year, for example:

  • Scientists closely tracked gene activity within fish and frog embryos, a step toward the longstanding goal of understanding how a single fertilised egg can produce an animal. One study compiled results from more than 92 000 zebrafish embryonic cells.
  • Other researchers revealed details of the physical connection between pregnant women and the foetus, giving potential clues for understanding some causes of stillbirth.
  • A study found a pattern of gene activity in some melanoma cells that let them resist immunotherapy, the practice of unleashing the body’s immune system on cancer. That might lead to finding a way to render those cells vulnerable.

And a pair of other studies may affect research into cystic fibrosis, the genetic disease that causes lung infections and limits breathing ability. Scientists have long known that the disease stems from a faulty version of protein called CFTR. The studies identified a type of rare cell in the airway that makes large amounts of CFTR, surpassing earlier but only dimly understood indications that such cells existed.

The discovery offers great potential for guiding the development of new treatments, said Dr William Skach, senior vice president of research affairs for the Cystic Fibrosis Foundation. Single-cell techniques will be important in studying them further for coming up with new therapies, he said. (Two co-authors of one paper are from the foundation).

At the MD Anderson Cancer Center of the University of Texas, Nicholas Navin uses single-cell DNA studies to reveal different patterns of mutations in various cells of a single tumour. That lets him reconstruct when and where those mutations appeared as the tumour evolved from benign cells. And he can identify cells that contain combinations of mutations that make them the most lethal.

Someday, such research should indicate what treatments to use for particular patients, or which patients have the highest risk of the disease progressing, he says. It might also allow doctors to check how well their treatments are working against a cancer over time. A decade or two from now, it might let doctors detect cancers very early by picking up and analysing the DNA of rare cells in blood tests, he says.

Thousands of genetic variants

Meanwhile, the ability to produce single-cell results for hundreds of thousands of cells at a time has opened the door to a huge effort to catalogue every cell type in the human body. More than 1 000 scientists from 57 countries have joined the Human Cell Atlas Consortium, which estimates it will eventually profile at least 10 billion cells found in both healthy and sick people.

Why do this? It’s a natural follow to the big project that catalogued all the human genes, says co-organizer Aviv Regev, a biology professor at the Massachusetts Institute of Technology and researcher at the Broad Institute of MIT and Harvard. (Her salary is paid by the Howard Hughes Medical Institute, which also supports The Associated Press Health & Science Department.)

The gene map led to identifying thousands of genetic variants that raise or lower the risk of many diseases. But to turn that into therapies, scientists have to know in which cells those variants act, she said. And to run down those cells in the human body, “we have to map all of them”.

Some cells are rarer than others, but these can be just as critical for a functioning body as their more plentiful neighbours, she said.

She hopes for a first draft of the cell atlas in about five years, focused on certain organs and tissues of the body. To finish the job might take about a decade, she figures. Regev won’t hazard a guess about how many cell types will be found for the entire human body.

“This is not going to cure all disease immediately,” she said, but “it is a critical stepping stone.”

Image credit: iStock

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