Experts associate negative emotions with cancer

Chinese researchers have revealed the mechanism of how chronic stress promotes breast cancer development, shedding light on future clinical treatment for cancer.

Cancer patients often suffer negative emotions such as anxiety, despair and fear, which are risk factors facilitating tumour growth as well as promoting cancer progression. However, the specific mechanisms of how chronic stress affects cancer development remains unknown yet.

Researchers found that chronic stress might increase epinephrine levels, which enhances lactate dehydrogenase A (LDHA) and promotes breast cancer stem-like cells, it was reported.

Using a drug screen that targeted LDHA, they found that Vitamin C reversed the chronic stress-induced cancer stem-like phenotype.

The study demonstrates the critical importance of psychological factors in promoting stem-like properties in breast cancer cells and provides a promising therapeutic approach for breast cancer, according to a researcher.

The LDHA-lowering agent Vitamin C can be a potential approach for combating stress-associated breast cancer, the researcher said.

This team has been engaged in the dynamic regulation of cancer stem cells research as well as the mechanism of psychological behaviour affecting tumour development.

The researcher noted that patients with breast cancer, ovarian cancer and stomach cancer often have negative emotions, which in turn accelerates the development of their own tumours.

It is necessary to monitor their chronic stress comprehensively by taking psychological assessments as well as conducting blood tests which include epinephrine levels, he said.

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Chinese researchers have revealed the mechanism of how chronic stress promotes breast cancer development, shedding light on future clinical treatment for cancer.

Cancer patients often suffer negative emotions such as anxiety, despair and fear, which are risk factors facilitating tumour growth as well as promoting cancer progression. However, the specific mechanisms of how chronic stress affects cancer development remains unknown yet.

Researchers from the Dalian Medical Universi ..

Read more at:
//economictimes.indiatimes.com/articleshow/68814458.cms?utm_source=contentofinterest&utm_medium=text&utm_campaign=cppst

Chinese researchers have revealed the mechanism of how chronic stress promotes breast cancer development, shedding light on future clinical treatment for cancer.

Cancer patients often suffer negative emotions such as anxiety, despair and fear, which are risk factors facilitating tumour growth as well as promoting cancer progression. However, the specific mechanisms of how chronic stress affects cancer development remains unknown yet.

Researchers from the Dalian Medical Univers ..

Read more at:
//economictimes.indiatimes.com/articleshow/68814458.cms?utm_source=contentofinterest&utm_medium=text&utm_campaign=cppst

New method better predicts tumour growth rate in 12 cancers

In a new research, scientists have come up with a new formula that predicts tumour growth rate more accurately, a crucial statistic used to schedule screenings and set dosing regimens in cancer treatment.

The mathematical method successfully estimated the doubling time, the amount of time for a tumour to double in size, for 12 types of cancer, ranging from breast and prostate cancers to melanoma.

"This novel method allows clinicians and drug development scientists to use routinely-generated clinical data to infer doubling times of solid tumours. This parameter can be used to design individualised dosing regimens and develop reliable models for anticancer therapeutics," said the Dr.

Tumour doubling time can significantly affect the outcome of anticancer therapy, but the rate is challenging to determine. Current methods calculate doubling time by measuring the size of a tumour at two points in time and assuming cancer will grow at an exponential rate.

However, most doubling times calculated using this method are overestimated, and tiny changes in tumour size can make determining growth rates difficult.

The error impacts the ability of clinicians to schedule optimal follow-up screenings, set effective dosing regimens, and determine whether surgery, chemotherapy or radiation therapy  is the best form of treatment.
 
The researchers instead base their method on data extracted from progression-free survival  plots - the length of time during and after treatment that cancer does not grow or spread.

Progression-free survival plots explained the Dr., inherently contain information that could help identify tumour growth rates.

The investigators examined data from 47 clinical trials that reported plots for any of 12 cancer types: melanoma; pancreatic, lung, prostate, gastric, colorectal and three forms of breast cancer; hepatocellular (liver) and renal cell (kidney) carcinoma; and glioblastoma multiforme (brain).

The cancer growth rates predicted by the researchers using progression-free survival plots were within close range to the reported actual tumour doubling times. 

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Researchers pinpoint a set of enzymes involved in colon cancer growth

Food science researchers have pinpointed a set of enzymes involved in tumor growth that could be targeted to prevent or treat colon cancer.

"We think this is a very interesting discovery," says an assistant Prof. of food science, whose study was published recently. "Our research identifies a novel therapeutic target and could help to develop novel strategies to reduce the risks of colon cancer."

Colon cancer is the third most common cancer and the second leading cause of cancer-related death in the United States, according to the Centers for Disease Control and Prevention, claiming some 50,000 lives each year. Those statistics emphasize the need to discover new cellular targets that are crucial in the development of colon cancer, he says.

In their study, researchers tested their hypothesis that once present, colon cancer was increased by enzymes known as cytochrome P450 (CYP) monooxygenases and the fatty acid metabolites they form, epoxyoctadecenoic acids (EpOMEs). The researchers compared healthy mice and mice with colon cancer by performing metabolomics, a comprehensive and complex analysis of metabolites, which are produced when food and chemicals are broken down.

In recent years, metabolomics has emerged as a powerful technology in precision medicine because it can offer a detailed picture of biological processes and molecular phenotypes, or characteristics. Precision medicine tailors treatment to an individual's unique genetic and molecular profile.

As they suspected, the researchers found that certain fatty acid metabolites were more abundant in colon cancer. "If a mouse has colon cancer, the plasma and colon concentrations of EpOMEs are very dramatically increased and the EpOME-producing enzymes, CYP monooxygenases, are overexpressed in the colon," he says.

Researchers also studied human colon cancer cells, comparing them to normal colon cells, and found the same results: an overexpression, or plethora, of the CYP monooxygenase enzymes.

Next, using pharmacological and genetic approaches, the researchers removed or inhibited the CYP monooxygenase enzymes in mice with colon cancer and found that tumor growth was suppressed. "If you block the enzyme, colon cancer can be significantly reduced," he says.

In an effort to determine which metabolites were involved in the colon cancer-enhancing effects, researchers studied the biological actions of CYP monooxygenase metabolites. In an in vitro test, they found that EpOME, but not other CYP monooxygenase metabolites, increased inflammation in both inflammatory and colon cancer cells. They then treated cancer-induced mice with EpOME and found an increase in the number and size of tumors. "We showed that at a low dose this metabolite can make colon cancer more aggressive," he says.

Taken together, the results of the research demonstrate "that the previously unappreciated CYP monooxygenase pathway" could be explored for preventing or treating colon cancer, he concludes.

He points out that previous studies have shown that some FDA-approved drugs inhibit CYP monooxygenases, including Micardis, a blood pressure medication, and Lopid, which is used to lower cholesterol. "That suggests that these drugs could be repurposed for preventing or treating colon cancer," he says. "And novel monooxygenase inhibitors could be developed for use in humans."

Using data from his groundbreaking research, he has received a $406,000 USDA grant to study how dietary fats may regulate colon cancer. EpOMEs are metabolites of linoleic acid, which are found in vegetable oils and red meat.

"Based on our findings, overconsumption of linoleic acid could increase tissue concentrations of EpOMEs, which have potent effects to exaggerate inflammation and tumor growth in the colon," he says.

More research is needed in animal models, which can be controlled more easily than human studies. "We need to better understand this pathway in colon cancer, which ultimately may help us suggest nutritional and therapeutic approaches to reduce the risks of colon cancer," he says.

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Cancer: new DNA sequencing technique analyses tumours cell by cell to fight disease

A new DNA sequencing technique lets scientists track genetic errors in individual cancer cells. For the first time, they can reconstruct a tumour’s life history and understand how an error in a cell’s DNA led to the uncontrollable growth of a tumour. This new technology will help doctors understand how a particular cancer has evolved and personalise treatments for each patient, to make them more effective and successful.

We are made of billions of cells that work together to build every part of our body. Occasionally, one of these cells acquires an error in its genetic code and this error, or mutation, can sometimes make this abnormal single cell divide and grow faster than the healthy ones, causing a tumour to develop. During this process, cells can continue to evolve and accumulate many more mutations that make it more dangerous than the original one.

Previously, when researchers studied cancer, they used to take a piece of the tumour and analyse it as a whole. Without understanding the life history of each tumour, science could only give us an incomplete picture of the cancer, where the different cells are mixed and averaged, to get an idea of how dangerous the cancer was. But it didn’t tell us anything about how the tumour had evolved and what type of cells it was made of, making it hard for doctors to select the right treatment for each patient. 

This is the reason many cancer treatments don’t work, and when they do, cancer sometimes regrows within a few months or years, coming back a lot more aggressive than the previous one and much more difficult to treat.

Seeing the whole picture

As the entire tumour couldn’t be beaten as a whole, five years ago, researchers started using a different strategy: divide and conquer. They began dividing the tumours into single cells and analysing each cancer cell separately to try and understand which types of cells made up each tumour.
But even with this advance, they still only had two main tools to analyse single cancer cells. One tool allowed them to read the genetic code of a single cell at a time, identifying which cells have genetic mutations. The other tool helped them understand which genes were active in each cancerous cell, and what their role in the cells was. However, neither of these tools revealed the whole picture. Using them, you could either get the genetic errors from each cell, or the genes that are active and functional – but not both. This made it impossible to understand which genes are activated as a result of genetic errors in each cell. 

A team of researchers, developed a new single-cell sequencing technique that allowed them to see the whole picture. It lets scientists analyse the genetic errors that each cell in a tumour has accumulated while also understanding its gene activity and cell function. This will allow researchers to see in fine detail every aspect of the tumour.

In their latest study, they used this new technique, called TARGET-seq, to analyse many thousands of cells from 11 patients whose blood-making cells had become cancerous. Their analysis provided a detailed picture of the cell types that made up blood cancers. Thanks to its high resolution, they could reconstruct the complete life history of each tumour and identify the molecules that were active during the first steps of tumour development. They also found that cells that appeared healthy, as they didn’t have cancerous mutations, were behaving like malignant cells and activating abnormal genes because they were in a tumour environment. 

Scientists are now using TARGET-seq to analyse different types of aggressive leukemias for which there are no effective treatments. They are hoping to understand how to eliminate the cells that started and sustained the tumour, to be able to completely eradicate them. In the future, we hope that this technique will be used by oncologists to determine the exact mixture of cancer cells that makes up each tumour and customise the right treatment for each patient.

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Cancer cells thrive in stiff tissue

Stiffer breast tissue creates an environment more prone to cancer by enabling the disease to interfere with the surrounding healthy cells, according to a recent study.

Scientists studying tumor growth and metastasis fabricated a human tissue model to examine how cancer cells interact with connective tissue in the breast. The model allowed the team to control the stiffness of the tissue, mimicking both healthy and cancerous breast tissue structures. They found manipulation of fat cells to be stiffness-dependent.

"One of the interesting things we're looking at is how cancer interacts with surrounding cells and how it manipulates those cells to its own benefit," said an assistant professor. "The goal of these tissue engineered cancer models is to mimic the physiological environment of the tumor, so we can use them as a platform to study breast cancer in the human tissue microenvironment."

Fat cells, collagen fibers and epithelial cells make up the micro-environment of breast tissue. Cancer typically appears around the epithelial cells. Previous studies looking at differences between healthy and cancerous tissue found that the cancerous tissue differed in stiffness. According to the study, stiff tissue can present a micro-environment susceptible to tumor growth by enabling the cancer cells to modulate its surrounding connective tissue cells.

"If you have a stiffer environment, the cancer cell can do more manipulation of its immediate micro-environment," the Prof. said. "The model allowed us to study varying levels of stiffness in the tissue. In tissue with normal stiffness, the cancer cells did not interfere with the state of the surrounding stromal cells. In tests where the tissue was stiffer, the cancer halted the differentiation process of the surrounding fat stem cells, favoring a more stem cell-like state creating a micro-environment that favors a tumor to grow."

Researchers have typically conducted similar studies using animal models. While these tests can help advance an understanding of the disease, the Prof. said they could also pose a challenge.

"Animals and humans are quite different," she said. "If you're looking at tissue environment, mobility and the immune system, mouse models, for example, are as different to human models as the pancreas is to the lung."

Those models can also pose a challenge to drug discovery. A fraction of the drugs proven effective in mice actually makes it through clinical trials when tested on humans, she said. The results of this study could help make the case for tissue engineered human disease models to be used as part of a parallel approach to drug screening before administering those drugs in clinical trials.

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Wild berries help in the fight against cancer

Finnish experts in a study found that pigments, reinforcing actions sirtuin-6 – an enzyme involved in building a DNA that is able to actively deal with the genes affected by cancer, and slow tumor growth. Large concentrations of such pigments, scientists found in some wild berries. Unique compounds contain blueberries, raspberries, cranberries and black currants. Consumption of these berries increases the production sirtuin-6 more than 50 times, which helps the body in fighting cancer cells.

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