Tag: cancer

Categories : CancerTags :

Study Discovers How Melanoma Cells Hide From Immune System

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Melanomas in some patients do not respond well to immunotherapy treatments, and now researchers have discovered that a defect in STING gene expression in melanoma cells helps them escape immune cell surveillance.

Cancer cells use a variety of recently discovered mechanisms to avoid detection and destruction by immune cells, including defective detection and destruction of T cells, losses in expression of critical proteins on tumour cells and defective cell signaling in both immune and tumor cells.

The interferon signaling pathway is an important signaling pathway in interactions between tumour and immune cells. This pathway increases expression of molecules allowing tumour cells to be targeted by immune cells. One of the interferon signaling pathway’s key molecules is STING, which is activated by the protein cGAS.

Previously Moffitt researchers showed that STING activity is suppressed and altered in a subset of melanomas, rendering tumour cells invisible to the immune system.

Using a process called epigenetic modification to turn genes on or off with methylation groups, the researchers sought to improve the understanding of alterations in STING signaling in melanoma and find out how STING expression is suppressed. 

The researchers performed a series of laboratory experiments and discovered that the DNA regulatory region of the STING gene is highly modified by methylation groups resulting in loss of STING gene expression in certain melanoma cell lines. Importantly, they confirmed these findings in patient clinical samples of early and late-stage melanomas and showed similar methylation events and loss of expression of the upstream STING regulator cGAS.

The researchers demonstrated the possibility of reactivating STING and/or cGAS expression with a demethylating drug or genetic approaches. These successfully reactivated STING activity, resulting in increased interferon levels when triggered by STING agonist drugs that enabled the melanoma cells to now be recognised and targeted by immune cells.

“These studies show the critical importance of an intact STING pathway in melanomas for optimal T cell immunotherapy success, and how to overcome a notable STING defect in melanoma cases of gene hypermethylation by a combination therapy,” said senior author James J. Mulé, PhD, and Associate Center Director, Translational Science, H. Lee Moffitt Cancer Center & Research Institute.”Unless patients’ melanomas are pre-screened for intact versus defective STING, it is not at all surprising that clinical trials of STING agonists have, to date, uniformly failed.”

Source: News-Medical.Net

Journal information: Falahat, R., et al. (2021) Epigenetic reprogramming of tumor cell–intrinsic STING function sculpts antigenicity and T cell recognition of melanoma. Proceedings of the National Academy of Sciences. doi.org/10.1073/pnas.2013598118.

Categories : CancerTags :

Most Glucose Consumption in Non-cancer Cells, Upending Century-old View

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A study has found that cancer cells are not the main consumers of glucose in tumours, challenging an observation held for over a century.

“The field of cancer metabolism has really exploded over the last 20 years, but it has been based on this observation that Otto Warburg published in 1922—that cancer cells can consume glucose at a very high rate,” said Jeffrey Rathmell, PhD, Cornelius Vanderbilt Professor of Immunobiology and director of the Vanderbilt Center for Immunobiology. “We now know that tumors include many types of cells, and it’s surprising that non-cancer cells are actually the major glucose consumers in the tumor.”

One application of the Warburg effect is where cancer cells are picked out based on their glucose metabolism in positron emission tomography (PET), a radioactive tracer of glucose (FDG). However, this doesn’t always yield the results expected by clinicians.

“I had been curious about why PET scans are ‘hot’ or ‘not hot’ for many years because the kidney cancer type that I study, from what we understand about the biology, should light up hot on PET and often doesn’t,” said W. Kimryn Rathmell, MD, PhD, Hugh J Morgan Professor and Chair of the Department of Medicine. “Jeff and I have had many conversations about which cells are using the glucose: is it the cancer cells; is it the immune cells; how does it all fit together? You can just imagine our dinner table.”

A pair of MD-PhD students from their labs, Bradley Reinfeld and Matthew Madden, decided to resolve this conundrum. They administered two different PET tracers (one for glucose, one for glutamine) to mice with tumours, isolated the tumors and separated them into various cell types and then measure the radioactivity in the cells. Six different tumour models were used, including colorectal, kidney and breast cancer. The results showed that, in each case, myeloid immune cells (primarily macrophages) had the highest uptake of glucose, followed by T cells and cancer cells. Cancer cells, in contrast, had the highest glutamine uptake.

“We think this is a general phenomenon that extends across cancer types,” Madden said.

The researchers showed that, instead of limiting nutrients, certain cellular signaling pathways drove the differences in glucose and glutamine uptake. The prevailing view is rather of metabolic competition taking place in the tumour microenvironment, where the cancer cells “win” to deplete nutrients and suppress immune cells.

“The idea has been that the cancer cells are gobbling up all of the glucose, and consequently, immune cells can’t get enough glucose and can’t do their job,” Madden said. “Our data suggest that nutrients aren’t limiting. Instead, cells are programmed to consume certain nutrients, and there is partitioning of nutrients between cells: cancer cells pick up glutamine and fatty acids; immune cells pick up glucose.”

Knowing that cells in the tumour microenvironment use different nutrients “may allow for specifically targeting particular cell types—for new therapies or for imaging people’s tumors,” Reinfeld said.

Kimryn Rathmell added, “We’re in a good place now to be able to have more sophisticated PET radiotracers. It’s time to think about testing fluoridated glutamine or other nutrient probes in patients.”

The study’s findings also have implications for interpreting FDG-PET imaging results, she said. “We order FDG-PET scans all the time, and we need to have a good sense of what that information is providing us. We use it to judge tumor response, but it may be telling us about inflammatory response and not tumor response.”

Source: Medical Xpress

Journal information: Cell-programmed nutrient partitioning in the tumour microenvironment, Nature (2021). DOI: 10.1038/s41586-021-03442-1

Categories : CancerTags :

A Cellular Communication Network Allows Tumour Regrowth

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Scientists at the University of Missouri and Yale University have discovered that one of the mutations in the RAS family of genes, which impede treatment options, is also responsible for allowing tumour regrowth following genotoxic therapy.

Genotoxic therapies cause DNA damage inside cancer cells in order to destroy them . To avoid being eliminated, cells will stop replicating and try to repair the damage, but if they fail to do so, they will trigger cell death, relying on a protein called “p53”.  

While RAS gene mutations have been studied for over three decades, scientists today have a better understanding of how they work. However, many of them still consider these mutations to be “undruggable” or resistant to therapeutic treatment, according to the National Cancer Institute.

“Most of our knowledge of how cells respond to DNA damage is mainly derived from studies looking at the single cell level,” said Yves Chabu, an assistant professor in the MU College of Arts and Science. “Therefore, we don’t know much about how tumour cells respond to DNA damage in the broader context of the tissue level, and what possible implications these responses might have on a tumor’s relapse following genotoxic therapies. To address this, we looked at how tissues containing patches of cells carrying oncogenic RAS mutations respond to DNA damage. We focused on oncogenic RAS because it is associated with cancers relapse and resistance to genotoxic therapies in humans. This approach has allowed us to identify novel cell-to-cell communication within the tissue that instructs tumour cells in tissues to regrow. It’s something we would not have identified if we were only looking at the single cell level.”

“We found that in oncogenic RAS tissues, cells elevate the levels of the p53 protein to varying degrees in response to DNA damage,” said Prof Chabu, whose appointment is in the Division of Biological Sciences. “Further analyses revealed that cells with high p53 protein levels, or more extensive DNA damage, do not simply die in response to the DNA damage. Instead, they release a growth signal called interlukin-6 into the tumor environment. Interlinkin-6 instructs cells with low p53 levels, or cells with less DNA damage, to activate JAK/STAT, a growth-amplifying signal, and drive tumor regrowth after treatment. We essentially have a situation where cells that are vulnerable to the treatment are instructing the more robust cells to take over and grow.”

Prof Chabu, who has been studying oncogenic RAS mutations for more than a decade, said that this further suggests that adding JAK/STAT inhibitors to genotoxic therapies inhibit the regrowth ability of RAS tumours. He said another interesting aspect of their findings is that p53 is traditionally considered as a tumour suppressor protein.

“A loss of p53 activity, due to genetic mutation, causes cells to grow uncontrollably while accumulating even more DNA mutations,” said Prof Chabu. “So, naturally one would think that having more p53 activity is a good thing because it prevents pre-cancerous cells from growing and forming cancers. Yet, here we find that too much of a normal, not mutated, p53 can signal the surrounding RAS tissues to overgrow.”

Source: Medical Xpress

Journal information: Yong-Li Dong et al, Cooperation between oncogenic Ras and wild-type p53 stimulates STAT non-cell autonomously to promote tumor radioresistance, Communications Biology (2021). DOI: 10.1038/s42003-021-01898-5

Categories : Cancer Cardiovascular DiseaseTags :

Antihypertensive Drugs Not Linked to Cancer Risk

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A review of 33 clinical studies  showed that antihypertensive drugs did not have a consistent association with cancer risk.

Patients treated with any of five different classes of antihypertensive drugs had essentially the same cancer risk as those receiving placebo. Comparisons of each antihypertensive class against all the others showed no association with an increased risk of cancer, save for calcium channel blockers (CCBs), which had only a modestly higher risk versus the other drug classes (HR 1.06, 95% CI 1.01-1.11).

The data do not conclude the issue, since some comparisons had insufficient data to exclude the possibility of excess cancer risk, reported Kazem Rahimi, DM, of the University of Oxford in England, and colleagues in Lancet Oncology.

“Our study has addressed an ongoing controversy about the safety of blood pressure-lowering medication with respect to cancer risk, using the largest sample of individual-level randomized evidence on blood pressure-lowering treatment to date, to our knowledge,” they wrote. “The main implication of our study is that patients using antihypertensive medication should continue to take their medications because concerns about increased cancer risk seem to be unfounded.”

The author of an accompanying commentary noted that the findings could have been due to chance. The number of trials per drug class varied greatly, and small sample sizes were used in analyses by type of cancer.

“Taken together, these limitations raise a more fundamental question about how the findings of randomised controlled trials should be interpreted,” wrote Laurent Azoulay, PhD, of McGill University in Montreal.

Randomised trials are the “gold standard” for assessing drug efficacy, but are not typically designed to assess safety, he continued. This is especially important for outcomes like cancer, which have a delayed onset. Since the median follow-up was only 4.2 years , “a potential association between cancer and the long-term use of antihypertensive drugs cannot be ruled out.”

“Such analyses are necessary to understand the short-term effects of these drugs on cancer incidence,” Azoulay concluded. “However, moving forward, these studies will need to be complemented with well-designed, real-world studies in heterogeneous patient populations who are followed up for extended periods of time to fully understand their carcinogenic potential.”

Several meta-analyses have yielded conflicting evidence, Rahimi and colleagues stated. The Blood Pressure Lowering Treatment Trialists’ Collaboration (BPLTTC) is the world’s largest individual patient-level data on blood pressure-lowering trials, and data from this formed the basis for the meta-analysis.

The authors identified 33 trials for inclusion in the meta-analysis, which comprised 260 447 patients with available data on cancer outcomes. CCBs were the antihypertensive class most commonly represented in the trials (n=19), followed by ACE inhibitors (15), angiotensin-receptor blockers (ARBs, 11), thiazide diuretics (six), and beta-blockers (five). Median follow-up ranged from 4 to 5 years across the trials, grouped by drug class.

Patient age ranged between 64 and 68 by drug class, and pretreatment systolic blood pressure ranged from 147mm Hg (ACE inhibitors) to 166mm Hg (beta-blockers).

Across the five classes of antihypertensive drugs, individual comparisons for cancer risk versus the other drug classes yielded only a maximum hazard ratio of 1.06 for CCBs.

“We found no consistent evidence that antihypertensive medication use had any effect on cancer risk,” the authors stated.

Source: MedPage Today

Journal information 1: Copland E, et al “Antihypertensive treatment and risk of cancer: An individual participant data meta-analysis” Lancet Oncol 2021; DOI: 10.1016/S1470-2045(21)00033-4.

Journal information 2: Azoulay L “Elucidating the association between antihypertensive drugs and cancer: A need for real-world studies” Lancet Oncol 2021; DOI: 10.1016/S1470-2045(21)00085-1.

Categories : Cancer PaediatricsTags :

Blood Mutation Explains High Leukaemia Rates in Children with Down’s

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According to a new study by researchers at the Linda Crnic Institute for Down Syndrome, the reason that children with Down syndrome have a drastically elevated risk of leukaemia is due to a more prevalent condition increasing blood stem cell mutation.

Children with Down syndrome are 20-times more likely to develop acute lymphocytic leukaemia (ALL) and 150-times more likely to develop acute myeloid leukaemia (AML) compared to their typical peers. The researchers found that the reason for this is that they are more likely to present with clonal haematopoiesis (CH), a process in which a blood stem cell acquires a genetic mutation that promotes replication.  

The findings add to a growing body of evidence linking immune dysregulation to a very different disease spectrum, whereby people with Down syndrome are highly predisposed to certain diseases such as leukaemia and autoimmune disorders, while being highly protected from others, such as solid tumours.

“We found a higher-than expected rate of CH in individuals with Down syndrome between the age of one to 20 years old,” said study author Dr Alexander Liggett, who as a doctoral candidate led the study in the lab of Dr James DeGregori, Professor of Biochemistry and Molecular Genetics. “It is a surprising finding, as the phenomenon is typically only observed in elderly people.”

The researchers used an advanced sequencing technique that they had developed, called FERMI, to blood samples from the Crnic Institute Human Trisome Project Biobank. Mutations were more likely to be detected in Down’s syndrome and also more likely to be oncogenic. In elderly people, oncogenic mutations are commonly found in the genes DNMT3A, TET2, ASXL1, TP53, and JAK2. In people with Down’s syndrome, oncogenic CH was found to be dominated by mutations of the TET2 gene.

“Given the increased risk of leukaemia that accompanies clonal expansion of blood cells carrying oncogenic mutations, these expansions may become an important biomarker of cancer risk in the future,” said Dr Liggett.

The study also found that CH in Down syndrome is associated with immune dysregulation biosignatures linked to diseases co-occurring with Down’s syndrome, including thyroiditis, Alzheimer’s disease, and leukaemia. This discovery opens new avenues in understanding the way CH impacts an array of health outcomes in Down syndrome and how to potentially counteract its effects.

“This is truly transformative. This team has identified a new trait of Down syndrome that has strong implications for understanding the appearance of comorbidities more common in this population, such as leukaemia and premature ageing,” said Dr. Joaquin Espinosa, Executive Director of the Crnic Institute. “The next step is to define the long-term impacts of this precocious clonal hematopoiesis and how to prevent its harmful effects.”

Source: News-Medical.Net

Journal information: Liggett, L.A., et al. (2021) Precocious clonal hematopoiesis in Down syndrome is accompanied by immune dysregulation. Gut. doi.org/10.1182/bloodadvances.2020003858.

Categories : CancerTags :

The Effect of Hypoxia on Cancer Cells is a Matter of Timing

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A new study from the University of Colorado School of Medicine shows that the effect of hypoxia on cancer cells varies in the short term versus the long term, opening new possibilities for cancer treatment.

How cancer cells adapt to hypoxia, where insufficient oxygen reaches cells, is a key aspect of cancer biology.

“Most tumours cannot grow unless they figure out a way to induce formation of new blood vessels to supply them with oxygen and other nutrients,” explained Matthew Galbraith, PhD. “So, what happens inside of solid tumours is they undergo intermittent periods of low oxygen between rounds of new blood vessel formation.”

Previous research focussed on hypoxia in the long term, characterising it as oncogenic, or cancer promoting. However some studies showed that hypoxia-sensing factors, known as hypoxia inducible factors, or HIFs, can in some situations suppress tumour growth. To solve this, senior researcher Joaquin Espinosa, PhD and colleagues studied the immediate acute response to hypoxia.

“We employed a cutting-edge genomics technology that nobody had employed in this field before that allowed us to see what happens to cancer cells within minutes of depriving them of oxygen,” Dr Espinosa said.

Employing this technology, they identified hundreds of hypoxia-inducible genes activated shortly upon oxygen deprivation. Using computational biology approaches on large, publicly available datasets, they inferred the function of these genes on hundreds of lab-grown cancer cell lines and hundreds of tumour samples from cancer patients.

They found that when a cell is hypoxic, it reacts by ceasing growth to preserve its existing nutrients and oxygen. Thus, hypoxia causes a tumour-suppressive reaction at this point, mostly by preventing protein synthesis. Only after prolonged periods of hypoxia do cells metastasise and spread out in search of oxygen.

“There’s been a lot of debate about whether these hypoxia-inducible factors promote tumour growth or prevent tumour growth,” Dr Espinosa said. “The conclusion we came to is that everyone was right to a degree. Hypoxia-inducible factors can suppress tumour growth by preventing protein synthesis early on, but they can also advance tumour growth at later stages by promoting the ability of cancer cells to invade neighboring tissues. It depends on when you’re looking at it.”

The tumour suppression and promotion mechanisms elicited by HIFs can be exploited as drug targets. Tumour suppression is mediated by inhibition of an enzyme known as mTOR, which in turn can be inhibited by available drugs often used in cancer therapies. “mTOR inhibitors could mimic the tumour suppressive effects of HIFs,” Dr Galbraith explained.

When deprived of oxygen for a longer amount of time, the HIFs switch on a set of enzymes that can degrade the extracellular matrix that holds them in place, allowing the cancer cells to escape the oxygen-deprived tumour. The cancer cells can then enter the bloodstream and invade nearby tissues.

“These results emphasise the importance of developing inhibitors of hypoxia-inducible enzymes that degrade collagen and other components of the extracellular matrix,” Espinosa said.

Dr Espinosa and his team hope that their research will help new cancer treatments to be developed, which also target the cancer at the right times. 

“People have been trying to target the hypoxia-inducible factors with different therapeutics, but this research would suggest that you may want to exercise some caution about when you apply those therapeutics, given that the HIFs can be tumour suppressive in the early stages of hypoxia,” Dr Galbraith said.

“Since the hypoxic response can be tumour suppressive in some contexts and oncogenic in other contexts, it’s not a good idea to issue a blanket statement that we should always try to shut it down,” Dr Espinosa added. “Instead, we should be thinking about what aspect of the hypoxic response to target, and that’s the aspect where hypoxia drives invasion and metastasis.”

Hoping that other researchers would make use of the map his team developed, Dr Espinosa said, “I would say this is a definitive improvement in the mapping of the early events of hypoxia. And the beauty of that is that once you have a good map of the land, a lot of people can use it.”

Source:  Medical Xpress

Journal information: Zdenek Andrysik et al, Multi-omics analysis reveals contextual tumor suppressive and oncogenic gene modules within the acute hypoxic response, Nature Communications (2021). DOI: 10.1038/s41467-021-21687-2

Categories : COVID General InterestTags :

Pandemic Steals the Enjoyment of Terminally Ill Patients’ Last Years

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Welsh grandmother Maggie Shaftoe has a terminal brain tumour and doctors have told her she has less than two years to live.

Life with a terminal illness during the coronavirus pandemic and being in lockdown has caused difficulties for one couple making final memories.

Macmillan Cancer Support calls it an “acutely challenging time” for people living with a terminal diagnosis.

In 2017, the 63-year-old great-grandmother was diagnosed with an Anaplastic Pleomorphic Xanthoastrocytoma (APXA) brain tumour, which is very rare and most commonly occurs in children and young people with an average age for diagnosis at 12 years old. Her cancer was discovered by chance through a regular epilepsy check up and an MRI scan.

Mrs Shaftoe said that she has not seen her 11 grandchildren and great-granddaughter and she’s “just waiting for things to get back to normal”.

Together for more than 50 years, Mrs Shaftoe and her husband Chris first met as teenagers in a church choir in London. Mr Shaftoe said at this stage they “should be making the most of the time she has left and making memories with our family”.

“I think we’d like to go somewhere like Disneyland, or Lapland to see the northern lights or she’d love to go to the Cheddar Gorge,” said Mr Shaftoe, 65.

“But the pandemic has buried us in a great big hole and I don’t expect the situation to change.

“We’re noticing that Maggie’s memory is fading quite quickly now and she is getting worse day by day, and we understand what is coming,” he said.

In 2017 Mrs Shaftoe had an operation to remove the tumour and the following year had radiotherapy.

But Mr Shaftoe said this has only “delayed the inevitable” and his wife’s life expectancy “hangs on the effectiveness” of two anti-cancer drugs.

Since the operation, she has suffered difficulty with her memory, impaired speech, balance problems and is partially blind.

Doctors have told the couple that typically life expectancy for a patient with APXA would be five years.

Cancer Research UK said that the pandemic has had a “devastating impact on the lives of cancer patients”.

“Dealing with a cancer diagnosis and treatment is extremely difficult at any time, but the pandemic has added the stress of uncertainty, delays and shielding for some cancer patients,” said Martin Ledwick,  head information nurse at the charity.

Mrs Shaftoe remains positive despite the situation, saying it helps to laugh.

“If you can make a joke of something, make a joke of it,” she said, speaking during Brain Tumour Awareness month.

“You go out to make a cup of tea and you end up peeling potatoes, and come back in and wonder why I haven’t got a cup of tea – you have to laugh at silly little things.”

However managing during lockdown has been “very difficult” and mundane tasks could be a “major headache”, according to her husband, who has medical conditions of his own.

Mr Shaftoe says they now have a carer who comes for an hour each morning.

But he said: “We need more care. We have spent most of the pandemic without a carer and it has been absolutely nightmarish trying to get Maggie one.”

Macmillan Cancer Support in Wales said it has heard from many people in isolation, which makes “a challenging situation even more difficult”.

“We know this is an acutely challenging time for people with cancer, the NHS and cancer care, and particularly for people who are living with a terminal diagnosis,” said Richard Pugh, Macmillan’s head of partnerships.

Source: BBC News

Categories : Cancer COVIDTags :

Despite COVID, Cancer Screenings in the US Picked Up

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Woman Receives Mammogram. An Asian female technician positions an African-American woman at an imaging machine to receive a mammogram. Creator: Rhoda Baer

In an encouraging sign, the RAND corporation reports that despite COVID, cancer screenings in the United States rebounded in the wake of the first wave.

There has been concern since the COVID pandemic was keeping people from going in for routine cancer screening, resulting in more undetected cancers to progress unchecked and an increase in cancer deaths. As some 600 000 Americans were expected to die of cancer in 2020, any impact on screening is a considerable health concern.

In a statement, Ryan McBain, PhD, of the RAND Corp. in Santa Monica, California, said: “These are the first findings to show that, despite real fears about the consequences of drop off in cancer screens, health facilities figured out how to pick this back up after the initial pandemic restrictions. Our study shows that health systems were able to recalibrate resources and protocols in a relatively short interval to deliver these important services.”

In Spain, cancer diagnoses were down 38% in the first half of 2020, according to one study. The pandemic’s impact on cancer screening that required in-person examinations, such as mammography and colonoscopy, were a particular concern, McBain and co-authors noted. Moreover, little was known about the magnitude of the decline in screening rates or longer-term trends in screen.

Using data on Castlight Health beneficiaries from January 15 to July 31, 2020, the researchers calculated weekly screening rates per 10 000 eligible beneficiaries. Before the declaration of national emergency in the US on March 13, screening mammography weekly rate was 87.8 per 10 000, falling to a low of 6.9 per 10 000 in April. Thereafter, screening rates began a steady recovery, to 88.2 per 10 000 at the end of July.

Over the same time period, weekly colonoscopy screenings fell from 15.1 to 0.9 per 10 000, before rebounding to a weekly median of 12.6 per 10 000 by July 31, 2020.

Multivariable regression analyses confirmed the significant declines in screening mammography and colonoscopy. A larger decline in colonoscopy was observed in high-income counties. Otherwise, the analyses showed no significant demographic variations.

Laura Makaroff, DO, of the American Cancer Society in Atlanta, said that the pandemic’s ultimate impact on cancer screening and cancer care is still largely unknown.

“We have seen similar data showing some rebound in cancer screening rates last summer and fall, but even those turnarounds show an approximate 30% decrease in cancer screening compared with pre-pandemic rates,” she said to MedPage Today in an email. “We also don’t yet know the full impact of the late fall and winter surges on disruptions in cancer screening and diagnosis.”

“The COVID-19 pandemic has had numerous consequences secondary to the disease itself, including reduced access to care for other illnesses,” Dr Makaroff added. “While these measures were necessary, delays in cancer screening, diagnosis, and treatment due to reduced healthcare access will likely result in a short-term drop in cancer diagnoses followed by increases in late-stage diagnoses and preventable cancer deaths.

“The full impact of the COVID-19 pandemic on cancer prevention and early detection will not be known until population-based nationwide data become available in the years to come,” she said.

Source: MedPage Today

Journal information: McBain RK, et al “Decline and rebound in routine cancer screening rates during the COVID-19 pandemic” J Intern Med 2021; DOI: 10.1007/s11606-021-06660-5.

Categories : Cancer Environmental EffectsTags :

Low-dose Radiation May be Beneficial to Humans

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A study has found that cancer rates go down and life expectancy increases in areas of the US with high natural background radiation, flying in the face of decades of accepted theory that low-dose radiation is still harmful.

Natural background radiation exists from sources in the environment. This is the first large-scale study looking at terrestrial radiation (coming from radioactive elements in rocks, which vary across regions) and cosmic radiation (which increases with altitude). The Ben-Gurion University of the Negev (BGU) researchers found that life expectancy is approximately 2.5 years longer for those who live in areas of naturally high background radiation vs those who live in areas of low radiation.

The linear no-threshold (LNT) hypothesis has guided radiation protection policy in the US since the 1960s. This assumes that health risk from radiation is linear and incremental, meaning that there is no safe minimum dose – all ionising radiation is assumed to be harmful. However, numerous studies have contended that radiation at low doses initiates a protective hormesis effect.

Reduced levels of a number of types of cancers were found when in areas of high background radiation levels as opposed to lower. In both sexes, there was a significant decrease in lung, pancreatic, colon and rectal cancers. Among men, there were additional decreases in brain and bladder cancers. However, no decreases in cervix, breast or prostate cancers or leukaemia were observed.

“Decades of scientific theory are potentially being disproven by the remarkable researchers at BGU. These findings might even provide a sense of relief for those who reside in areas in the U.S. with higher-than-average background radiation,” said Doug Seserman, Chief Executive Officer, American Associates, BGU.

Using the United States Environmental Protection Agency’s radiation dose calculator, the researchers retrieved data background radiation on all 3,29 US counties. Cancer rate data were retrieved from the United States Cancer Statistics, while life expectancy data were retrieved from the Institute for Health Metrics and Evaluation at the University of Washington Medical Center.

“It is reasonable to suggest that a radiation threshold does exist, yet it is higher than the upper limit of the natural background radiation levels in the US (227 mrem/year),” the researchers wrote. “These findings provide clear indications for re-considering the linear no-threshold paradigm, at least within the natural range of low-dose radiation.”

Source: News-Medical.Net

Journal information: David, E., et al. (2021) Background radiation impacts human longevity and cancer mortality: reconsidering the linear no-threshold paradigm. Biogerontology. doi.org/10.1007/s10522-020-09909-4.

Categories : Pain ManagementTags :

Electroacupuncture Tops Standard Care for Cancer Pain

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Image by wei zhu from Pixabay

A study found that electroacupuncture was superior to both auricular acupuncture and standard care for skeletal muscle pain management in cancer survivors.

Electroacupuncture reduced pain by 1.9 points on the 0-10 scale of the Brief Pain Inventory (BPI), compared to standard care. Auricular acupuncture, which was developed by the US military, reduced pain by 1.6 points compared to standard care, and was associated with more adverse effects (AE). Standard care consisted of analgesics, physical therapy, and steroid injections.

“The magnitude of effect of electroacupuncture was clinically important and durable,” the authors wrote. “This finding is consistent with evidence from other large acupuncture trials for chronic pain in the general population. Electroacupuncture has been shown to influence endogenous opioid release, which provides a mechanistic basis for chronic pain management.”

“The present trial includes a large and diverse group of cancer survivors and provides evidence that electroacupuncture provides additional benefits beyond usual care, including not only reduction in pain severity, but also improvements in physical function and quality of life and reductions in analgesic use.”

The PEACE Study enrolled patients with a history of cancer who had experienced musculoskeletal pain for at least three months and at least 15 of the preceding 30 days, with a worst pain intensity within the past week of ≥ 4 (moderate or greater) on the BPI.

Patients were randomised 2:2:1 to receive either electroacupuncture, auricular acupuncture (which were both delivered by licensed, experienced practitioners) or standard care. 

In electroacupuncture procedure, needles were placed at four sites near the location of pain and four additional sites elsewhere on the body to address comorbid symptoms. The treatments consisted of 10 weekly 30-minute sessions.

The auricular acupuncture, also known as ‘battlefield acupuncture’ had a standardised procedure where a single needle was inserted into the cingulate gyrus of one ear. The patient then walked for one minute, and if pain remained ≥ 1 on the BPI, another needle was inserted into the other ear. The process was repeated for the four remaining ear acupuncture points.

Mean baseline BPI scores ranged from 5.0 to 5.6. At week 12, mean BPI score had declined by 0.48 in the standard care group, 2.39 in the electroacupuncture group (P < 0.001), and 2.03 in the auricular acupuncture group (P < 0.001). The 0.36 difference between the two acupuncture groups exceeded the prespecified noninferiority margin of 0.657 for auricular versus electroacupuncture.

Source: MedPage Today

Journal information: Mao JJ, et al “Effectiveness of electroacupuncture or auricular acupuncture vs usual care for chronic musculoskeletal pain among cancer survivors: the PEACE randomized clinical trial” JAMA Oncol 2021; DOI: 10.1001/jamaoncol.2021.0310.