Tag: cancer

Categories : Cancer GeneticsTags :

Comprehensive Genome Sequencing Can Improve Cancer Outcomes

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Image source: National Cancer Institute

Researchers from St Jude Children’s Research Hospital have demonstrated the feasibility of comprehensive genomic sequencing for all paediatric cancer patients, which maximises the lifesaving potential of precision medicine.

All 309 patients who enrolled in the study were offered whole genome and whole exome sequencing of germline DNA. For the 253 patients for whom adequate tumour samples were available, whole genome, whole exome and RNA sequencing of tumour DNA was carried out.

Overall, 86% of patients had at least one clinically significant variation in tumour or germline DNA. Those included variants related to diagnosis, prognosis, therapy or cancer predisposition. An estimated 1 in 5 patients had clinically relevant mutations that would not have been picked up with standard sequencing methods.

“Some of the most clinically relevant findings were only possible because the study combined whole genome sequencing with whole exome and RNA sequencing,” said Jinghui Zhang, PhD, St Jude Department of Computational Biology chair and co-corresponding author of the study.

While such comprehensive clinical sequencing is not widely available, as the technology becomes less expensive and accessible to more patients, comprehensive sequencing will become an important addition to paediatric cancer care.

“We want to change the thinking in the field,” said David Wheeler, PhD, St Jude Precision Genomics team director and a co-author of the study. “We showed the potential to use genomic data at the patient level. Even in common pediatric cancers, every tumor is unique, every patient is unique.

“This study showed the feasibility of identifying tumour vulnerabilities and learning to exploit them to improve patient care,” he said.

Tumour sequencing resulted in a change in treatment for 12 of the 78 study patients for whom standard of care was unsuccessful. In four of the 12 patients, the treatment changes stabilised disease and extended patient lives. Another patient, one with acute myeloid leukaemia, went into remission and was cured by blood stem cell transplantation.

“Through the comprehensive genomic testing in this study, we were able to clearly identify tumor variations that could be treated with targeted agents, opening doors for how oncologists manage their patients,” said co-corresponding author Kim Nichols, MD, St Jude Cancer Predisposition Division director.

The results of the study were published online in the journal Cancer Discovery.

Source: St. Jude Children’s Research Hospital

Journal information: Newman, S., et al (2021) Genomes for Kids: The scope of pathogenic mutations in pediatric cancer revealed by comprehensive DNA and RNA sequencing. Cancer Discovery. doi.org/10.1158/2159-8290.CD-20-1631.

Categories : CancerTags :

Organ-on-a-chip Enables Rapid Cancer Treatment Evaluation

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Researchers at Texas A&M University are advancing organ-on-a-chip devices to new levels, which may change the way clinicians approach cancer treatment, particularly for ovarian cancer.

The research team, led by Abhishek Jain, an assistant professor in the Department of Biomedical Engineering with a joint appointment in the College of Medicine, has developed a device focusing on platelets. The ovarian tumour microenivornment-chip (OTME-Chip) is about the size of a USB and models the properties of a tumour in a laboratory setting. The microdevice is able to recreate events within platelets circulating in the blood as they approach the tumour, making it more potent and metastatic.

“We claim several novelties in technological design as well as biological capabilities that didn’t exist in prior organs-on-chips,” Prof Jain said.

Advances in organ-on-a-chip microdevices allow researchers to discover more about cancer outside the human body. These organs-on-chips serve as a model of the state a cancer patient is in, giving clinicians a chance to find the correct treatment before administering it to the patient.

“We are creating a platform technology using the organ-on-a-chip approach where tumour biology can be advanced, and new drugs can be identified by recreating the platelet-tumor and platelet-tumour-drug interactions under the influence of flow, supporting blood vessels and the extracellular matrix,” Jain said.

Ovarian cancer is one of the leading causes of cancer deaths for women in developed countries. Tumours typically form deep inside a patient’s tissue, and it can be difficult to obtain real-time information of the tumour’s properties and its interaction with blood cells. Ovarian tumours can also rapidly metastasise, meaning that analysis and intervention must be prompt.

The OTME-Chip builds on current understanding of how blood platelets move inside tumour tissue and what triggers them to spread outside the tumour. The actual mechanism behind this process, however, had remained mostly unknown, until now.

“For the first time, we identified a crucial interaction between platelets and the tumor via their surface proteins,” Prof Jain said. “By applying high-resolution imaging, advanced cell and molecular readouts and RNA sequencing methods leveraging the OTME-Chip, we discovered the actual genetic signaling pathways behind the blood cell triggered metastasis of ovarian cancer and a new drug strategy to stop this process.”

Their study was recently published in the journal Science Advances.

Prof Jain said the OTME-Chip has several applications, both in observing cancer cells interactions with vascular and blood cells and testing novel complementary ways to treat cancer.

“This multimodal OTME-Chip is going to provide an ideal platform to the health care researchers to evaluate their anti-cancer, vascular and haematological drugs individually or in combination in an artificially created human-level tumor microenvironment,” Prof Jain said.

Source: Texas A&M University

Journal information: Saha, B., et al. (2021) Human tumor microenvironment chip evaluates the consequences of platelet extravasation and combinatorial antitumor-antiplatelet therapy in ovarian cancer. Science Advances. doi.org/10.1126/sciadv.abg5283.

Categories : Ageing GeneticsTags :

Junk DNA Yields Insights into Ageing and Cancer

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Findings from a new study into ‘junk DNA’ have brought scientists one step closer to solving the mysteries of ageing and cancer.

Jiyue Zhu, a professor in the College of Pharmacy and Pharmaceutical Sciences, led a team which recently identified a DNA region known as VNTR2-1 which seems to drive activity of the telomerase gene, which has been shown to prevent ageing in certain types of cells. The study was published in the journal Proceedings of the National Academy of Sciences (PNAS).

The telomerase gene controls the activity of the telomerase enzyme, which helps produce telomeres, the caps at the end of each strand of DNA that protect the chromosomes within our cells and which shorten over time until cells are no longer able to divide.

However, in certain cell types, such as reproductive cells and cancer cells, the telomerase gene’s activity ensures that telomeres are reset to the same length when DNA is copied. This is essentially what restarts the aging clock in new offspring but is also the reason why cancer cells can continue to multiply and form tumors.

Understanding how the telomerase gene is regulated and activated and why it is only active in certain types of cells could someday be the key to understanding how humans age, as well as how to stop the spread of cancer. That is why Prof Zhu has focused the past 20 years of his career as a scientist solely on the study of this gene.

Zhu said that VNTR2-1’s discovery is especially noteworthy due to the type of DNA sequence it represents.

“Almost 50% of our genome consists of repetitive DNA that does not code for protein,” noted Prof Zhu. “These DNA sequences tend to be considered as ‘junk DNA’ or dark matter in our genome, and they are difficult to study. Our study describes that one of those units actually has a function in that it enhances the activity of the telomerase gene.”

In previous work, deleting the DNA sequence from human and mouse cancer cells caused telomeres to shorten, cells to age, and tumours to stop growing. They conducted a subsequent study measuring the length of the sequence in DNA samples taken from Caucasian and African American centenarians and control participants in the Georgia Centenarian Study, a study that followed a group of people aged 100 or above between 1988 and 2008. The researchers found that the length of the sequence ranged from as short as 53 repeats of the DNA to as long as 160 repeats.

“It varies a lot, and our study actually shows that the telomerase gene is more active in people with a longer sequence,” Prof Zhu said.

Since very short sequences were found only in African American participants, they looked more closely at that group and found that there were relatively few centenarians with a short VNTR2-1 sequence as compared to control participants. However, Prof Zhu said that a shorter sequence does not necessarily translate to a shorter lifespan, since the telomerase gene is less active with possibly a shorter telomere length which could reduce cancer risk.

“Our findings are telling us that this VNTR2-1 sequence contributes to the genetic diversity of how we age and how we get cancer,” Prof Zhu said. “We know that oncogenes–or cancer genes–and tumor suppressor genes don’t account for all the reasons why we get cancer. Our research shows that the picture is a lot more complicated than a mutation of an oncogene and makes a strong case for expanding our research to look more closely at this so-called junk DNA.”

Prof Zhu observed that many African Americans in the United States for generations have Caucasian ancestry, which could have added this sequence. So he and his team hope to next be able to study the sequence in an African population.

Source: Washington State University

Journal information: Xu, T., et al. (2021) Polymorphic tandem DNA repeats activate the human telomerase reverse transcriptase gene. PNAS. doi.org/10.1073/pnas.2019043118.

Categories : CancerTags :

MRI Clear Cell Likelihood Score Matches Renal Carcinoma Growth

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Photo by MART PRODUCTION from Pexels

According to a new study, the MRI-derived standardised non-invasive clear cell likelihood score (ccLS) is correlated with the growth rate of small renal masses (cT1a, <4 cm) and could help guide personalised management.

The study was published in the American Roentgen Ray Society’s American Journal of Roentgenology. Extracted from clinical reports, “the ccLS scores the likelihood that the small renal mass represents clear cell renal cell carcinoma, from 1 (very unlikely) to 5 (very likely),” explained corresponding author Ivan Pedrosa from the University of Texas Southwestern Medical Center at Dallas. “Small renal masses with lower ccLS may be considered for active surveillance, whereas small renal masses with higher ccLS may warrant earlier intervention.”

The team’s retrospective study included consecutive small renal masses assigned a ccLS on clinical MRI exams performed from June 2016 to November 2019. Tumour size measurements were obtained from available prior and follow-up cross-sectional imaging examinations, up to June 2020.

Among 389 small renal masses in 339 patients (198 men, 141 women; median age, 65 years) on active surveillance that were assigned a ccLS on clinical MRI examinations, those with ccLS4-5 grew significantly faster (9% diameter, 29% volume yearly) than those with ccLS1-2 (5% diameter, p<.001; 16% volume, p<.001) or ccLS3 (4% diameter, p<.001; 15% volume, p<.001).

With a lack of validated imaging markers to characterise biologic aggressiveness of small renal masses hindering medical decision making, “growth is associated with ccLS in small renal masses,” the authors reiterated, “with higher ccLS correlating with faster growth.”

Source: EurekAlert!

Categories : Antibiotics CancerTags :

Old Antibiotics as New Weapons against Melanoma

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Researchers may have hit upon a new weapon in the fight against melanoma: antibiotics that target a vulnerability in the ‘power plants’ of cancer cells when they try to survive cancer therapy.

“As the cancer evolves, some melanoma cells may escape the treatment and stop proliferating to ‘hide’ from the immune system. These are the cells that have the potential to form a new tumor mass at a later stage,” explains cancer researcher and RNA biologist Eleonora Leucci at KU Leuven, Belgium. “In order to survive the cancer treatment however, those inactive cells need to keep their ‘power plants’—the mitochondria—switched on at all times.” As mitochondria derive from bacteria that, over time, started living inside cells, they are very vulnerable to a specific class of antibiotics. This is what gave us the idea to use these antibiotics as anti-melanoma agents.”

The researchers implanted patient-derived tumors into mice, which were then treated with antibiotics, either as alone or in combined with existing anti-melanoma therapies. Leucci observed: “The antibiotics quickly killed many cancer cells and could thus be used to buy the precious time needed for immunotherapy to kick in. In tumors that were no longer responding to targeted therapies, the antibiotics extended the lifespan of—and in some cases even cured—the mice.”

The researchers made use of nearly antibiotics rendered nearly obsolete because of antibiotic resistance. However, this does not affect the efficacy of the treatment in this study, Leucci explained. “The cancer cells show high sensitivity to these antibiotics, so we can now look to repurpose them to treat cancer instead of bacterial infections.”

However, patients with melanoma should not try to experiment, warned Leucci. “Our findings are based on research in mice, so we don’t know how effective this treatment is in human beings. Our study mentions only one human case where a melanoma patient received antibiotics to treat a bacterial infection, and this re-sensitized a resistant melanoma lesion to standard therapy. This result is cause for optimism, but we need more research and clinical studies to examine the use of antibiotics to treat cancer patients. Together with oncologist Oliver Bechter (KU Leuven/UZ Leuven), who is a co-author of this study, we are currently exploring our options.”

Source: KU Leuven

Journal information: Roberto Vendramin et al, Activation of the integrated stress response confers vulnerability to mitoribosome-targeting antibiotics in melanoma, Journal of Experimental Medicine (2021). DOI: 10.1084/jem.20210571

Categories : CancerTags :

Aspirin Could Cut Cancer Deaths by 20%

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Photo by HalGatewood.com on Unsplash

Patients with a wide range of cancers who take aspirin as part of their treatment could have their risk of death decrease by 20%, according to a major review of existing research.

Researchers at Cardiff University carried out a huge  systematic review of 118 published observational studies in patients with 18 different cancers. Pooling the results, 250 000 patients with cancer who reported taking aspirin, which was associated with a reduction of about 20% in cancer deaths.

The review said the available body of evidence regarding its efficacy and safety “justifies its use” as a supplementary treatment in a wide range of cancers—and that patients should be made aware of this.

Lead author Professor Peter Elwood, Honorary Professor at Cardiff University who has studied the effects of aspirin for over five decades, said: “In recent years, my research team and I have been struck by the actions of aspirin on the biological mechanisms relevant to cancer—and these seem to be the same in many different cancers.

“We therefore wanted to review the scientific evidence available on the use of aspirin as an additional treatment for a wide range of cancers.

“Overall, we found that at any time after a diagnosis of cancer, about 20% more of the patients who took aspirin were alive, compared with patients not taking aspirin.”

The team took into consideration aspirin taking risks and wrote to an author on each of the papers asking about any stomach or other bleeding episodes.

A minority of patients had experienced a bleed, but no evidence of any excess deaths attributable to bleeding in the patients on aspirin was found, the review noted.

“Our research suggests that not only does aspirin help to cut risk of death, but it has also been shown to reduce the spread of cancer within the body—so-called metastatic spread,” said Prof Elwood.

“There is now a considerable body of evidence to suggest a significant reduction in mortality in patients with cancer who take aspirin—and that benefit appears to not be restricted to one or a few cancers.

“Aspirin therefore appears to deserve serious consideration as an adjuvant treatment of cancer and patients with cancer and their carers should be informed of the available evidence.

“However, we must also stress that aspirin is not a possible alternative to any other treatment.”

It started in 1974 when a research team led by Professor Elwood and Professor Archie Cochrane at the Medical Research Council’s Unit in Wales showed for the first time that taking an aspirin tablet a day reduced deaths from heart disease and stroke by about 24%.

In 1990, the finding gained global traction and was judged by the BMJ to have been one of the top 50 most important research studies published since 1945. A meta-analysis of 13 randomised controlled studies found a major adverse cardiovascular event risk reduction for statin users (12%), non-smokers (10%) and males (11%).

Prof Elwood said his original study stimulated a new phase of research work on aspirin. At the time of the report about 100 clinical research studies on aspirin were published each year—but now, in excess of 1 000 are reported each year. He said a number of new clinical trials had been set up to test aspirin treatment in several cancers and the results of these should offer further clear evidence.

“Further research into aspirin and cancer would clearly be of great value, and new studies should be encouraged, especially if focused on some of the less common cancers,” said Prof Elwood.

Source: Medical Xpress

Journal information: Peter C Elwood et al, Aspirin and cancer survival: a systematic review and meta-analyses of 118 observational studies of aspirin and 18 cancers, ecancermedicalscience (2021). DOI: 10.3332/ecancer.2021.1258

Categories : CancerTags :

In Vitro Cancer Cells Differ to Those in Body

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Photo by Drew Hays on Unsplash

A new study has shown that most cancer cells grown in vitro have little in common genetically with cancer cells in humans.

Human cancer cells grown in culture dishes have the least genetic similarity to their human sources, according to a new computer-based technique developed by researchers at John Hopkins.

According to the researchers, the finding should help shift more resources to cancer research models such as genetically engineered mice and balls of human tissue known as ‘tumouroids’ to better evaluate human cancer biology and treatments, and the genetic errors responsible for cancer growth and progress.

“It may not be a surprise to scientists that cancer cell lines are genetically inferior to other models, but we were surprised that genetically engineered mice and tumouroids performed so very well by comparison,” says Patrick Cahan, PhD, associate professor of biomedical engineering at The Johns Hopkins University and the Johns Hopkins University School of Medicine and lead investigator of the new study.

The new computer modelling technique, CancerCellNet, compares the RNA sequences of a research model with data from a cancer genome atlas to see how closely the two sets match up.

On average, genetically engineered mice and tumouroids have RNA sequences most closely aligned with the genome atlas baseline data in 4 out of every 5 tumour types they tested, including breast, lung and ovarian cancers.

This adds to evidence that cancer cell lines grown in the laboratory have less parity with their human source due to the many differences between a human cell’s natural environment and a laboratory growth environment, the researchers said. “Once you take tumours out of their natural environment, cell lines start to change,” said Prof Cahan.

Around the world, scientists depend on a range of research models to enhance their understanding of cancer and other disease biology, and to develop treatments for conditions. Of these, one of the most widely used is cell lines created by extracting cells from human tumours and growing them with various nutrients in laboratory flasks.

Other methods involve mice that have been genetically engineered to develop cancer, or implanting human tumours into mice, known as xenografting, or use tumouroids.

To investigate the accuracy of these models, scientists often transplant lab-cultured cells or cells from tumouroids or xenografts into mice and see if the cells behave as they should — that is, grow and spread, retaining the genetic hallmarks of cancer. However, the researchers contend that this process is expensive, time-consuming and scientifically challenging and so they developed a more streamlined method. The new technique is based on genetic information about cellular RNA.

“RNA is a pretty good surrogate for cell type and cell identity, which are key to determining whether lab-developed cells resemble their human counterparts,” said Prof Cahan. “RNA expression data is very standardised and available to researchers, and less subject to technical variation that can confound a study’s results.”

To start, Prof Cahan and his team had to choose a standard set of data that acted as a baseline to compare the research models. They used data from The Cancer Genome Atlas as ‘training’ data, which includes RNA expression information of hundreds of patient tumour samples, and other information on the tumour.

They also tested their CancerCellNet tool by applying it to data where the tumour type was already known, such as from the International Human Genome Sequencing Consortium.

The John Hopkins researchers combed through The Cancer Genome Atlas data to select 22 types of tumours for study, and used that data as the baseline for comparing RNA expression data from cancer cell lines, xenografts, genetically engineered mouse models and tumouroids.

Some differences observed included prostate cancer cells from a line called PC3 that started to look genetically more like bladder cancer, Prof Cahan noted. It’s also possible, he said, that originally  the cell line was simply labelled incorrectly, or else it could have in fact been derived from bladder cancer. But, from a genetic standpoint, the prostate cancer cell line was not a representative surrogate for what happens in a typical human with prostate cancer.

According to a 0-1 scoring method, cell lines had, on average, lower scoring alignment to atlas data than tumouroids and xenografts.

Prof Cahan said he and his team will be improving the reliability of CancerCellNet by adding additional RNA sequencing data.

Source: John Hopkins Medicine

Journal information: Da Peng et al, Evaluating the transcriptional fidelity of cancer models, Genome Medicine (2021). DOI: 10.1186/s13073-021-00888-w

Categories : GeneticsTags :

Key Genetic Repair Protein Removes Traps

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Image source: Pixabay

Researchers have discovered that a key genetic repair protein also cleans up ‘traps’ left by another protein, its partner in genetic repair.

DNA is constantly getting damaged: the delicate strands that carry life’s genetic code take quite a beating as they jumble about in the course of their work. Errors can accumulate if left untreated, with fatal consequences — such as cancerous tumors — for the cell and the organism.

Two key proteins are involved in preventing the damage from getting out of hand: PARP — or poly ADP ribose polymerase — acts as a marker for a trouble spot, allowing XRCC1 — or X-ray repair cross-complementing protein 1 — to locate the damage and start repairs.

The repair functions of these two proteins have been known for some time. The importance of this has been recognised with the 2015 Nobel prizes for chemistry, as this knowledge allowed the development of anti-cancer drugs, known as PARP inhibitors, that disrupt the growth of certain kinds of tumours.

Although these key proteins had been identified, their precise roles were not well understood. It took a team of scientists at Tokyo Metropolitan University, the University of Sussex, and Kyoto University to revealed how exactly XRCC1 accomplishes its work — and it was a surprising discovery.

“PARP turns out to be something of a villain,” explained Kouji Hirota at Tokyo Metropolitan. “The spots it marks become ‘PARP traps’, which left un-repaired lead to disfunction and cell death.”

It seems that XRCC1 doesn’t just simply repair DNA, it goes about disarming PARP traps. The scientists compared cells without the XRCC1 gene to those without PARP as well as to still others which lacked both proteins. The team found that without XRCC1 on patrol, PARP traps accumulate like landmines.

“PARP exerts toxic effects in the cell and XRCC1 suppresses this toxicity,” Hirota elaborated.

The team aims to further explore these processes, with the goal of aiding development of future cancer treatments.

KyotoU’s Shunichi Takeda said: “These results indicate that XRCC1 is a critical factor in the resolution of PARP traps and may be a determinant of the therapeutic effect of PARP inhibitors used in the treatment of hereditary breast and ovarian cancer syndromes.”

Source: Kyoto University

Journal reference: Demin, A. A., et al. (2021) XRCC1 prevents toxic PARP1 trapping during DNA base excision repair. Molecular Cell. doi.org/10.1016/j.molcel.2021.05.009.

Categories : Cancer Lab Tests and ImagingTags :

An Easy to Swallow Detection Method for Oesophageal Cancer

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Image by Natural Herbs Clinic from Pixabay

In the UK, a “game-changer” method to sample cells for the detection of oesophageal cancer is being trialled in a mobile unit.

The cytosponge, a pill containing a sampling sponge, was developed at the and collects cells which are tested at a laboratory. Details on its development were published in The Lancet. In a previous trial with more than 13 000 participants receiving either the cytosponge or usual care from a GP, the odds of detecting oesophageal cancer were ten times higher than with usual care.

It is hoped the test will be much more efficient and quicker than the current detection method, requiring an endoscopy in hospital.

Prof Rebecca Fitzgerald from the University of Cambridge, which developed the test, said it was “really simple and straightforward”.

Early signs of cancer of the oesophagus are often mistaken for heartburn. It is the sixth most common cause of death from cancer worldwide.

A mobile unit will perform the test at GP surgeries at different locations around the UK.

Prof Fitzgerald, who specialises in cancer prevention, said the cytosponge “can diagnose cancer of the oesophagus really early”.

“Usually you would have to go to the hospital and get an endoscopy, with all that entails, and our idea was could you make something that was so simple you could go to a mobile unit or GP surgery,” Prof Fitzgerald said.

“The simplicity is the absolute key of this – we know the power of diagnosis is in the cells you collect.”

She added that due to COVID, “some endoscopy has been completely on hold so you might have to wait months” for the procedure, where a long, thin tube with a camera is sent down the patient’s mouth and throat.

Prof Fitzgerald explained: “You swallow the capsule on a string with water and it will go down to the top of the stomach.

“The capsule will dissolve in five to seven minutes, and as it dissolves out pops a sponge which has been compressed in that capsule. The nurse simply pulls the sponge out with the string and it will collect about a million cells on its way out.

“We put that sponge into a preservative, send it to the laboratory where it is tested to see whether there are Barrett cells or not and whether the cells look like they are turning to pre-cancer. Then we can let the patient know and if there is anything to worry about they can have an endoscopy and treatment.”

The procedure takes about 10 minutes to perform in total.

Source: BBC News

Categories : Cancer COVIDTags :

Cancer Patients Have a Higher Mortality Risk from COVID

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Photo by Tima Miroshnichenko from Pexels

Patients hospitalised with active cancer are more likely to die from COVID than those with a cancer history or diagnosis, according to a new study.

The findings published by Wiley early online in CANCER, a peer-reviewed journal of the American Cancer Society, also indicate that the greatest risk of death due to COVID was in those with active blood cancers. No mortality risk increase was found in patients who received cancer treatments in the three months (or longer) prior to hospitalisation.

To find out how cancer, or the various therapies used to treat it, could affect the health of patients with COVID infections, a team analysed the NYU Langone Medical Center’s records of 4184 hospitalised patients who tested positive for SARS-CoV-2, the virus that causes COVID.

This group included 233 patients who had a current, or ‘active’, cancer diagnosis. They found that more patients with an active cancer diagnosis (34.3 percent) were likely to die from COVID than those with a history of cancer (27.6 percent) and those without any cancer history (20.0 percent).

Among patients with active cancer, those with blood-related cancers had the greatest risk of death. However, undergoing systemic anticancer therapy, including chemotherapy, molecularly targeted therapies, and immunotherapy, within three months prior to hospitalisation was not linked to a higher risk of death, and the investigators found there were no differences according to the type of cancer therapy being received.

Senior author Daniel Becker, said, “We completed a large chart review-based study of patients hospitalised with COVID and found that patients with active cancer, but not a history of cancer, were more likely to die. Notably, however, among those hospitalised with active cancer and COVID, recent cancer therapy was not associated with worse outcomes.”

“People with active cancer should take precautions against getting COVID, including vaccination, but need not avoid therapy for cancer.”

Source: Wiley