Severe SARS-CoV-2 Infection as a Marker of Undiagnosed Cancer

News Release, World Mitochondria Society, Berlin - Germany – June 7, 2023

This population-based study by Dugerdil et al, published in scientific reports, investigated if a severe SARS-CoV-2 infection represents a marker of an undiagnosed cancer.

The SNDS database was used, identified from 02/15/2020 to 08/31/2021, 41,302 individuals hospitalized in intensive care unit due to SARS-CoV-2 (ICU-gr) and 713,670 control individuals not hospitalized for SARS-CoV-2 (C-gr). Individuals were matched according to year of birth, sex and French department.The cancer incidence was compared in the two groups during the follow-up period, using Cox proportional hazards models adjusted on matching variables, socioeconomic characteristics and comorbidities.

In the ICU-gr, 2.2% was diagnosed with a cancer in the following months, compared to 1.5% in the C-gr. The ICU-gr had a 1.31 higher risk of being diagnosed with a cancer following hospital discharge compared to the C-gr. A global similar trend was found when competing risk of death was taken into account. A significant higher risk was found concerning renal, hematological, colon, and lung cancers.

The obtained results suggest that a severe SARS-CoV-2 infection may represent a marker of an undiagnosed cancer.

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Image credits: by kjpargeter on Freepik

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Iron & Cancer : Targeting Mitochondria

 News Release, World Mitochondria Society, Berlin - Germany – May 8, 2023

In their new paper published in Science Advances, Subhadip Mukhopadhyay and colleagues from NYU and Harvard, highlighted a critical link between autophagy, iron metabolism, and mitochondrial function that may have implications for Pancreatic ductal adenocarcinoma (PDAC)  progression.

PDAC cells maintain a high level of autophagy, allowing them to thrive in an austere microenvironment. However, the processes through which autophagy promotes PDAC growth and survival are still not fully understood. 

Subhadip Mukhopadhyay and his research team showed that autophagy inhibition in PDAC alters mitochondrial function by losing succinate dehydrogenase complex iron sulfur subunit B expression by limiting the availability of the labile iron pool.  PDAC uses autophagy to maintain iron homeostasis, while other tumor types assessed require macropinocytosis, with autophagy being dispensable.

The researchers observed that cancer-associated fibroblasts can provide bioavailable iron to PDAC cells, promoting resistance to autophagy ablation. To overcome this cross-talk, they used a low-iron diet and demonstrated that this augmented the response to autophagy inhibition therapy in PDAC-bearing mice.

In summary, this work supports the model in which the iron-autophagy/lysosome axis represents a metabolic vulnerability in PDAC. It specifically demonstrated the feasibility of targeting this metabolic dependency in vivo and mechanistically defined the distinct regulation of iron homeostasis in different tumor types, which has implications for how one would approach this therapeutically. 

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Targeting Mitochondria 2023 will extensively cover the implication of mitochondria in cancer and its potential in cancer therapy. Submit a related abstract.

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New study outlines how brain cancer cells take mitochondria from healthy cells to grow and survive

GBM cells acquire mitochondria from astrocytes

Glioblastoma cancer cells use mitochondria from the central nervous system to grow and form more aggressive tumors, according to new Cleveland Clinic-led findings published in Nature Cancer.

The research showed that it is common for healthy astrocytes – a type of glial cell with important functions in the central nervous system – to transfer the energy-producing organelles to glioblastoma cancer cells. When this process happens, it makes the cancer more deadly and the tumors more likely to grow. Researchers found that acquiring mitochondria boosted energy production and amplified cancer stem cells – cells with properties that already make cancer more difficult to treat.

"Defining the complex interactions glioblastoma cells have with the brain and nervous system is critical for developing new treatments for this highly aggressive form of brain cancer" says Justin Lathia, PhD, staff in Cardiovascular & Metabolic Sciences and the Melvin H. Burkhardt Endowed Chair for Neuro-Oncology Clinical Research. “We knew that this type of transfer was theoretically possible, but we didn’t know how relevant and dangerous it was in brain tumors.”

Cancers, including glioblastoma, are resilient in part because of resources in the environment, capitalizing on the body’s natural defenses to protect cancer cells. By determining how cancer cells interact with healthy cells to survive, researchers can design new treatments to block cancer from growing or resisting treatment.

This study investigated mitochondria transfer in glioblastoma, the most common and deadly type of primary brain cancer. The paper’s first co-authors are Dionysios C. Watson, MD, PhD, and Defne Bayik, PhD, both previously of Cleveland Clinic and now at University of Miami’s Sylvester Comprehensive Cancer Center.

Mitochondria are essential components of normal cells, so-called “powerhouses” that also play a major role in signaling processes like cell death. There are thousands of mitochondria in each cell. Mitochondria transfer between cells is part of an emerging type of cell-to-cell interaction that is still being explained.

Mitochondria are essential to cancer cells too; chemotherapy and radiation can target mitochondria to destroy tumors. Previous studies established that mitochondria transfer can also happen in other neurological conditions, like stroke, but ongoing research is figuring out the impact of transfer on disease and how it happens.

When cancer cells receive mitochondria, it affects the processes that produce energy. The study found in glioblastoma, this boost supports cancer stem cell properties including self-renewal and tumorigenicity, Dr. Lathia says.

“Cancer – and cancer treatment – does not exist in a vacuum,” Dr. Lathia says. “You’re not just treating and researching the tumors alone, instead tapping into a diverse ecosystem. Further research into this pathway can identify new strategies for treating glioblastoma, but also has potential for understanding other types of cancer.”

Targeting Mitochondria 2023 will extensively cover the implication of mitochondria in cancer and its potential in cancer therapy. Submit a related abstract.

News source: Cleavland Clinic.

Image source: Watson et al. Nature Cancer (2023)

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Rescuing Corneal Cells from Death with the Help of Mitochondria

News Release, World Mitochondria Society, Berlin - Germany – April 20, 2023

Fuchs' endothelial corneal dystrophy, a degenerative eye disease, causes progressive vision loss that can induce blindness. It is the leading cause of corneal transplantation, but the scarcity of grafts hinders its treatment. A research team from Université Laval and Université de Montréal has identified a way to slow the disease and even avoid transplantation if diagnosed at an early stage.

In people with the disease, the endothelial cells at the back of the cornea die more quickly than in healthy people.

"Everyone loses them at a slow rate, slow enough to make it to the end of our lives without problems. For sick people, depletion is accelerated by factors not yet understood at the molecular level. Since the cells do not divide, they do not replace themselves," says Patrick J. Rochette, full professor at the Faculty of Medicine at Université Laval and a researcher at the CHU de Québec-Université Laval Research Center, who conducted the study.

These endothelial cells play an essential role in vision. They ensure that the cornea remains transparent by keeping it partially dehydrated. When the cells die, the cornea becomes wet and cloudy, which can lead to complete blindness.

In a previous study, the research team showed that mitochondria were central to the disease. "In people with the disease, the mitochondria become depleted rapidly, leading to cell death. The more cells die, the more the mitochondria in other cells have to compensate, which accelerates their depletion. It's a vicious circle," explains Patrick J. Rochette.

Reduce mortality rate

The research team wondered whether injecting healthy mitochondria into cells could delay the progression of Fuchs' dystrophy. To test their hypothesis, the scientists used diseased endothelium removed during a corneal transplant. "We were able to save cells close to death, going from a 60% mortality rate to 10%," Rochette said. These results demonstrate a high therapeutic potential for the injection of mitochondria.

The strength of this approach lies in the automatic recycling of diseased mitochondria without injecting healthy ones directly into the cell. "Cells eat mitochondria as if their life depended on them. Any cell, even if it is dying, will take them up. The replacement happens by itself. After 24 hours, only healthy mitochondria remain," says the researcher.

In the study, the healthy mitochondria were grown under controlled conditions, but the research group is developing an approach to extract them from the patient's blood.

If Fuchs' dystrophy is diagnosed at an early stage, when most endothelial cells are still alive, the approach could maintain vision without a transplant. The injection of mitochondria would be a benign procedure, much less invasive than surgery.

The paper is published in the journal Scientific Reports.

Targeting Mitochondria 2023 will adress the latest research that targets the mitochondria in ophthalmology. You can submit a related abstract.

Source: Press release by the University of Laval.

Image Credits: Freepik

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