NEWS FROM MEDICAL SCIENCE (b)


(BEING CONTINUED FROM 30/04/18)

A)Research sheds new light on how brain stem cells are activated

Source: University of Plymouth

Our brains are notoriously bad at regenerating cells that have been lost through injury or disease. While therapies using neural stem cells (NSCs) hold the promise of replacing lost cells, scientists need to better understand how NSCs behave in the brain in order to develop effective treatments.

Now research led by the University of Plymouth helps to shed new light on the mechanisms used by NSCs to ‘wake up’ – going from their usual dormant state to one of action.

NSCs produce neurons (nerve cells) and surrounding glial cells in the brain. By understanding how NSCs work, it could pave the way for therapies to speed up the neurons’ and glial cells’ regeneration.

The new study, conducted using Drosophila fruit flies, shows that molecules that form a complex called STRIPAK are essential to promote reactivation in NSCs. STRIPAK (Striatin-interacting phosphatase and kinase) is found in organisms from fungi to humans, and the team uncovered it when comparing the genetic messages of dormant and reactivated NSCs in live fly brains.

The researchers then discovered that STRIPAK components act as a switch to turn off dormancy (or quiescence) and turn on reactivation.

Lead author Dr Claudia Barros, from the Institute of Translational and Stratified Medicine at the University of Plymouth, acknowledges there is still a long way to go until such findings can be translated into human treatments. But she explains the significance of the new work:

“So little is currently known about how neural stem cells coordinate cues to become active and direct the production of more brain cells,” she said. “These stem cells last throughout life mainly in a dormant state, so learning how they work is critical to our understanding of cell regeneration.

This shows neural stem cells

A confocal microscope image showing small/ quiescent and enlarged/ reactivating Neural Stem Cells expressing membrane-tagged GFP (green) and the cell cycle marker Cyclin B (red) in the young Drosophila larval brain. The image is credited to Dr. Claudia Barros, University of Plymouth.

“This study reveals that STRIPAK molecules are essential to enable reactivation in NSCs, and we are very pleased with the outcomes. But we are only at the beginning. We are working to expand our findings and bring us closer to the day when human neural stem cells can be controlled and efficiently used to facilitate brain damage repair, or even prevent brain cancer growth that is fuelled by stem-like cells.”

Funding: The work was supported by the University of Plymouth, Faculty of Medicine and Dentistry; the Leverhulme Trust; the Biotechnology and Biological Sciences Research Council (BBSRC) the DFG German Research Foundation and the Johannes Gutenberg University, Germany.

The work of Dr Barros and her team takes place within the Brain Tumour Research Centre of Excellence at the University of Plymouth.

B)Aging delayed in older mice given blood component from young mice

New research has identified a novel approach to staving off the detrimental effects of aging, according to a study from Washington University School of Medicine in St. Louis.

The study suggests that a protein that is abundant in the blood of young mice plays a vital role in keeping mice healthy. With age, levels of this protein decline in mice and people, while health problems such as insulin resistance, weight gain, cognitive decline and vision loss increase. Supplementing older mice with the protein obtained from younger mice appears to slow this decline in health and extend the life spans of older mice by about 16 percent.

The study is published June 13 in the journal Cell Metabolism.

The circulating protein is an enzyme called eNAMPT, which is known to orchestrate a key step in the process cells use to make energy. With age, the body’s cells become less and less efficient at producing this fuel — called NAD — which is required to keep the body healthy. Washington University researchers have shown that supplementing eNAMPT in older mice with that of younger mice appears to be one route to boosting NAD fuel production and keeping aging at bay.

“We have found a totally new pathway toward healthy aging,” said senior author Shin-ichiro Imai, MD, PhD, a professor of developmental biology.

“That we can take eNAMPT from the blood of young mice and give it to older mice and see that the older mice show marked improvements in health — including increased physical activity and better sleep — is remarkable.”

Imai has long studied aging, using mice as stand-ins for people. Unlike other studies focused on transfusing whole blood from young mice to old mice, Imai’s group increased levels of a single blood component, eNAMPT, and showed its far-reaching effects, including improved insulin production, sleep quality, function of photoreceptors in the eye, and cognitive function in performance on memory tests, as well as increased running on a wheel. Imai’s group also has shown other ways to boost NAD levels in tissues throughout the body. Most notably, the researchers have studied the effects of giving oral doses of a molecule called NMN, the chemical eNAMPT produces. NMN is being tested in human clinical trials.

“We think the body has so many redundant systems to maintain proper NAD levels because it is so important,” Imai said. “Our work and others’ suggest it governs how long we live and how healthy we remain as we age. Since we know that NAD inevitably declines with age, whether in worms, fruit flies, mice or people, many researchers are interested in finding anti-aging interventions that might maintain NAD levels as we get older.”

This shows the mice from the video

Imai’s research has shown that the hypothalamus is a major control center for aging throughout the body, and it is directed in large part by eNAMPT, which is released into the blood from fat tissue. The image is adapted from the WUSTL video.

Imai’s research has shown that the hypothalamus is a major control center for aging throughout the body, and it is directed in large part by eNAMPT, which is released into the blood from fat tissue. The hypothalamus governs vital processes such as body temperature, thirst, sleep, circadian rhythms and hormone levels. The researchers have shown that the hypothalamus manufactures NAD using eNAMPT that makes its way to the brain through the bloodstream after being released from fat tissue. They also showed that this eNAMPT is carried in small particles called extracellular vesicles. As levels of eNAMPT in the blood decline, the hypothalamus loses its ability to function properly, decreasing life span.

In an intriguing finding, Imai and first author Mitsukuni Yoshida, a doctoral student in Imai’s lab, showed that levels of eNAMPT in the blood were highly correlated with the number of days the mice lived. More eNAMPT meant a longer life span, and less meant a shorter one.


Scientists are seeking new ways to extend healthy life spans, and a new study in mice suggests a novel strategy. Researchers at Washington University School of Medicine in St. Louis have shown that supplementing older mice with an enzyme called eNAMPT from younger mice extends life spans in the older mice. The active mouse in the video was given the enzyme; the less active mouse was given saline. The mice are the same age. Credit: WUSTL.

The researchers also showed increased life span with delivering eNAMPT to normal old mice. All mice that received saline solution as a control had died before day 881, about 2.4 years. Of the mice that received eNAMPT, one is still alive as of this writing, surpassing 1,029 days, or about 2.8 years.

“We could predict, with surprising accuracy, how long mice would live based on their levels of circulating eNAMPT,” Imai said. “We don’t know yet if this association is present in people, but it does suggest that eNAMPT levels should be studied further to see if it could be used as a potential biomarker of aging.”

The study also found sex differences in levels of eNAMPT, with female mice consistently showing higher levels of the enzyme.

“We were surprised by the dramatic differences between the old mice that received the eNAMPT of young mice and old mice that received saline as a control,” Imai said. “These are old mice with no special genetic modifications, and when supplemented with eNAMPT, their wheel-running behaviors, sleep patterns and physical appearance — thicker, shinier fur, for example — resemble that of young mice.”

Imai and his colleagues, including co-author Rajendra Apte, MD, PhD, the Paul A. Cibis Distinguished Professor of Ophthalmology and Visual Sciences, noted that eNAMPT also is carried in extracellular vesicles in humans. As such, future studies should be done to investigate whether low levels are associated with disease in aging people and whether supplementing eNAMPT in extracellular vesicles could serve as an anti-aging intervention in older people, they said.

Funding: This work was supported by the Diabetes Research Center, grant number P30 DK020579; and Nutrition Obesity Research Center, grant number P30 DK56341. This work was mainly supported by grants from the National Institute on Aging, grant numbers AG037457 and AG047902; the American Federation for Aging Research, and the Tanaka Fund. A part of this study also was performed in a facility supported by the NCRR grant C06 RR015502. Further support was provided by JSPS KAKENHI, grant number JP18H03186; AMED, grant number JP18gm5010001h0001; the Takeda Science Foundation; and the Research Fund for Longevity Sciences from the National Center for Geriatrics and Gerontology (28-47). Imai and Satoh also are collaborating in the Project for Elucidating and Controlling Mechanisms of Aging and Longevity, organized by the Japan Agency for Medical Research and Development (AMED). Further support was provided by the Intellectual and Developmental Disabilities Research Center, grant numbers U54 HD087011; the NIH R01 EY019287, P30 EY02687, Vision Core Grant; the Starr Foundation; the Carl Marshall Reeves and Mildred Almen Reeves Foundation; the Bill and Emily Kuzma Family Gift for retinal research; a Physician-Scientist Award and a Nelson Trust Award from Research to Prevent Blindness; the Jeffrey Fort Innovation Fund; the Thome Foundation; and an unrestricted grant from Research to Prevent Blindness to the Department of Ophthalmology and Visual Sciences of Washington University School of Medicine. Further support was provided by the Washington University Medical Scientist Training Program, NIH grant number T32 GM007200; the Washington University Institute of Clinical and Translational Sciences, grant numbers UL1 TR002345 and TL1 TR002344; and the VitreoRetinal Surgery Foundation. Apte is a co-founder of Metro Midwest Biotech. All other authors have no financial interests.

Source:
WUSTL
Julia Evangelou Strait – WUSTL
Image Source:
The image is adapted from the WUSTL video.

Original Research: Closed access
“Extracellular Vesicle-Contained eNAMPT Delays Aging and Extends Lifespan in Mice”. Mitsukuni Yoshida, Akiko Satoh, Jonathan B. Lin, Kathryn F. Mills, Yo Sasaki, Nicholas Rensing, Michael Wong, Rajendra S. Apte, and others.
Cell Metabolism. doi:10.1016/j.cmet.2019.05.015

Abstract

Extracellular Vesicle-Contained eNAMPT Delays Aging and Extends Lifespan in Mice

Highlights
• Circulating levels of eNAMPT decline with age in both mice and humans
• Increasing eNAMPT promotes NAD +, counteracts aging, and extends healthspan in mice
• eNAMPT is contained exclusively in extracellular vesicles (EVs) in mice and humans
• Supplementing eNAMPT in EVs improves physical activity and extends lifespan in mice

Summary

Aging is a significant risk factor for impaired tissue functions and chronic diseases. Age-associated decline in systemic NAD + availability plays a critical role in regulating the aging process across many species. Here, we show that the circulating levels of extracellular nicotinamide phosphoribosyltransferase (eNAMPT) significantly decline with age in mice and humans. Increasing circulating eNAMPT levels in aged mice by adipose-tissue-specific overexpression of NAMPT increases NAD + levels in multiple tissues, thereby enhancing their functions and extending healthspan in female mice. Interestingly, eNAMPT is carried in extracellular vesicles (EVs) through systemic circulation in mice and humans. EV-contained eNAMPT is internalized into cells and enhances NAD + biosynthesis. Supplementing eNAMPT-containing EVs isolated from young mice significantly improves wheel-running activity and extends lifespan in aged mice. Our findings have revealed a novel EV-mediated delivery mechanism for eNAMPT, which promotes systemic NAD + biosynthesis and counteracts aging, suggesting a potential avenue for anti-aging intervention in humans.

SOURCE https://neurosciencenews.com

C)Viruses that can lead to cancer

Viruses are very small organisms; most can’t even be seen with an ordinary microscope. They are made up of a small number of genes in the form of DNA or RNA surrounded by a protein coating. A virus must enter a living cell and “hijack” the cell’s machinery in order to reproduce and make more viruses. Some viruses do this by inserting their own DNA (or RNA) into that of the host cell. When the DNA or RNA affects the host cell’s genes, it can push the cell toward becoming cancer.

In general, each type of virus tends to infect only a certain type of cell in the body. (For example, the viruses that cause the common cold only infect the cells lining the nose and throat.)

Several viruses are linked with cancer in humans. Our growing knowledge of the role of viruses as a cause of cancer has led to the development of vaccines to help prevent certain human cancers. But these vaccines can only protect against infections if they are given before the person is exposed to the cancer-promoting virus.

Human papilloma viruses (HPVs)

Human papilloma viruses (HPVs) are a group of more than 150 related viruses. They are called papilloma viruses because some of them cause papillomas, which are more commonly known as warts. Some types of HPV only grow in skin, while others grow in mucous membranes such as the mouth, throat, or vagina.

All types of HPV are spread by contact (touch). More than 40 types of HPV can be passed on through sexual contact. Most sexually active people are infected with one or more of these HPV types at some point in their lives. At least a dozen of these types are known to cause cancer.

While HPV infections are very common, cancer caused by HPV is not. Most people infected with HPV will not develop a cancer related to the infection.

HPV infections of the mucous membranes can cause genital warts, but they usually have no symptoms. There are no effective medicines or other treatments for HPV, other than removing or destroying cells that are known to be infected. But in most people, the body’s immune system controls the HPV infection or gets rid of it over time. To learn more, see HPV and HPV Testing.

HPV and cervical cancer

A few types of HPV are the main causes of cervical cancer, which is the second most common cancer among women worldwide. Cervical cancer has become much less common in the United States because the Pap test has been widely available for many years. This test can show pre-cancerous changes in cells of the cervix that might be caused by HPV infection. These changed cells can then be destroyed or removed, if needed. This can keep cancer from developing. Doctors may now also test for HPV, which can tell them if a woman might be at higher risk for cervical cancer.

Nearly all women with cervical cancer show signs of HPV infection on lab tests, but most women infected with HPV will not develop cervical cancer. Even though doctors can test women for HPV, there is no treatment directed at HPV itself. If the HPV causes abnormal cells to start growing, these cells can be removed or destroyed.

See HPV and HPV Testing for more information on this topic.

HPV and other cancers

HPVs also have a role in causing some cancers of the penisanusvagina, and vulva. They are linked to some cancers of the mouth and throat, too. Again, although HPVs have been linked to these cancers, most people infected with HPV never develop these cancers.

Smoking, which is also linked with these cancers, may work with HPV to increase cancer risk. Other genital infections may also increase the risk that HPV will cause cancer.

You can get more details in HPV and Cancer.

Vaccines against HPV

Vaccines are now available to help protect against infection from the main cancer-causing HPV types. These vaccines are approved for use in females and males from age 9 up to their mid-20’s. They’re given as a series of injections (shots).

The vaccines can only be used to help prevent HPV infection – they do not stop or help treat an existing infection. To be most effective, the vaccine series should be given before a person becomes sexually active (has sex with another person).

American Cancer Society recommendations for HPV vaccination

  • Routine HPV vaccination for girls and boys should be started at age 11 or 12. The vaccination series can be started as early as age 9.
  • HPV vaccination is also recommended for females 13 to 26 years old and for males 13 to 21 years old who have not started the vaccines, or who have started but not completed the series. Males 22 to 26 years old may also be vaccinated.*
  • HPV vaccination is also recommended through age 26 for men who have sex with men and for people with weakened immune systems (including people with HIV infection), if they have not previously been vaccinated.

*For people 22 to 26 years old who have not started the vaccines, or who have started but not completed the series, it’s important to know that vaccination at older ages is less effective in lowering cancer risk.  

See HPV Vaccines for more on this.

Epstein-Barr virus (EBV)

EBV is a type of herpes virus. It is probably best known for causing infectious mononucleosis, often called “mono” or the “kissing disease.” In addition to kissing, EBV can be passed from person to person by coughing, sneezing, or by sharing drinking or eating utensils. Most people in the United States are infected with EBV by the end of their teen years, although not everyone develops the symptoms of mono.

As with other herpes virus infections, EBV infection is life-long, even though most people have no symptoms after the first few weeks. EBV infects and stays in certain white blood cells in the body called B lymphocytes (also called B cells). There are no medicines or other treatments to get rid of EBV, nor are there vaccines to help prevent it, but EBV infection doesn’t cause serious problems in most people.

EBV infection increases a person’s risk of getting nasopharyngeal cancer (cancer of the area in the back of the nose) and certain types of fast-growing lymphomas such as Burkitt lymphoma. It may also be linked to Hodgkin lymphoma and some cases of stomach cancer. EBV-related cancers are more common in Africa and parts of Southeast Asia. Overall, very few people who have been infected with EBV will ever develop these cancers.

Hepatitis B virus (HBV) and hepatitis C virus (HCV)

Both HBV and HCV cause viral hepatitis, a type of liver infection. Other viruses can also cause hepatitis (hepatitis A virus, for example), but only HBV and HCV can cause the long-term (chronic) infections that increase a person’s chance of liver cancer. In the United States, less than half of liver cancers are linked to HBV or HCV infection. But this number is much higher in some other countries, where both viral hepatitis and liver cancer are much more common. Some research also suggests that long-term HCV infection might be linked with some other cancers, such as non-Hodgkin lymphoma.

HBV and HCV are spread from person to person in much the same way as HIV (see the section on HIV below) — through sharing needles (such as during injection drug use), unprotected sex, or childbirth. They can also be passed on through blood transfusions, but this is rare in the United States because donated blood is tested for these viruses.

Of the 2 viruses, infection with HBV is more likely to cause symptoms, such as a flu-like illness and jaundice (yellowing of the eyes and skin). Most adults recover completely from HBV infection within a few months. Only a very small portion of adults go on to have chronic HBV infections, but this risk is higher in young children. People with chronic HBV infections have a higher risk for liver cancer.

HCV is less likely to cause symptoms than HBV, but it is more likely to cause chronic infection, which can to lead to liver damage or even cancer. An estimated 3.2 million people in the United States have chronic HCV infection, and most of these people don’t even know they have it. To help find some of these unknown infections, the US Centers for Disease Control and Prevention (CDC) recommends that all people born between 1945 and 1965 (as well as some other people at high risk) get blood tests to check for HCV. (For a more complete list of who should get tested for HCV, visit the CDC website at: www.cdc.gov/hepatitis/C/cFAQ.htm.)

Once an infection is found, treatment and preventive measures can be used to slow liver damage and reduce cancer risk. Both hepatitis B and C infections can be treated with drugs. Treating chronic hepatitis C infection with a combination of drugs for at least a few months can get rid of HCV in many people. A number of drugs can also be used to help treat chronic hepatitis B. Although they don’t cure the disease, they can lower the risk of liver damage and might lower the risk of liver cancer as well.

There is a vaccine to prevent HBV infection, but none for HCV. In the United States, the HBV vaccine is recommended for all children. It’s also recommended for adults who are at risk of exposure. This includes people infected with HIV, men who have sex with men, injection drug users, people in certain group homes, people with certain medical conditions and occupations (such as health care workers), and others. (For a more complete list of who should get the HBV vaccine, visit the CDC website at: http://www.cdc.gov/hepatitis/B/bFAQ.htm.)

For more information, see Liver Cancer.

Human immunodeficiency virus (HIV)

HIV, the virus that causes acquired immune deficiency syndrome (AIDS), doesn’t appear to cause cancers directly. But HIV infection increases a person’s risk of getting several types of cancer, especially some linked to other viruses.

HIV can be spread through semen, vaginal fluids, blood, and breast milk from an HIV-infected person. Known routes of spread include:

  • Unprotected sex (oral, vaginal, or anal) with an HIV-infected person
  • Injections with needles or injection equipment previously used by an HIV-infected person
  • Prenatal (before birth) and perinatal (during birth) exposure of infants from mothers with HIV
  • Breastfeeding by mothers with HIV
  • Transfusion of blood products containing HIV (the risk of HIV from a transfusion is less than 1 in a million in the United States due to blood testing and donor screening)
  • Organ transplants from an HIV-infected person (donors are now tested for HIV)
  • Penetrating injuries or accidents (usually needle sticks) in health care workers while caring for HIV-infected patients or handling their blood

HIV is not spread by insects, through water, or by casual contact such as talking, shaking hands, hugging, coughing, sneezing, or from sharing dishes, bathrooms, kitchens, phones, or computers. It is not spread through saliva, tears, or sweat.

HIV infects and destroys white blood cells known as helper T-cells, which weakens the body’s immune system. This might let some other viruses, such as HPV, thrive, which might lead to cancer.

Many scientists believe that the immune system is also important in attacking and destroying newly formed cancer cells. A weak immune system might let new cancer cells survive long enough to grow into a serious, life-threatening tumor.

HIV infection has been linked to a higher risk of developing Kaposi sarcoma and cervical cancer. It’s also linked to certain kinds of non-Hodgkin lymphoma, especially central nervous system lymphoma.

Other types of cancer that may be more likely to develop in people with HIV infection include:

Some other, less common types of cancer may also be more likely to develop in people with HIV.

Because HIV infection often has no symptoms for years, a person can have HIV for a long time and not know it. The CDC recommends that everyone between the ages of 13 and 64 be tested for HIV at least once as part of their routine health care.

There is no vaccine to prevent HIV. But there are ways to lower your risk of getting it, such as not having unprotected sex or sharing needles with someone who has HIV. For people who are at high risk of HIV infection, such as injection drug users and people whose partners have HIV, taking medicine (as a pill every day) is another way to help lower your risk of infection.

For people already infected with HIV, taking anti-HIV drugs can help slow the damage to the immune system, which may help reduce the risk of getting some of the cancers above.

For more information, see HIV Infection, AIDS, and Cancer.

Human herpes virus 8 (HHV-8)

HHV-8, also known as Kaposi sarcoma–associated herpes virus (KSHV), has been found in nearly all tumors in patients with Kaposi sarcoma (KS). KS is a rare, slow-growing cancer that often appears as reddish-purple or blue-brown tumors just underneath the skin. In KS, the cells that line blood and lymph vessels are infected with HHV-8. The infection makes them divide too much and live longer than they should. These types of changes may eventually turn them into cancer cells.

HHV-8 is transmitted through sex and appears to be spread other ways, such as through blood and saliva, as well. Studies have shown that fewer than 10% of people in the US are infected with this virus.

HHV-8 infection is life-long (as with other herpes viruses), but it does not appear to cause disease in most healthy people. Many more people are infected with HHV-8 than ever develop KS, so it’s likely that other factors are also needed for it to develop. Having a weakened immune system appears to be one such factor. In the US, almost all people who develop KS have other conditions that have weakened their immune system, such as HIV infection or immune suppression after an organ transplant.

KS was rare in the United States until it started appearing in people with AIDS in the early 1980s. The number of people with KS has dropped in the US since peaking in the early 1990s, most likely because of better treatment of HIV infection.

For more information on KS, see Kaposi Sarcoma.

HHV-8 infection has also been linked to some rare blood cancers, such as primary effusionlymphoma. The virus has also been found in many people with multicentric Castleman disease, an overgrowth of lymph nodes that acts very much like and often develops into cancer of the lymph nodes (lymphoma). (For more information, see Castleman Disease.) Further study is needed to better understand the role of HHV-8 in these diseases.

Human T-lymphotrophic virus-1 (HTLV-1)

HTLV-1 has been linked with a type of lymphocytic leukemia and non-Hodgkin lymphoma called adult T-cell leukemia/lymphoma (ATL). This cancer is found mostly in southern Japan, the Caribbean, central Africa, parts of South America, and in some immigrant groups in the southeastern United States.

In addition to ATL, this virus can cause other health problems, although many people with HTLV-1 don’t have any of them.

HTLV-1 belongs to a class of viruses called retroviruses. These viruses use RNA (instead of DNA) for their genetic code. To reproduce, they must go through an extra step to change their RNA genes into DNA. Some of the new DNA genes can then become part of the chromosomes of the human cell infected by the virus. This can change how the cell grows and divides, which can sometimes lead to cancer.

HTLV-1 is something like HIV, which is another human retrovirus. But HTLV-1 cannot cause AIDS. In humans, HTLV-1 is spread in the same ways as HIV, such as unprotected sex with an HTLV-1-infected partner or injection with a needle after an infected person has used it. Mothers infected with HTLV-1 can also pass on the virus to their children, although this risk can be reduced if the mother doesn’t breastfeed.

Infection with HTLV-1 is rare in the United States. Fewer than 1% of people in the US are infected with HTLV-1, but this rate is much higher in groups of people at high risk (such as injection drug users). Since 1988, all blood donated in the United States has been screened for HTLV-1. This has greatly reduced the chance of infection through transfusion, and has also helped control the potential spread of HTLV-1 infection.

Once infected with HTLV-1, a person’s chance of developing ATL can be up to about 5%, usually after a long time with no symptoms (20 or more years).

Merkel cell polyomavirus (MCV)

MCV was discovered in 2008 in samples from a rare and aggressive type of skin cancer called Merkel cell carcinoma. Most people are infected with MCV at some point (often in childhood), and it usually causes no symptoms. But in a few people with this infection, the virus can affect the DNA inside cells, which can lead to Merkel cell cancer. Nearly all Merkel cell cancers are now thought to be linked to this infection.

It is not yet clear how people become infected with this virus, but it has been found in a number of places in the body, including normal skin and saliva.

For more information, see Skin Cancer: Merkel Cell Carcinoma.

Viruses with uncertain or unproven links to cancer in humans

Simian virus 40 (SV40)

SV40 is a virus that usually infects monkeys.Some polio vaccines prepared between 1955 and 1963 were made from monkey cells and were later found to be contaminated with SV40.

Some older studies suggested that infection with SV40 might increase a person’s risk of developing mesothelioma (a rare cancer of the lining of the lungs or abdomen), as well as some brain tumorsbone cancers, and lymphomas. But the accuracy of these older studies has been questioned.

Scientists have found that some lab animals, such as hamsters, developed mesotheliomas when they were intentionally infected with SV40. Researchers have also noticed that SV40 can make mouse cells grown in the lab become cancerous.

Other researchers have studied biopsy specimens of certain human cancers and found fragments of DNA that look like they might be from SV40. But not all researchers have found this, and fragments much like these can also be found in human tissues that show no signs of cancer.

So far, the largest studies looking at this issue have not found any increased risk for mesothelioma or other cancers among people who got the contaminated polio vaccines as children. For example, the recent increase in lung mesothelioma cases has been seen mainly in men aged 75 and older, most of whom would not have received the vaccine. Among the age groups who were known to have gotten the vaccine, mesothelioma rates have actually gone down. And even though women were just as likely to have had the vaccine, many more men continue to be diagnosed with mesothelioma.

The bottom line: even though SV40 causes cancer in some lab animals, the evidence so far suggests that it does not cause cancer in humans.

  • Written by

The American Cancer Society medical and editorial content team

Our team is made up of doctors and oncology certified nurses with deep knowledge of cancer care as well as journalists, editors, and translators with extensive experience in medical writing.

(TO BE CONTINUED)

About sooteris kyritsis

Job title: (f)PHELLOW OF SOPHIA Profession: RESEARCHER Company: ANTHROOPISMOS Favorite quote: "ITS TIME FOR KOSMOPOLITANS(=HELLINES) TO FLY IN SPACE." Interested in: Activity Partners, Friends Fashion: Classic Humor: Friendly Places lived: EN THE HIGHLANDS OF KOSMOS THROUGH THE DARKNESS OF AMENTHE
This entry was posted in SCIENCE=EPI-HISTEME and tagged , , , , . Bookmark the permalink.

Leave a Reply

Please log in using one of these methods to post your comment:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

This site uses Akismet to reduce spam. Learn how your comment data is processed.