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Category Archives: viruses

Quora contributions from August 2016 to March 2017

Quora is a question-and-answer site. You can view all my contributions here; selected highlights are listed below. I encourage you to check out the other answers submitted for each question, too!

Epigenetics

What molecular mechanisms regulate methylase activity?

Why is the epitranscriptome (epigenetic marks on mRNA) important when mRNA molecules last so transiently?

What is the difference between histones and nucleosomes?

What’s “Histone modification”?

What is the difference between acetylation and methylation?

Why does acetylation remove the positive charge on histones?

Why does trimethylation of histone H3 on lysine 27 (K27) result in chromatin repression?

Should histone modifications be labeled as an epigenetic modification? Or just a chromatin modification?

Are epigenetics a type of post-translational modification?

Could stem cells just be epigenetic?

I want to start learning about epigenetics. Where should I start?

What are the best books on epigenetics, for a layperson?

Cancer

Can cancer cells evolve resistance to treatment?

Why are familial tumors usually multiple compared to sporadic cases, even when the same mutation is responsible for both types?

Why can’t people with cancer donate their organs?

Viruses

Can we use mRNA silencing techniques to inhibit the HIV genome?

Other scientific topics

Once we insert a desired gene into the human genome, how is its expression limited to the specific target organs where the gene is needed?

Do our parents have the same DNA as us?

Do red blood cells have functional miRNAs?

My ex-husband and I both have blood type O (positive and negative). How is it possible that our son has type B+?

Miscellaneous

Do you think Goodreads should ask a few questions from a book before letting anyone rate it?

 

 

 

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Quora activity for January 2015 – August 2016

Quora is a question-and-answer site. You can view all my contributions here; selected highlights are listed below. I encourage you to check out the other answers submitted for each question, too!

Cancer

Would it be possible to avoid cancer by modifying our DNA?

Is whole genome sequencing of any use in cancer diagnostics?

If our body can detect cancerous cells, why do people still get cancer? Does it mean that we can improve our body’s defenses against cancer before even getting sick?

If 2/3 of cancers are caused by chance mutations, why should I work to help prevent cancer?

Is it possible that cancer is not actually a disease to be “cured”, but it is actually an inherent defect of genetics?

Is cancer an intrinsic feature of life?

Is worrying about cancer the biggest cause of cancer?

What are the chances (if any), that a blind person getting cancer in the eye would allow them to see again?

What cure would be most beneficial to discover: HIV/AIDS or cancer?

Can Ebola be treated with cancer drugs?

Epigenetics

If two people have identical DNA fingerprints, what other molecular evidence does forensics use to distinguish between biological samples?

Can a methylation pattern be sequenced?

What could potentially be the most exciting application of epigenetic research?

Why hasn’t Lamarck been acknowledged in the face of the burgeoning advances made in the science of epigenetics?

In what way does histone methylation prevent transcription?

Is the epigenetic system of a person heritable?

Is there a meaningful way to diagnostically test a patient for epigenetic changes caused by long term use of medications?

Other Scientific Subjects

Is it a possibility that parents of genotype AA have an offspring with AS?

What is the reason that viruses are inactive when not inside any organism? What is the mechanism?

Will the final solution to HIV be to just accept it as part of the human genome?

What can you tell about a gene based on its tissue expression patterns?

What are some interesting examples of people becoming infected with typically fatal diseases (e.g. Ebola, HIV/AIDS, rabies, anthrax) through unusual means or at long odds?

Could cellular environment (pH, temperature, molecular crowding, redox state) affect a cell’s interactome?

What causes mutation in viruses?

Which (multicellular) animal is most deadly to humans?

What would happen if all the DNA in my body suddenly disappeared?

What are the most useful lab hacks, tips and tricks for molecular biology/biochemistry?

Do viruses have nutritional value for any organism?

What will next-generation sequencing be called a generation from now?

When will we be able to sequence the genome of every living vertebrate on Earth?

What are the oddest organisms?

Biochemistry: Why does the yeast two-hybrid system system have low specificity?

About Scientific Research and Careers

What does a principal investigator at a molecular biology lab spend time doing during the day?

How common is it for scientists to hire people to write their grant proposals?

How do I improve my grant writing?

I want to apply for a grant for a project, but I have no idea how to write a proper grant proposal. How can I go about this?

What is your favorite annual scientific conference?

Does a biochemist/biologist have to know all the reactions of cellular respiration or other general topics by heart after graduating?

Miscellaneous

Is there racism in Canada? Why?

What’s the best story about “fighting fire with fire”?

What are some of the best moments while taking exams?

Why do people believe in the ancient aliens theory?

If cloning of people was legal, whom would you choose and why?

What are some great optical illusions?

Which is the best way to pass the PMP exam?

Why do some people choose to use Quora over writing a blog?

 

Can a trigger-happy immune system cause cancer after viral infection?

(Originally published on Occam’s Corner at Guardian Science, in June 2014)

Friendly fire: while the immune system tries to protect us from viruses, it could be causing cancer

The immune system is a fickle thing, both hero and villain.

The ability of our ancestors to survive plague and pestilence was one of the forces that shaped the evolution of the human species into its current form. But many of us now find ourselves in environments where many of the biggest infectious threats have been neutralised by a combination of vaccination programmes, improved hygiene, and (temporarily) effective treatments. With their usual duties cut back so drastically, our evolutionary superstar immune systems sometimes lash out at innocuous perceived threats. This can cause allergies, multiple sclerosis, and other auto-immune disorders in the process – sins of commission, if you will.

But at least our immune systems are still pretty good at protecting us from infections and most cancers, right?

Well, much of the time, yes. The importance of the immune system in protecting us from cancer is evident from the increased rates of the disease in people with reduced immunity due to HIV/Aids or followingorgan transplants. And yet the immune system’s sins of omission mean that far too many cancer cells slip through the net – and we still get colds and the dreaded norovirus, too.

This week, though, new research from University College London (UCL) suggests for the first time that the immune system also commits sins of commission when it comes to cancer.

The research, published in the journal Cell Reports on Thursday, concerns a class of genes called the APOBEC family. These genes code for proteins that attack invading viruses by mutating their DNA, a tactic that can stop or at least slow the replication and spread of the virus. The mutations caused by APOBEC proteins occur in a characteristic pattern – a pattern that also shows up in some types of cancer, including types that are often caused by infection with human papilloma viruses (HPV). Could the mutations in these cancers be caused by misfiring antiviral defences?

Papilloma Virus (HPV) EM
Human papilloma virus. Photograph: Laboratory of Tumor Virus Biology/Wikimedia Commons

Drs Stephen Henderson, Tim Fenton and their teams at UCL have now demonstrated that there is indeed an association between the presence of HPV in some cancer cells, elevated activity of the APOBEC proteins in those cells, and the presence of the characteristic APOBEC-mediated mutation pattern. These findings support the idea that HPV infection triggers an anti-viral attack that not only hits the intended target – the viral genes –but also the cell’s own DNA. The UCL team also found that mutations caused by APOBEC have a strong tendency to hit genes such as PIK3CA that help to regulate the growth and division of the cell, and whose mutation is associated with the development of cancer.

“It is not clear why HPV infection causes the APOBEC genes to misbehave and mutate PIK3CA,”says Dr Henderson. “It could be that the body responds to HPV infection with increased ABOBEC activity, simply making ‘friendly fire’ more likely. Alternatively, there may well be something about the virus that causes the APOBEC response to wrongly target the body’s own genes for mutation.”

The good news is that these new findings open up new avenues for researchers working on diverse aspects of the cancer problem: there are known inherited variations in a member of the APOBEC family that have been linked with an elevated risk of developing breast cancer; other viral infections may also be associated with cancer, possibly via the same mechanism; and drugs that target mutated versions of the PIK3CA protein are already being developed.

Meanwhile, if you don’t want to give your trigger-happy immune system a shot at the human papilloma virus, effective vaccines are now available.

 
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Posted by on 2014/09/14 in cancer, genetics, viruses