10 things scientists really want everyone to know

These days there are a lot of scientists, and therefore science, in the media. In pop culture, we have shows like the The Big Bang Theory, filled with characters like Sheldon Cooper and his rag-tag team of scientist-friends. Meanwhile, Bill Nye the Science Guy just released his own show on Netflix. Sheldon and Bill, among others, are great at bringing science into the light. However, as a scientist watching (and enjoying) these shows, we know there are a few truths about being a scientist that are often lost in translation.

1. Scientists fail. All the time.

No really. We fail all the time. The media tends to shares science success stories but science is riddled with optimization, trial and error (emphasis on error), and false leads. Ask any scientist and they’ll confirm that only a small portion of their work in the lab is ever published. The rest remain stuck on our computers and in lab notebooks, despite being vital in the journey to scientific discovery.

2.  “Negative” data is important.

Having a spotlight on scientific advances and discoveries is great but these advances represent positive data. Neglected are the tales of our negative data (data that fails to disprove your null hypothesis). And as much as we hate when experiments don’t support our hypotheses, we value negative data. It helps us narrow down the scope of our research and gives us more focus. So though its frustrating, we must give it a due nod of acknowledgement.

3. Scientists are a single cog in the science discovery machine.

There are usually one or two faces attached to each scientific discovery in the news. However, if you ever look at the authors of a scientific paper, you’ll rarely (if ever) see just one or 2 scientists listed. Plus, often times, the bigger the discovery, the more scientists involved. Collaborations are true driving forces in science.  

4. Scientists have a healthy level of skepticism (about science).

Of course scientists talk about science in a positive light! We are fiercely passionate about our work and want to spread the love! However, science has so many unforeseen plot twists that can never be anticipated. It is why seasoned scientists develop a healthy level of skepticism. It forces us to be critical of our findings, question our own bias (and those of others), and helps promote quality control on our research.     

5. Scientists define “complete” differently from a non-scientist when it comes to their scientific work.

Science aims to understand the unknown. Fortunately for science, the unknown is seemingly infinite. Ergo a scientist’s job is never done. When we say we are done with a project, it means that we/our team feel we collected sufficient evidence to propose a new theory to explain an observation in regards to a FEW specific hypotheses we tested. Unfortunately, it is hard for us to say we are “done” because we know there are remaining hypotheses we want to test (and any new ones we collected along the way).

6. A scientist is defined by the way they think, not the facts they know.

Scientists follow the scientific method: make observations, formulate hypotheses, test hypotheses, develop new theories, re-evaluate hypotheses and repeat. This is what makes us scientists. So, if and when a scientist happen to know a lot of facts, it is because s/he is curious and an active learner. Their love of knowledge goes beyond their own work. They are driven by a desire to understand everything thoroughly.

7. Scientists say “I don’t know” a lot.

Scientists in the media are often portrayed as know-it-alls and sure, there are a few out there. But if you ever hear scientists talking among themselves at science conferences, there is a good chance you will hear us say, “I don’t know. Good question!” After months (often years) of working on our own research, we invite new perspectives to evaluate our work and help find strengths and weakness we overlooked. The end result is overall better science.   

8. Diseases are complicated. Scientific questions are complicated. Science is complicated.

Everyone (including scientists) wants solutions for diseases and other tough scientific questions. Unfortunately, a lot of science is about studying the variables that affect an observation and, though we test variables we know, there are all the ones we have yet to realize are important still remaining! Successful science is a combination of hard work, innovation, MULTIPLE inquisitive minds, and time. Hence why:

9. Science is SLOW.

Even as a scientist with all our skepticism, we are determined and plan ambitious projects because we are EXCITED and we WANT to do EVERYTHING in our power to try to answer every question we have. But with just the points above, by now you must see that science is slow! Good science is a step-by-step process that takes time and shortcuts are usually non-existent.      

10. Scientists are normal people.

I think this is (hopefully) more and more apparent… but scientists are NORMAL people. We have families, religions, personal experiences, likes and dislikes, personal biases, insecurities, hopes, dreams, and a whole lot more. These traits shape how we work, think and the science we do. Without this diversity of minds, science would never move forward.

All this to say: these are a few truths to keep in mind when you hear about science in the mainstream media. The news and media are evolving and there are great pockets of accurate science representation out there but sensationalized news is often louder. Keep in mind that science is big, complicated, messy, and powerful. Scientists are the mere mortals trying to figure out its mysteries.

Science Now + Beyond

Was it wrong for scientists to make a pig-human hybrid?

Biomedical researchers are constantly trying to find answers in the lab for several health-related issues like organ shortages. One possible solution, at least in theory, is to grow tissues and organs in the lab. Recently, scientists from the renowned Salk Institute in San Diego, California announced a big step forward in this field: They made the first successful effort combining human induced stem cells into a large animal — a pig!

These hybrids are commonly known as chimeras, coming from Greek mythology where chimeras are creatures made up of multiple animals. For a scientist, a chimera is an organism that is made up of cells from different organisms. So when you read in the news that scientists made the first human-pig chimera, it is not necessarily what it may sound like. Understanding the actual science behind the news will help demonstrate how momentous this advancement is and yet how much more work there is left to do.

How did scientists get human cells inside a pig?

Stem cells are defined by two main characteristics: 1) they make more of themselves via cell division (proliferate) and 2) they can become any type of cell in the body (pluripotent). Embryonic stem cells (ESCs) are the ones most often surrounded by controversy. When you look at a textbook picture of a blastocyst, the mound of cells in the middle is called the inner cell mass (ICM).

The cells in ICM ultimately become the entire organism, but early on the ICM houses stem cells. At this point, these cells are “undifferentiated” meaning that they have not determined a cell fate. Depending on the messages they receive from surrounding cells and the environment, they will begin to change (differentiate) into specific types of cells (brain, heart, kidney, pancreas, skin, etc).

After a stem cell chooses a fate, they cannot naturally become a stem cell again. However, in 2006 Japanese researchers from Kyoto University identified conditions necessary to “reprogram” cells back into a stem cell-like state. These cells are called induced pluripotent stem cells (iPSCs). For researchers, one major benefit of this model is that differentiated cells (like skin cells) can be isolated from patients, transformed into iPSCs, and then used to model diseases and develop drugs. Since these cells are from the patient, the hope is that the patient’s body will also be less likely to reject them.

The best part is that iPSCs overcome the ethical complications of embryonic stem cells. This Nobel Prize winning discovery has great implications for regenerative medicine. Scientists and clinicians hope to use these cells to create tissues to repair or entirely replace those damaged in the body.

But how can scientists take the cells and turn them into an organ outside of the body? Truthfully, they can’t yet. They still need to understand more about the environmental signals that instruct cells to become a specific organ. One way scientists hope to possibly grow these organs and tissues is by using animals to provide the environment for the stem cells to develop. The work done by these Salk scientists is the first steps in the right direction.

What exactly did these scientists do?


The team first used rodent models to test their hypothesis. They were able to grow rat organs in a mouse to replace mouse organs that were missing! However, mice and rats have biological limitations when it comes to biomedical research. Rats and mice are similar but unfortunately, humans and rodents are not so growing human organs in a mouse is unlikely.

This is why scientists turned to pigs, which are more comparable to humans. In these experiments, they injected human iPSCs into pig blastocysts. Excitingly, they saw that these cells could incorporate with the ICM. Then the pig blastocysts were re-introduced to a female pig and embryos were examined. Unfortunately, these embryos were sickly and small. But the human cells were incorporated into cells that would eventually give rise to different organs! This is the first time scientists have successfully been able to do this with human cells in a large animal.

So when can we use this in modern medicine?

This is a huge accomplishment in biomedical research but there is still a long way to go. First of all, “incorporated cells” are different from a full and functional organ or tissue, which is the ultimate goal. Plus the success rate of even these experiments was low. Can these cells actually grow into a fully functional organ? Can scientists direct these cells to grow into specific organs? How similar will these resulting organs be to the patient’s organ? There are so many variables in play that still need to be understood going forward!

As always, exciting science and technology comes with heavy ethical and social questions. One major issue is that these chimeras are not naturally occurring so scientists must question if it is appropriate. This also opens up a whole new area of animal rights and welfare. Even now, for scientists to conduct any level of animal research on rodents or any other animal, there are strict guidelines that are tightly regulated. As science evolves these issues will be continuously reevaluated and questioned. None of these scientific or ethical questions have a single, simple answer. Even for scientists, these questions are complicated and hotly debated.

In the meantime, science will discover new insight and develop new technologies that will reshape research in ways we cannot even imagine. Only time will tell how these findings will shape modern medicine!

Science Now + Beyond

ASK A SCIENTIST: What is mitochondrial DNA and why is it important?

Nuclear DNA, or DNA that’s found in the nucleus, is probably the only type you learned about in high school bio. It carries all of an organism’s genetic information, which is used for proper growth, development, functioning, and reproduction. We get a set of DNA from each of our parents: one set from mom and one set from dad. In this Ask A Scientist piece, we delve into research on our third set of DNA: mitochondrial DNA.

Recently, there was news of the first baby born with DNA from three parents. The mother lost her first two babies to Leigh syndrome, which is associated with mutations in mitochondrial DNA. In attempt to circumvent this, doctors removed the nucleus from one of the mother’s eggs, placed it in a donor mother’s egg (after removing the donor egg’s nucleus), and fertilized this egg with the father’s sperm. The successful transplant led to the world’s first baby with DNA from three parents: mom and dad’s nuclear DNA and a donor’s mitochondrial DNA.


What is mitochondrial DNA?

Eukaryotic cells (which we are made of) contain a nucleus and other organelles. Organelles are “little organs” in the cell that carry out specific functions. Mitochondria, one of these organelles, generate energy for the cell in the form of ATP. This is why know it as the “powerhouse of the cell.” However, mitochondria are unique organelles because they have their own genetic material — independent to that in the nucleus!

Mitochondrial DNA (mtDNA) is different from nuclear DNA in a lot of ways. mtDNA is generally circular, while nuclear DNA is linear. Nuclear DNA has 3.3 billion DNA base pairs (the building blocks of DNA) – the mitochondrial genome is only made up of ~ 16,569 base pairs and only encodes for 37 genes. You might remember that there’s only one nucleus in a cell, where the DNA is tightly packed into chromosomes. We have two copies of each chromosome (46 chromosomes total). However, a single cell can have multiple mitochondrion and each of them has dozens of copies of the mitochondrial genome. Plus, mtDNA isn’t in the nucleus.

Why do we have mtDNA?

Given the shape of mtDNA and its independence from nuclear DNA, it’s possible that mitochondria came from bacteria. This theory claims that over a billion years ago, mitochondria were actually small aerobic (oxygen related) bacteria that were engulfed by a larger cell. Instead of digesting the small cell, the big and small cells developed a relationship. Perhaps that first big cell benefited from the smaller cell’s ability to use oxygen to produce energy! This theory originated from professor Lynn Margulis in the mid-1900s.

Thank your mother for your mtDNA!

Interestingly, unlike nuclear DNA, which comes from both your mother and father, only maternal mtDNA is passed down (maternal inheritance). Since this is unique to the maternal lineage, scientists think that they can trace human lineage through mtDNA inheritance. This might help us identify one ancient woman who is the most common female ancestor of all modern people. She is aptly named “Mitochondrial Eve” (the male equivalent is the “Y-chromosomal Adam”).

By C. Rottensteiner - TiGen, CC BY-SA 3.0,
By C. Rottensteiner – TiGen, CC BY-SA 3.0

Even though mtDNA is passed down by maternal inheritance, males still have it. We know paternal mtDNA gets eliminated but nobody knows why. Excitingly, earlier this year a group of scientists found a potential explanation. They observed that in C. elegans (a type of roundworm), paternal mitochondria are eliminated when the sperm and egg fuse. If this process was disturbed, embryo survival rates decreased. This is the first time a study showed experimental evidence to suggest that maintaining paternal mtDNA may be harmful.

mtDNA and biomedical research

Because of the number of mtDNA, there’s a much higher mutation rate in mitochondrial DNA. A mutation is a change in DNA sequence and is not necessarily always bad. However, when a mutation occurs in an important gene and alters the ability of the gene to function normally, it can contribute to genetic diseases. These mutations can occur spontaneously, due to errors in DNA replication and repair, or as a result of exposure to chemicals.

Since offspring inherit mom’s mitochondrial DNA, fathers with mitochondrial diseases aren’t at risk to pass on the disorder to offspring. However, since a single cell contains many mitochondria, each with multiple copies of mtDNA, symptoms of mitochondrial diseases can vary. Given that the role of mitochondria is to produce power for the cell, mitochondrial DNA diseases often affect tissues requiring lots of energy like the heart, brain, and muscles. Just last month, a group from Cornell University published a study suggesting a link between mtDNA and some forms of autism spectrum disorder. Right now, treatment options for mitochondrial diseases are limited but as the understanding of mtDNA and its effect on diseases grow, so does our ability to target and come up with potential treatments.

Science Now + Beyond

Why haven’t we cured cancer yet?

Cancer is bad. It is scary, sad, depressing, maddening, frustrating, terrifying, and so much more. It is a unique “disease” that can strike anyone at any age in any tissue. And despite the progress made in cancer research, we are still waiting for a complete “cure”.

But why is that? What is it about cancer that makes it such a widespread, common, and deadly disease? And why is it that there is so much cancer research and yet, we seem to still understand so little?

Cancer is a genetic disease that tampers with the cellular machinery of healthy cells. To understand what cancer is and why we haven’t cured it, we have to first understand how healthy cells work.


Cells are the basic building blocks of our bodies. One of the most important cellular structures is the nucleus. It contains most of the cells’ genetic material (DNA). The DNA is tightly coiled and stored in structures called chromosomes that act like a book filled with instructions (genes) that control the cell’s identity and actions.

In humans, there are two copies (alleles) of every gene – one from each biological parent. Among these genes include those that strictly deal with cell growth, division, and survival. When healthy cells are old, become damaged, or are no longer needed, they have genes that instruct repair or cell death (i.e apoptosis).

What goes wrong in cancer cells?

Changes in DNA, or mutations, happen. Generally, not all mutations are bad; they can actually be good! And all of us have mutations. It’s how we have genetic diversity. However, mutations in genes that control cell growth destroy the cell’s ability to detect damage and regulate growth. So you end up with uncontrolled cell growth and abnormal masses of cells, called tumors. Fortunately, not all odd cell masses are cancerous; they can be benign. Cancerous tumors are malignant, meaning they can spread to other tissues.

There are three main categories of genes that contribute to cancer.

Proto-oncogenes are genes important for cell growth and differentiation. In healthy cells, they regulate

necessary cell division and growth. They also control when cells stop dividing and take on more specific identities and functions (differentiation). If these genes are mutated, they can become an ‘oncogene’. Oncogenes promote uncontrolled cell growth. As you can imagine, oncogenes can lead to tumors.

Healthy cells also have tumor suppressor genes. A tumor suppressor gene tells cells to stop dividing and growing. Cells need to know when to stop cell growth, even under normal conditions. Damage to a tumor suppressor gene is often a “loss of function”: the cells lose their ability to stop growth. Usually these types of mutations are recessive, meaning that both copies of this gene (one from each parent) must be damaged to fully lose function.

The third category of genes commonly mutated or damaged in cancer is DNA repair genes. Normal cell division includes replication and manipulation of DNA with every cycle. Mistakes in DNA therefore occur regularly, but luckily there are DNA repair genes ready to correct and minimize damage. So, a mutation in ONE oncogene or tumor suppressor gene alone can be fixed to prevent disease. But remember- in cancer, if genes in all three categories of genes are damaged, all of the cellular checkpoints are broken, facilitating further DNA damage and cellular dysregulation.

What does this all mean?

Knowing that cancer is characterized by multiple mutations in multiple genes caused by multiple sources, how do we “cure cancer”? Each case is unique and can result from an endless combination of genetic changes. Mutations that cause cancer can be both sporadic or DNA damage caused by the environment. But even within those, the same cancer causing risks can create mutations in different genes for different people. Plus, there are so many cancer-causing factors and these are just the ones we know! We use the word ‘cancer’ as though it is one disease but it is not a singular disease.

This is part of the struggle scientists face. They can study patterns and correlations of specific genes and mutations and how they manifest in people or investigate if certain environmental factors increase risks but it will take time before scientists understand enough to make a “cure”, if it is possible. Luckily, scientists thrive on the challenge of the unknown. With this determination, scientists will continue to chase cancer to find a cure and continue to further the ever-evolving field of cancer biology.

But in the meantime, finding a cure for cancer will continue to be a bit complicated.