An Interview With p53: A Celebrity In The Cancer World

Well, as you might have guessed by now, I am a bit fascinated with p53. So, I took some time out and built myself a machine that shrunk me down to the molecular level, with the help of my good friends Hank Pym and Wayne Slazinski. I took a violent journey through one of my cells in my friend Kev’s body (you know, molecules are so jittery in there, it’s like a chemical mosh pit). I had to get an appointment to meet p53 in person for an interview and had to wait for a long time before I saw him. He’s busy, you know? It was a really short interview. Although, it was all worth it, in the end. p53 is an interesting molecule, for sure.

So, this is how it went.

Hello, Mr. p53. It’s an absolute pleasure to meet you!

Yes, it’s a pleasure to meet you, too. You look strange, though. New around here?

Yes, Sir.

Well, I have been informed that you’re here to interview me. Go on, then. I have no time to waste.

Sure. First of all, how did you get the name p53?

Well, you know. We don’t really have names here. But, humans love classifying stuff. So, they made me squeeze through a mesh of gel once, while I was being chased by electricity. Later, they said I weighed 53 kilodaltons. And gave me the name p53 for protein, 53 kilodaltons. And I don’t even weigh 53 kilodaltons! I weigh 43, and some. Do I look fat? No, right?

Are you happy with your name?

No, I’m not. It’s boring. There’s this fellow I know who works at Neuron District, they named him “Pikachurin“. Now, that’s a good name. Who doesn’t love Pokemon? And there’s my good friend, who they’ve named Sonic Hedgehog. With all the work I do, the least they could’ve done is call me DragonSlayer or something.

So, Mr p53. People want to know what you do in Cell City. Could you elaborate on that, please?

Well, it is quite complex. And I don’t really think you’ll understand. But here’s the gist of it, okay? At the heart of Nucleus Town, we’ve got the blueprint for Life, that we’ve received from our forefathers. It’s our holy scripture. You call it the Genome. That is the foundation of All Life. I wouldn’t want to get philosophical, but it’s beautiful. The information to give me life is also stored there, in Chapter TP53. You call these chapters Genes.

Sure, but you still haven’t told us what you do?

Well, while we try to replicate the scripture everytime we expand, some errors do happen. When that happens, shit hits the fan.

Mr p53, I would advise you to kindly refrain from using profanity.

Sorry. I mean, change is necessary. You know? That’s how you improve. If nothing changes, everything will be boring. We do encourage experimentation with the Genome for improvements. That’s how we’ve managed to make it so far. But, sometimes, changes can be bad. Like, I know some fellows here, who are really nice, like Ras. Something goes wrong in his genes [you call it mutation], and he starts acting all weird. Suddenly, he just wants to expand without checking for errors. And he won’t stop. Fortunately, that’s where I come in.

Finally! We get to know what you do!

Will you stop interrupting, man? You mess up my flow.


See, I basically look for errors, and if I find them, and act accordingly. The Scripture must remain safe, that’s the plan. So, I either ask my subordinates to correct the error, or I stop the expansion midway. There are many of us involved in this, each of us doing something. Sometimes, when we can’t do anything about the error, we destroy the Cell. It’s painful to watch. But that’s for our own good.You call it apoptosis. It’s named after a Greek word that describes leaves falling in Autumn. Or petals falling from a flower. It’s the balance of life, you see. Birth and death. Ying and yang, you know?

So, is that why they call you Guardian of the Genome? 

Yes. I make sure the Genome is replicated faithfully, and nothing like cancer happens. That is essential. Cancer is when we start expanding endlessly and invade other worlds. I try to stop that and usually succeed. But sometimes, something goes wrong in my gene, and I get sort of like, lazy. I don’t do what I’m supposed to do. So if something goes wrong, I don’t really care anymore. So, basically, I am what you call a ‘tumour suppressor‘. If all versions of me go wrong in a body, it can lead to disaster. Anyhow, in about 50% or more cancer, there’s something wrong with me. *sighs*

You’ve been voted “Molecule of the Year” in 1993 by Science Magazine. How do you feel about that?

Well, it was quite an honour, obviously. I felt like all these years of hard work was finally being recognised. And now I’m sort of a celebrity. Like, it’s 22nd January, 2017 today, and already 427 article about me have been published since 1st Jan, 2017. So, you could say I’m quite famous. *winks*

Thank you so much for your time, Mr p53. 

No problem, buddy. Be careful when leaving. People who are new get lost in this City. Goodbye!


And, I was back. So, that’s the story of how I met my hero.

What do you think about Mr p53? Leave it in the comments below!


Five Books on Cancer Every Booklover Must Read!

What are some good books on cancer?

A good way to learn about any subject is to read good books about it. The same goes for cancer. Below, I’ve listed five of my favourite popular science books that feature cancer. However, I apologise for having avoided fiction (saving it for another day). So, if you’re expecting to see The Fault in Our Stars, you’re in the wrong place.

Please note that the following list is not a countdown.

1. The Emperor of All Maladies: A Biography of Cancer by Siddhartha Mukherjee

This Pulitzer Prize winning book chronicles one of humanity’s oldest battles: the fight against cancer. Written by scientist and physician Dr Mukherjee, the book takes the reader on a journey spanning thousands of years, peeling through layers of history surrounding the emperor of all maladies and giving us a hopeful glimpse into the future. This book is a must-read for anyone hoping to get an idea of where we are in the race against cancer.

2. The Cancer Chronicles by George B. Johnson

When journalist George Johnsons’s wife Nancy was diagnosed with a rare form of uterine cancer, he was faced with a feeling of utter hopelessness and fear. Hoping to learn more about the disease, Johnson spent the next few years documenting its impact on people in the past and the present. This book is a personal story and speaks of the fears and hopes of someone who’s losing a loved one to cancer.

3. p53: The Gene that Cracked the Cancer Code by Sue Armstrong

p53 is one of the most famous genes and its role in cancer development is as important as it is complex. This book is a tribute to the world’s most studied gene, taking the reader through its discovery and role in cancer development. It is an interesting book that gives the reader a peek into the lives of cancer biologists and how sometimes, serendipity can lead to great discoveries.

4. One Renegade Cell by Robert Weinberg

One of the best popular science books on cancer, One Renegade Cell is authored by none other than Robert Weinberg, who discovered the first human oncogene. Written in simple and accessible language, the book focuses on how one renegade cell can lead to cancer. This is a must-read for anyone who wishes to acquire a basic understanding of the nature of cancer.

5. The Immortal Life of Henrietta Lacks by Rebecca Skloot

This book is about Henrietta Lacks, an African-American woman who was the unwitting donor of cells derived from her cervical cancer. These cells gave rise to the first immortal cell line called HeLa. The book traces the history of Henrietta Lacks amidst issues such as medical ethics, consent and privacy. Though not entirely cancer-centric, the book is an interesting read for science non-fiction readers.

EXTRA: If you have a bit of a background in biology, and want to know more about cancer from a technical perspective, a good introductory paper would be The Hallmarks of Cancer by D. Hanahan and R. Weinberg. Also, if you like, The Emperor of All Maladies has been made into a three-part documentary that is available online.

What’s your favourite book on cancer? 

Chemotherapy: The Good, The Bad and The Future


Is it true that chemotherapy can give you cancer?

Someone asked me this once, and announced that if they were to ever get cancer, they would reject chemotherapy because they wouldn’t want to “lose their dignity”. When we think about chemotherapy, we think of alopecia (hair loss), nausea, weakness, weight loss, immunodeficiency, among other terrible things. Some patients fear chemotherapy more than the cancer itself. What makes chemo so scary? Why does it have to be this way? I try to answer some of these questions briefly, and comment on targeted therapies as cancer treatments of the future (I’m being quite optimistic here).

According to the website WebMD, chemotherapy is defined as a type of treatment that uses drugs to destroy cancer cells. Simple, right? Not really.

Chemotherapy is one of the most effective ways of treating some cancers. However, the treatment has a dark side because of its effect on healthy cells. When Sidney Farber, the father of modern chemotherapy, used aminopterin to treat childhood leukaemia in 1947, the trial was viewed with equal amounts of enthusiasm and concern.  In the original study, Farber expressed his concerns over non-specific cytotoxicity (cell killing), stating “The toxic effects are stressed in these histories, and the temporary nature of the remission is emphasised.”

But why do chemotherapy based treatments conveniently ignore the fundamental doctrine of medicine, i.e. Primum non nocere (First, do no harm)? This can be explained by introducing what is called the “therapeutic window”. It is defined as “the range of dose which produces a therapeutic effect without causing any significant adverse effects to the patient”. Simply, antibiotics have a wider therapeutic window due to the significant differences between human and bacterial cells, leading to drugs that can target the foreign cell, leaving the host cell unharmed. Cancer cells, however, are so similar to their originators (normal human cells) that designing a drug specific to them has been an exceptionally daunting task.

This means that almost all chemotherapeutic drugs developed initially were non-specific. While the success of conventional chemotherapy lies in producing cytotoxicity, the narrow therapeutic window implies that normal cells would inevitably caught in the crossfire. Simply, the question is: How many cancer cells can we kill, without killing the organism itself?

Most chemotherapeutic drugs inhibit cell proliferation by affecting the synthesis of DNA, or by introducing damage to the genetic material. Since cancer cells divide much rapidly as compared to normal cells, the drugs seem to work by producing DNA copying errors leading to cell death. However, other tissues that contain fast-dividing cells are also affected, including the lining of the gut and hair follicles. This leads to baldness and nausea, some of the side effects most commonly associated with chemotherapy in cancer. There are other side effects involved with chemotherapy, which differ based on the drug used. If you have been advised chemotherapy, kindly ask your Doctor for advice.

Coming to the initial question. Yes, some chemotherapy drugs can, in fact, increase the risk for secondary cancers. Quite ironic, indeed. Due to their method of action involving DNA damage, these drugs can sometimes lead to the development of secondary cancers unrelated to the primary cancer. While chemotherapy induced secondary cancers are usually blood cancers (such as leukaemia), some solid tumors can also result from chemotherapy, such as testicular cancer. This web page by briefly deals with chemotherapy and its link with secondary cancers, and is worth looking at.

While I have taken time to write a blog post about the side effects of chemotherapy. I, by no means, intend to discourage anyone from receiving chemotherapy as treatment if advised. Chemotherapy can be an extremely powerful weapon against some form of cancers, and can lead to impressive regressions. Remember to always consult your Doctor regarding potential adverse effects and success rates, when in doubt. Make sure you make the right decision!

The next question is: What are we doing to help change this? With the advent of molecular biology, cancer has been classified and sub-classified based on subtle molecular differences. Some cancers can be addicted to a certain oncogene. Identifying such addictions can reveal a cancer’s weakness (Achilles heel, if you will). For example, CML’s (chronic myeloid leukaemia) addiction to the BCR/ABL protein lead to the development of imatinib, a targeted drug that has proved to be (sort of) a miracle drug for CML patients. Being tailored to target a cancer-specific molecule, targeted therapies widen the therapeutic window for cancer treatments, leading to impressive results.

The hunt is on for other targets, and improved personalised medicine may prove to be the elusive “cure” we’ve always hoped for. More about targeted therapies in the next post!

What comes to your mind when you think of the word ‘chemotherapy’? Do you have any other questions? Leave them in the comments below. 

Further reading:

How Chemotherapy Drugs Work – American Cancer Society

How Chemotherapy Works –  National Institute of Health

How to Cure Cancer at Home with Baking Soda!

Is it true that you can cure cancer with baking soda?

Well, yes. And today I’m going to show you how.

It’s absolutely simple!

Take baking soda, flour and salt in a bowl. In another large bowl, add melted butter, sugar, eggs, and vanilla and beat lightly.  Gradually beat in the flour mixture and combine. Add milk slowly, and combine. Put the mix in a pre-heated oven (350 degrees F/175 degrees C) for about 30-40 minutes, cool for 10 minutes and enjoy some delicious vanilla cake while reading the following rant on why home remedies for cancer don’t really work. (Complete recipe available on request!)

Every time I log on to facebook, I see at least one post about how “big pharma” is hiding the cure for cancer, which is X, to increase profits.

Now, X here, can be one of the following:

1.Baking soda

2. Grapes

3. Carrot juice

4. Vitamin B17 (LOL)

5. Black salve (Stay away from this)

6. Coconut oil (or specifically, lauric acid, a component of coconut oil)

7. Plenty of other random stuff

So, where do these social media scientists/concerned netizens/well-read researchers get these colourful ideas? Well, sometimes these ideas condense out of thin air like a magician conjuring rabbits from an empty hat. On most occasions, though, these ideas have some substance, actual scientific evidence that was a precursor to a bad interpretation and bad reporting. Old Wives’ Tales gone wrong, in the information age.

Why does it matter?

Because some of these articles can be persuasive enough to make people forego conventional treatment and go for a glass of coconut oil because an article on facebook convinced them to do so.

Also, they back their content with evidence: a peer-reviewed article about coconut oil killing cancer. I am not, however, criticising the article, it’s a perfectly okay article. Lauric acid (a component of coconut oil) does kill 90% of colon cancer cells. However, the lousy article on facebook skimmed over something crucial word in the original study: the words “in vitro”. This basically means that lauric acid kills 90% of colon cancer cells grown in a petri-plate, NOT WHEN INGESTED BY AN ORGANISM. The same argument can be extended to any cytotoxic compound, even cyanide, which would kill 100% of any cancer cell in vitro.


Speaking of cyanide, the new star of the sham campaign is vitamin B17 (not a vitamin, I swear). Vitamin B17 (pffft…), also known as laetrile, is the synthetic form of amygdalin, a compound naturally found in some nuts. According to Cancer Research UK, there is no evidence to support that laetrile cures cancer. Any evidence therefore, is anecdotal. And as a wise man once truly said, “The plural of anecdote is not data”. There is one study, however, where laetrile did kill cancer cells in vitro in the presence of an enzyme called glucosidase. Why? Because the enzyme breaks vitamin B17 down to produce cyanide. Yes, cyanide. Doesn’t sound too tempting now, does it?

What about baking soda, though? Well, the famous baking soda theory says that cancers cannot survive in an alkaline environment, so drinking a solution of baking soda can help you clear out cancer. Well, again, not entirely true. Baking soda is, for now, best used for baking (cupcakes, yay!).

Misinformation is running rampant on social media, and the results can be heartbreaking. A 1o-year-old girl in El Salvador died after her parents rejected conventional treatment for her liver cancer, opting for mud treatments rubbed on her abdomen and herbal teas, instead (story here). Another woman lost half of her nose while trying to use black salve (a corrosive herbal remedy) as a treatment for her skin cancer (story here: GRAPHIC CONTENT). And this doesn’t end with cancer treatment, there are multiple stories about how people mismanaged their illnesses, based on anecdotal hearsay.

Bottom line: Cancer is complex. If it wasn’t, we would’ve cured it long ago. No matter how smart you think you are, you must ALWAYS listen to a medical professional when it comes to your health. We are not controlled by big pharma, we are not hiding a cure, and we definitely don’t want to rip you off.  Conspiracies can be fun (I know you secretly love watching some David Icke videos for a good laugh), but please don’t make decisions on your health based on facebook stories or youtube videos. Okay? We love you.

DISCLAIMER: This blog post was sponsored by Big Pharma Industries


Wiping Out Cancer With Gold

Why do some cancers come back, and what can we do about it?

Conventional cancer therapy involves a combination of surgery (manual excision of a cancerous tumour), chemotherapy (administration of anti-cancer drugs) and radiotherapy (the use of high-energy rays to kill cancer). However, sometimes, residual cancer cells can evade therapy and grow back into tumours, giving rise to cancer again. This is true especially after surgical excisions, where microscopic residual clusters are left behind. This condition is known as microscopic residual disease (MRD). While several diagnostic methods are available to detect residual cancer cells to avoid a possible recurrence, it is difficult to identify a small population of cancerous cells and selective elimination poses another challenge. Unfortunately, there’s not much we can do about it, at the moment.

The future, however, looks promising. Recently, researchers from the US and Belarus have come up with an innovative solution to this problem. In their study, they’ve developed a system where gold nanoparticles to target cancer cells and selectively destroy them. The procedure, called Plasmonic NanoBubble (PNB) nanosurgery, uses gold nanoparticles bound to antibodies selective for the cancer cell’s receptors. The cancer cells engulf these nanoparticles by a method called “receptor mediated endocytosis”, which basically means the intake of foreign material into the cell using surface receptors.

Once the nanoparticles are inside the cell, the nanoparticles are heated using infrared lasers (yes, lasers). The surrounding fluid in the cell vaporises, causing it to create a nanobubble that rapidly expands and collapses. Depending on the number of gold nanoparticle clusters in the cell, multiple nanobubble explosions eventually lead to cell death. While this happens on a scale too small to be optically measured, researchers could detect the procedure’s efficacy by measuring sound waves created by the micro-explosions. In the original study, mouse models with 3 to 30 residual cancer cells and MRD were treated with PNB nanosurgery, resulting in 100% tumour-free survival, and no local recurrence.

According to an article on Physics Central, this method is sensitive enough to selectively mark and destroy cancer cell clusters containing as few as three cancerous cells. This can be extremely beneficial for targeting and selectively eliminating microscopic clusters of cancer cells post-surgery.

As with any development in cancer therapy, there have been concerns regarding safety and selectivity. In an article published in Science, it has been mentioned that the procedure has been fine-tuned to enhance selectivity and avoid any damage to surrounding tissue. This has been achieved by two means: attaching an antibody to the gold nanoparticles to enhance selectivity and the use of ultrashort laser pulses to avoid collateral damage, as this avoids the heat from spreading to surrounding tissue.

PNB nanosurgery is going to undergo human trials in the next 2 years, and we’re all hoping that it passes the test.

As awesome as this sounds, what’s even more awesome (and so, so satisfying to watch) is a video of cancer cells exploding when hit by a laser pulse. Check out the following video, which describes the procedure in detail with snippets of exploding cells from the original study.

If you wish to, you can download a short (super-short) video of exploding cells from the original study by clicking here (DIE, CANCER, DIE!).

Do you have a question about cancer? Leave it in the comments below!

When Cancer Runs In The Family


Source: National Cancer Institute


Cancer is a genetic disease. It is caused by DNA mutations that lead to disruption of normal processes in the cell, leading to the uncontrolled growth of that cell. However, the words “genetic” and “hereditary” are often confused, leading people to believe cancer is inheritable.

Most cancers are caused by genetic factors, lifestyle choices and exposure to environmental carcinogens. Some forms of cancer, however, can be inherited. For example, approximately 45-90% of women with a faulty copy of BRCA1 or BRCA2 gene will develop breast cancer. Other cancers that seem to have an inheritable component include breast cancer, ovarian cancer, retinoblastoma, prostate cancer, etc. Find more details here.

But, what happens when you’re predisposed to have multiple cancers throughout your life? What happens when cancer runs in the family?

In 1969, two American physicians, Frederick P. Li and Joseph F. Fraumeni Jr., puzzled by a high incidence of cancer in some families, worked their way through medical records and death certificates of 648 childhood rhabdomyosarcoma patients. Rhabdomyosarcoma is a rare type of cancer that affects the musculoskeletal system.

Li and Fraumeni closely studied families with high incidence of soft tissue sarcomas, trying to establish an inheritable cause for the disease. They published their findings in Annals of Internal Medicine, where they suggested a familial cause for the high incidence of cancer in some families. But they did not know what was causing it.

I will briefly take you through the history of what is now called Li-Fraumeni Syndrome (LFS), which is responsible for an inheritable predisposition to multiple cancers.

In 1979, scientists discovered a gene they named TP53, while studying the oncogenic properties of SV40 viruses. It was later identified as the target of the SV40 virus, during the process of oncogenesis. It took a long time before scientists realised that p53 (another name for TP53) was a gene that contributed to preventing cancer, not causing it.

Ten years later, in 1989, Bert Vogelstein from John Hopkins School of Medicine revealed the true identity of p53 as a tumour suppressor, a protein that suppresses the development of cancer. An oncogene antagonist, if you may. In the following two to three years, studies on p53 increased dramatically, leading to a number of publications.

p53 is the most frequently mutated gene in human cancer, with a mutation present in almost 50% of cases. This has led to p53 being called the “Guardian of the Genome”. It is also the most studied gene in history, with 83,167 hits on PubMed!

Sometimes, a copy of the TP53 gene undergoes a germline mutation (heritable variation in germ cells). Children born from parents with a germline TP53 mutation are known to suffer from Li-Fraumeni Syndrome. Because p53 is responsible for maintaining genome integrity, loss of function of the p53 protein leads to multiple cancers throughout the life of the individual. p53 was pinpointed as being the cause of Li-Fraumeni syndrome in 1990, before which the syndrome was assumed to be caused by a virus.

People suffering from Li-Fraumeni Syndrome usually develop sarcomas, cancers of the breast, brain and adrenal glands. This is true for almost 80% of LFS cases. The risk for developing sarcomas and female breast cancer is almost 100 times greater than the general population.

In the early 1990s, Dr Maria Isabel Achatz studied a population in Brazil that had a high incidence of familial cancers, arising from a similar mutation, leading researchers to believe the population might have shared a common ancestor with the germline TP53 mutation. While this is perhaps the largest known population to have Li-Fraumeni Syndrome, Dr Achatz suggests there might be other populations with high incidence of familial cancers.

Being diagnosed with Li-Fraumeni Syndrome can be scary and depressing. In Sue Armstrong’s book p53: The Gene That Cracked The Cancer Code, Armstrong mentions a man with a family history of LFS, who after having himself tested for the mutation, committed suicide before he got the results. It was later found that he did not have the mutation.Dr Achatz has had patients with as many as 15 different tumours throughout their lives. This can be quite alarming, especially when it affects the patient at a young age. Usually, patients require counselling and emotional support from family and friends.

While Li-Fraumeni Syndrome appears to be rare, with only 400 cases reported since first being described in 1969, the effect it can have on someone suffering from the disease can be devastating. The George Pantziarka TP53 Trust in the UK is dedicated to providing support to people suffering from LFS in the UK. They also provide screening for people with supposed LFS, and help promote research related to the syndrome.

The TP53 Trust estimates that 1 in 10,000 or 1 in 25,000 people in the UK might be carriers of LFS, based upon predicted TP53 mutation rates. I am unsure about the validity of these claims, as I could not find sufficient supporting evidence.

For more information, buy Sue Armstrong’s book “p53: The Gene that Cracked the Cancer Code”. It’s an amazing book that chronicles the discovery of p53 in dizzying detail.

Do you have a question about cancer? Leave it in the comments below!

“Do plants get cancer?”

Photo credit: Dialysis Technician Salary


Before we try to answer that, let’s talk about what cancer is.

Cancer is an umbrella term used to describe a few hundred diseases with the same pathological origin: the uncontrolled growth of cells.

We have a few trillion cells in the adult human body, each containing a complete copy of our DNA, the genetic blueprint for life. The DNA is housed within the nucleus, and controls and regulates the workings of the cell.

Sometimes, due to intrinsic (errors in DNA replication, spontaneous mutation) or extrinsic factors (cigarette smoke, alcohol, asbestos), the DNA gets corrupted through mutation. These corrupted pre-cancerous cells seek one goal: immortality.

The cells proliferate rapidly, ignoring all signals to slow down or stop dividing, forming an aggregate or mass of cells, sometimes closely resembling their tissue of origin. This localised mass of cells is called a benign (fancy word for harmless) tumour. Bear in mind, this localised group of cells is not considered cancer, yet.

At some point, greed overtakes this population of cells, and everything spirals out of control. These cells break free from their original tumour, seeking refuge elsewhere. Chaos ensues. The process of migration from the tissue of origin to another tissue is called metastasis, and the cancer is now called metastatic cancer. Meanwhile, the tumour is now called a malignant tumour. This is the truest form of cancer.

So, do plants get cancer?

The simpler answer would be to say no.

Plants do have tumours, however.

Agrobacterium tumefaciens is a rod-shaped, Gram-negative, soil dwelling bacteria that can infect about 140 species of eudicot plants including grape vines, rhubarb, horse radish, etc.

This bacteria has a plasmid (an extra chunk of circular DNA) called the “Tumour inducing plasmid” or Ti plasmid. This plasmid overrides the plant’s DNA by integrating itself into the plant’s genome, leading to the formation of a tumour. The disease is called “crown gall disease”, which has also been described as a plant cancer. It might cause stunting of growth in seedlings or young plants.

While A. tumefaciens and its effects are widely studied, there are other fungal and bacterial pathogens that cause plant tumours as well.

From a wider perspective, a crown gall tumour might be classified as cancer. Similar to liver, stomach and cervical cancer in humans, caused by pathogens that stimulate uncontrolled growth and division of host cells.

However, human cancers are different. One of the hallmark characteristics of human or animal cancers, lacking in plants is metastatic invasion by the tumour. The process of metastasis in animals is facilitated by the movement of cells using the bloodstream or the lymphatic system to get around. Since plant cells have a thick cell wall, they are usually held in place. Lack of movement implies that a plant tumour cannot metastasize.

So, plants don’t really get cancer the way humans or other animals do. However, there’s a striking resemblance between plant tumours and premalignant animal tumours. A study published in 2010 suggests plant and animal tumours may have overlapping mechanisms and pathways that contribute to tumour formation. Interesting!

Do you have a question about cancer? Leave it in the comments below!



“Sniff, sniff!” “Is that Cancer?”


Source: Wikimedia Commons

Cancer sucks, it’s true.

But did you know, cancer stinks as well?

Someone asked me if cancer can affect our body odour. Well, yes.

Dogs, our furry friends with supernatural olfactory powers have demonstrated the ability to sniff out cancer, even during its early stages. Is there anything dogs can’t do?

So, how do they do it?

Cells require means for energy production and waste disposal to survive. This requires a complex series of chemical reactions called metabolic reactions (or metabolism) that can sometimes be intertwined in a web-like pattern.

Metabolism produces waste, molecules that are the products of careful processing by the cell (meticulous creatures, cells). Normally, the metabolic pathways in a cell are fixed, and for a normal population (of cells or people), they would be identical.

But because cancer is  weird, it likes to do stuff differently.

A characteristic of cancer cells is that they have altered metabolic pathways, that are sometimes beneficial for the cancer cell. For example, some cancer cells binge on glucose, because they process it in a different way, making the energy payoff extremely inefficient.

Okay, but how do they do it?

A widely accepted explanation is this: Because cancer cells have a weird metabolism, they produce metabolic waste that smells weird (to dogs, at least). And our friends with superpowers can (with some training) identify the funny smell of those little molecules that do not belong.

According to the website, compared to humans, the olfactory region of a dog’s brain is 40 times larger (that’s a lot!). This makes them much, much more sensitive to smell compared to us (estimates range from about 1,000 to 10,000,000 times more sensitive, depending on the breed). This helps them identify extremely faint odours, like those produced by the metabolic waste from cancer cells, or other biomarkers for various disorders.


A double-blind study published in the journal European Urology found that a Belgian Malinois shepherd could be trained to identify prostate cancer in patients by sniffing the odour of their urine. The dog (now my favourite superhero) could correctly identify prostate cancer in 30 of 33 cases (mind=blown).

Another study published in the journal Cancer Biomarkers, involving a group of four trained dogs, found that dogs could identify bladder cancer in urine samples with a sensitivity of up to 73%. This study also suggested the presence of volatile biomarkers in the urine, that help dogs identify cancer.

As if that wasn’t awesome enough, this study found that trained dogs could identify breast cancer and lung cancer with 88% and 99% accuracy, respectively. How? By sniffing the patient’s breath, of course! The study also showed that dogs could identify cancer during all 4 stages of the disease! If that isn’t amazing, I don’t know what is.

Coolest superpower ever, am I right?

Is this helpful?


A common non-invasive test for diagnosing prostate cancer is called the Prostate-Specific Antigen (PSA) test. It measures the amount of prostate-specific antigen (a protein produced by the prostate gland) in the serum, where a higher concentration of the protein usually correlates with the presence of cancer.

A review published in the Indian Journal of Surgical Oncology mentions the sensitivity of the PSA test to be 32% for detecting any prostate cancer and 68% for detecting high-grade cancers (sensitivities vary based on test parameters). When we compare this to the sensitivity of a sniff test (91%), we realise that using dogs as non-invasive means for preliminary diagnosis is a pretty good idea.

Also, consider cancers like bladder cancer, where invasive means of diagnosis are necessitated by a lack of non-invasive methods. The only non-invasive method for diagnosis of bladder cancer involves cytometry (a fancy word for cell counting), where cancer cells are manually counted in a blood or urine sample.  A simple sniff test, with a good enough sensitivity of 73% (as mentioned earlier) sounds like a great alternative.

Why aren’t we funding this?

Despite being a relatively new idea, disease detection (also called bio-detection) by dogs is gaining popularity. Apart from cancer, it has been reported that dogs can sniff out migrainesnarcolepsy, hypoglycaemia (fancy word for low blood sugar), seizures, etc. Dogs do this by recognising various volatile biomarkers.

Groups like Medical Detection Dogs and Assistance Dogs UK in the UK are actively involved in the promotion of dogs for assistance and diagnosis of medical conditions. There are many other international groups supporting bio-detection dogs and related research.

Dr Claire Guest, the founder of Medical Detection Dogs, discovered a lump in her left breast after her pet labrador kept nudging her breast with its nose. This led to an early confirmatory diagnosis, saving her life. She believes using dogs for early cancer diagnosis is a sure way to save lives. And I agree!

In conclusion, dogs are awesome.

UPDATE: Why aren’t we doing this, yet?

Because, the evidence, although promising, needs to be validated by means of critical evaluation by the scientific community. Some sceptics argue that present studies require precision. Volatile biomarkers need to be identified, and reliability of sniff tests needs to be assessed and compared against standard diagnostic methods.

P.S. While I do not suggest replacing traditional diagnostic methods with a sniff test, it might be useful to consider sniff tests as a preliminary test in diagnosing cancers.

And if you ever needed a reason to love dogs, you have one now.

Do you have a question about cancer? Leave it in the comments below.