Why are babies rarely born with cancer?

Why are babies rarely born with cancer?

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Childhood cancer is fundamentally a disease of dysregulated development. Why does it rarely occur during the fetal period, a time of enormous growth and development?

Nature tends to turn against cancer not towards it. Cancer exists when cells begin to multiply with abnormal features, without correction. Cancer is the consequence of many many harmful mutations, which inhibit the correct reading of DNA.

Cancer takes time to develop, not months, but years. Also, babies don't have old tissues, so there haven't been as many divisions, or as many opportunities for mutations, as a 5 yr old or a 10 yr old has gone through.

Although rare, Neuroblastoma is a cancer that babies CAN be born with. Nerve cells develop early, week 5 of fetal development.

Perhaps someone else could talk more about the biological mechanisms which really make cancer more a reality for older organisms, but probablistically, it doesn't make sense that a newborn baby would have cancer.

I looked up these links, to try and address your question.

cancer in general

why cancer takes time to develop

cancer in babies

In adults, lifestyle-related risk factors, such as smoking, being overweight, not getting enough exercise, eating an unhealthy diet, and drinking alcohol play a major role in many types of cancer. But lifestyle factors usually take many years to influence cancer risk, and they are not thought to play much of a role in childhood cancers.

A few environmental factors, such as radiation exposure, have been linked with some types of childhood cancers. Some studies have also suggested that some parental exposures (such as smoking) might increase a child’s risk of certain cancers, but more studies are needed to explore these possible links. So far, most childhood cancers have not been shown to have environmental causes.

Open questions in biology

BMC Biology has a scope that extends across all of biology and that is reflected in the varied expertise of our Editorial Board. Because their input is in turn crucial in the selection of both our research and our commissioned content, we invited all of our Editorial Board members to mark the tenth anniversary year of BMC Biology with short contributions representing their views on pressing or just interesting open questions in their fields, and thus to share their perspective with readers, contributors, and authors or potential authors of research submissions. Contributions will be added as new Editorial Board members join us.

Open questions: how do engineered nanomaterials affect our cells?

Our cells have evolutionarily conserved mechanisms that battle foreign and toxic materials to maintain cellular homeostasis and viability. How do these cellular machineries respond to engineered nanomaterials?

Authors: Daniela Barrios and Laura Segatori

Citation: BMC Biology 2020 18 :176

Published on: 24 November 2020

Open questions: how to get developmental biology into shape?

Recent technical advances have provided unprecedented insights into the selective deployment of the genome in developing organisms, but how such differential gene expression is used to sculpt the complex shape.

Authors: Timothy E. Saunders and Philip W. Ingham

Citation: BMC Biology 2019 17 :17

Published on: 22 February 2019

Open questions: why should we care about ER-phagy and ER remodelling?

The endoplasmic reticulum (ER) is one of the most complex organelles in the eukaryotic cell. Recent findings suggest that a process called ER-phagy plays a major role in maintaining the ER’s shape and function.

Citation: BMC Biology 2018 16 :131

Published on: 1 November 2018

Open questions: why are babies rarely born with cancer?

Childhood cancer is fundamentally a disease of dysregulated development. Why does it rarely occur during the fetal period, a time of enormous growth and development?

Citation: BMC Biology 2018 16 :129

Published on: 1 November 2018

Open questions: what are the genes underlying antagonistic coevolution?

Although the idea of coevolution was first presented 150 years ago, we still only vaguely understand the genetic basis of its workings. Identifying the genes responsible for coevolutionary interactions would e.

Citation: BMC Biology 2018 16 :114

Published on: 1 November 2018

Open questions: respiratory chain supercomplexes—why are they there and what do they do?

In the mitochondrial inner membrane the respiratory enzymes associate to form supramolecular assemblies known as supercomplexes. The existence of supercomplexes is now widely accepted—but what functional or st.

Citation: BMC Biology 2018 16 :111

Published on: 1 November 2018

Open questions: knowing who’s who in multicellular animals is not always as simple as we imagine

The ability of certain tumor cells of mammals and molluscs to spread from the original host to others reopens the question of distinguishing self from non-self. It is part of a wider phenomenon of cellular par.

Citation: BMC Biology 2018 16 :115

Published on: 15 October 2018

Open questions: CRISPR biology

CRISPR-Cas systems, the purveyors of adaptive immunity in archaea and bacteria and sources of the new generation of genome engineering tools, have been studied in exquisite molecular detail. However, when it c.

Citation: BMC Biology 2018 16 :95

Published on: 24 September 2018

Open questions: How many genes do we have?

Seventeen years after the initial publication of the human genome, we still haven’t found all of our genes. The answer turns out to be more complex than anyone had imagined when the Human Genome Project began.

Authors: Steven L. Salzberg

Citation: BMC Biology 2018 16 :94

Published on: 20 August 2018

Open questions: completing the parts list and finding the integrating signals

One of the great revelations of post-genomic biology has been the extent to which essential functions and mechanisms are conserved across vast phylogenetic distances. Because of this, we can look to the fruit .

Authors: Aurelio A. Teleman and Norbert Perrimon

Citation: BMC Biology 2017 15 :47

Open Questions: We don’t really know anything, do we? Open questions in sensory biology

Senses connect organisms to both the world and to each other, yet there is much we don’t know about them. Using examples drawn primarily from the author’s subfield of vision research, this article discusses fi.

Citation: BMC Biology 2017 15 :43

Open questions: Tackling Darwin’s “instincts”: the genetic basis of behavioral evolution

All of us have marveled at the remarkable diversity of animal behaviors in nature.

Authors: J. Roman Arguello and Richard Benton

Citation: BMC Biology 2017 15 :26

Published on: 3 April 2017

Open questions: how does Wolbachia do what it does?

A common symbiont of insects, the bacterium Wolbachia has been implicated in phenomena as diverse as sex determination, pathogen defence and speciation and is being used in public health programs to prevent mosqu.

Authors: Francis M. Jiggins

Citation: BMC Biology 2016 14 :92

Published on: 19 October 2016

Open questions: what about the ‘other’ Rho GTPases?

Rho GTPases have many and diverse roles in cell physiology, and some family members are very well studied, including RhoA, Rac1 and Cdc42. But many are relatively neglected, and fundamental questions about the.

Citation: BMC Biology 2016 14 :64

Published on: 4 August 2016

Open questions: seeking a holistic approach for mitochondrial research

In addition to their role as energy generators, mitochondria play critical and active roles in diverse signalling pathways, from immunity to cell survival and cell fate decisions. However, there remain many op.

Citation: BMC Biology 2015 13 :8

Published on: 5 February 2015

Open questions: The disrupted circuitry of the cancer cell

Citation: BMC Biology 2014 12 :88

Published on: 18 October 2014

Open questions: What has genetics told us about autism spectrum disorders?

Some of the most interesting questions in biology today, in my view, derive from the real advances in neuropsychiatry that have come largely from human genetics. Research in autism spectrum disorders (ASDs) ha.

Effects of premature birth can reach into adulthood

In the longest running U.S. study of premature infants who are now 23 years old, University of Rhode Island Professor of Nursing Mary C. Sullivan has found that premature infants are less healthy, have more social and school struggles and face a greater risk of heart-health problems in adulthood.

Sullivan has also found that supportive, loving parents and nurturing school environments can mitigate the effects of premature birth. She also found that premature babies are resilient and have a strong drive to succeed.

A research scientist at Women and Infants Hospital and an adjunct professor of pediatrics at the Alpert Medical School at Brown University, Sullivan has been studying a cohort of babies born prematurely at Women and Infants Hospital in the 1980s for 21 years. Since the lead study was launched by Brown University, the research has attracted a total of $7 million in federal grants. The study subjects are now 23 years old.

The latest investigation, funded by a $2.4 million National Institutes of Health grant to URI, is examining whether stresses experienced by pre-term babies lead to illnesses when they are adults.

In March, Sullivan presented her early findings at the Eastern Nursing Research Society in Philadelphia. Sullivan's co-investigator, cardiologist Jim Zeigler, will present their findings at the 27th Congress meeting of the European Group of Pediatric Work Physiology at Britain's University of Exeter Sept. 19 -- 23.

Her latest work is based on the "fetal origins hypothesis," which states that the stress response of pre-term infants, called the hypothalamic-pituitary adrenal (HPA) axis, is a mechanism underlying fetal origins of adult chronic diseases.

Pre-term birth sets up a stress response, which produces higher levels of the hormone cortisol, which is essential for regulating metabolism, immune response, vascular tone and homeostasis, Sullivan said. Her research is comparing cortisol levels in the adults who were born pre-term versus those born full-term and is assessing if cortisol levels among adults who were the sickest as premature infants are higher than those less medically and neurologically compromised.

Very low birth weight, repeated blood draws, surgery and breathing issues are among the major factors in stress levels for pre-term infants.

Among the early findings are:

  • Male gender and birth weight affect early adult pulmonary function.
  • The poorest pulmonary outcomes and higher resting blood pressure were for those born at extremely low birth weight.
  • Additional health data for age 23 years has not been analyzed yet, but data from age 17 revealed that physical health, growth, and subtle neurological outcomes were poorer in the preterm groups.
  • Infants with medical and neurological impacts had a 24 to 32 percent increase in acute and chronic health conditions.
  • Continued monitoring of adults born prematurely is warranted, not only during young adulthood but as they reach middle age.

Sullivan said one approach her team will undertake will be Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Risk Score at age 23 because it is strongly associated with coronary artery disease 10 to 15 years later.

"Continued monitoring of preterm survivors will enhance our understanding of the relative impact of prematurity and neonatal intensive care on later adult cardiopulmonary disease," Sullivan said.

"Since the beginning of the study, we have been asking the questions, can babies self-right themselves and do they have a resiliency that helps them overcome the challenges of pre-term birth?" Sullivan said. "Are there protective factors in the environment that mitigate the effects?"

Pre-term birth also affects even those infants not medically and neurologically ill in the following ways:

  • Effects of pre-term birth do not disappear after age 2 or even after pre-term children catch up physically with full-term babies.
  • Learning disabilities and other functioning issues often do not appear in premature babies until second grade and middle school years.
  • Pre-term infants with no medical conditions have more learning disabilities, struggles with mathematics and need more school services than full-term babies. One of Sullivan's studies determined that at least one-third of babies born pre-term needed school services at some point during their education. Out of that group, 22 percent of the healthy pre-term babies received school services. Almost one quarter of this group had an Individualized Education Plan (special education plan governed by federal and state law), with 15 percent receiving resources, 7 percent in self-contained classroom settings, and 11 percent receiving speech and language services.
  • Some children of pre-term birth are less coordinated, which may be related to brain development and effects of neonatal intensive care.
  • They have fewer friends and boys have more difficulty in school.

On the positive side, Sullivan found:

  • Children who were born pre-term have a persistent drive to succeed.
  • Children whose mothers provided a nurturing environment and who were strong advocates for them in school performed better academically, socially and physically. These are called protective factors and they work to counter the effects of pre-term birth.

"These findings are important for parents, nurses in the neo-natal intensive care units, teachers and staff in the schools, disability services offices in colleges and primary care providers," Sullivan said. "By identifying the issues pre-term babies face in childhood, adolescence and through adulthood, we can all be better prepared to take steps to mitigate their effects."

Story Source:

Materials provided by University of Rhode Island. Note: Content may be edited for style and length.

The case for genetically engineered babies

The first study to modify the genes of a human embryo, conducted at Sun Yat-sen University in China, has caused a furious backlash. Nature and Science, the world’s most prestigious scientific journals refused to publish the study, at least partly on ethical grounds. Instead they published commentaries calling for such research to be stopped. On Wednesday, the US government’s National Institutes of Health (NIH) restated their position that it will “not fund any use of gene-editing technologies in human embryos.” The NIH views such editing of the “germline” in human embryos as “a line that should not be crossed.” The stance will essentially stifle any research on gene editing in embryos in the US.

The ultimate goal of gene editing technologies is the capacity to make precise, controlled modifications to very specific areas of the genome. This would be a powerful ability. Gene editing unlocks access to an entirely novel way to fight disease which has been unreachable until now.

Around 7.9 million children each year are born with a serious birth defect that has a significant genetic contribution. If we could safely and easily correct these errors at the embryonic stage it would be possible to virtually eradicate this disease burden. In addition, 30% of all deaths worldwide are due to chronic diseases (such as heart disease, cancer, and diabetes) in those under 70. We all know of people who seem innately resistant to the perils of ageing and flourish well into their 80s and 90s. Gene editing could ensure we all have the best chance to live healthily into old age.

There are many challenges we must overcome to access the benefits of gene editing. The first and foremost is safety. Under agreed global research ethics standards, no experiments should be conducted where there is a high risk of harm to the participant, and a low chance of benefit. Gene editing is a long way from overcoming this barrier. Current techniques are imprecise, and lead to widespread damage to the genome. It would be highly unethical if a child was born whose genome was edited with current techniques.

However, we can still perform important research with current gene editing technologies in ways which harm no one. The pioneering Chinese study was performed entirely on abnormal, unviable IVF embryos that could never result in a live birth. Gene editing techniques could be greatly advanced by experiments conducted entirely in petri dishes, with embryos that would otherwise be destroyed and in accordance with existing regulations. The UK has a comprehensive and well-established regulatory framework for embryo research, including provisions that only embryos under 14 days old be used. This framework has successfully guided research involving embryos for over two decades.

Many fear that such research will lead us on a path to “designer babies”. People shudder at the thought of parents picking and choosing the genes of their children, just as they pick and choose the accessories for their nurseries. And we have good reasons to be concerned about this prospect. Widespread access to gene editing technologies could harm children and damage the gene pool. Genes fashionable in one generation may prove to be harmful in the next. In addition, parental control of the gene pool could reduce valuable forms of diversity. If every parent picks the same immunity genes for their children, it may make them collectively as vulnerable to pathogens as 19th century Irish potatoes.

But a fear of designer babies should not distract us from the goal of healthy babies. We know that some genes are bad in nearly every conceivable environment. There is no possible way that the gene which causes Tay-Sachs disease - a disease in which children develop normally for six months and then become progressively deaf, blind, unable to swallow, and paralytic, before dying at four - will benefit future generations. We lose nothing by editing this gene out of the human lineage.

There is no reason why we couldn’t restrict the use of gene editing technologies to removing valueless genes like this. For over two decades we have successfully used IVF and pre-implantation diagnosis (PGD) in this way. Regulations restrict the use of these technologies to the prevention of disease. Similar regulations could restrict gene editing technologies to therapeutic uses.

Some see unpredictable consequences, rather than designer babies, as the key risk in crossing the line to edited embryos. They see meddling with our genome as inherently dangerous – no matter which genes we target. Just dipping our toes in the gene pool will cause large ripples. These ripples will cause chaotic and uncontrollable consequences. According to this view it would be far wiser not to dip our toes in at all.

But the gene pool is a violent ocean rather than a peaceful pond. The human germline is in a constant state of flux. Every new birth adds new genetic variants, and each death removes some. Many permitted human activities, like delaying paternity, add to this chaos by increasing the number of random mutations in the germline. Any ripples caused by targeted therapeutic gene editing will likely be dwarfed by other factors.

No matter what is done in the UK, the line to edited embryos and intentional germline modifications will be crossed soon. In the US, work can go ahead with funding from foundations, charities, companies or private individuals. China will race ahead. Others will likely follow. If we want gene editing research to be done in a responsible way, we need countries with good regulatory systems leading the charge. The UK is one such country, where the Human Fertilisation and Embryology Authority can provide reassurance that no research or application proceeds without proper evaluation.

Whoever first crosses the line to edited embryos will find a powerful new resource in the fight against disease. Like many resources there are risks associated with its use. Indeed the risks are very high. However ignoring the resource is also risky. We may needlessly subject future generations to an endless cycle of suffering and disease.

What we ought to do is use this resource responsibly. We should harness its power to achieve good ends and restrict its use for purposes that are bad. This will not be achieved by simply withdrawing from research. It’s time to mount a responsible expedition across the line to edited embryos and the UK should lead the way.

Born with Cancer, Blessed with Life

When Rich and Stephanie Matthews were expecting their second child, a routine sonogram revealed that the developing baby might have a neuroblastoma—a sometimes deadly cancer that affects about 700 children a year.

How does a young couple handle such news? How did they brace themselves for the birth of a baby who might need surgery, chemotherapy or both? The couple described their journey for CURE, documenting the first year of life for their baby boy, Austin, in photos and words. Their story reminds us that cancer is not always the final victor.

[Stephanie] When that first sonogram showed we were having a boy, we knew what we would name our son: Austin, my grandmother’s maiden name.

[Rich] Time stops when you see and hear the heartbeat of your child for the first time. My mother was there for Austin’s first sonogram—Grandma’s first time seeing her grandson! It was an amazing moment. We left the doctor’s office as happy as could be.

[Stephanie] The call came to my desk phone in the newsroom, which was odd in itself because no one outside work calls on that line. The nurse said the doctor spotted something on my sonogram. “Nothing to worry about,” she said. It was probably just kidney cysts, which are common in boys. They wanted a specialist to check it out, just to be sure. I called Rich. He also told me not to worry. We had a healthy one-year-old girl, Avery, and would have a healthy baby boy.

[Stephanie] It was a few weeks later when we got in to see the neonatologist. Even though everyone told me not to worry, I did. After another sonogram, the doctor gave us what he called a differential diagnosis. That meant it could be several different things. First, it could be kidney cysts, but to him, the spots looked like they were above the kidneys. It could also be a sequestration, which is basically a piece of the lung that hadn’t formed properly. Then he gave us the final possible diagnosis: it could be neuroblastoma, a childhood cancer. But he was sure it wasn’t this, because neuroblastomas aren’t diagnosed this early in pregnancy. The next step, an MRI, would tell us more. So we left that appointment without the answers we‘d hoped to have.

We had the MRI with another doctor a few weeks later. The doctor called us back into her office to show us the scans. She focused on the area above one kidney, the adrenal gland. Then, in the kindest possible way, she dropped the bombshell: everything pointed to this being a neuroblastoma. “But neuroblastoma never shows up this early,” I insisted. She said it was rare to see it this early, but that’s what it looked like. I could feel the tears coming. Cancer? My child wasn’t even born yet, and already he had cancer? Rich grabbed my hand, and the doctor handed me a tissue. I was in a daze as she told us Austin might need surgery, chemotherapy or both. I left the appointment in a fog. I was supposed to return to work to produce the 10 o’clock news that night, but there was no way I could concentrate on work knowing the baby growing inside me likely had cancer.

[Rich] My wife and I are usually on the same page we are extremely close. But this challenge knocked the wheels off. Stephanie wanted to throw herself into preparing Austin’s room, putting together the crib, decorating. But I couldn’t bring myself to do it, fearing he would never make it home from the hospital. I wondered what we would do then—leave everything untouched as some tribute to our lost son? I knew I wouldn’t be able to bear moving things out of that room it would always be his even if years later we decided to have another child. For the first time in our relationship, we weren’t talking about it. Neither of us could sleep at all. We were sick for months.

[Stephanie] The next several months felt like I was running around in circles. I was getting sonograms every three weeks. The tumor was growing, but so was the baby, so it was hard to tell what that meant. I wanted to know what specialists I needed to see. I wanted to know who was going to deliver my baby and where. I wanted to make a plan, but no one could give me any answers. All the research I did online led me to heart-wrenching stories of children bravely battling cancer. I was at work one day, and an e-mail came in from a viewer. Her son had neuroblastoma, and her house was broken into while they were at the hospital. The e-mail included pictures of the toddler in a hospital bed attached to all sorts of machines. By then, I was seven months pregnant and very hormonal. I lost it. I started sobbing. I finally called my husband and asked him to come to work. We made a decision to take control of this situation. No more agonizing between appointments. No more surfing the Internet for answers. We were going to make our own plan.

She focused on the area above one kidney, the adrenal gland. Then, in the kindest possible way, she dropped the bombshell: everything pointed to this being a neuroblastoma.

He explained to us that neuroblastomas that are discovered during pregnancy are totally different than the ones that develop in toddlers and young children. He told us that new research showed neuroblastomas detected in utero often go away on their own.

[Rich] That night we found websites of a few local kids with neuroblastomas. Three of them wrote glowingly about the same pediatric oncologist. We called that doctor the next day, and they said they could see us that afternoon. On the elevator up to the office, a young patient was wheeled in beside us. She was riding in a red wagon just like the one we already had for our children. She was bald with a face full of pain but also hope. Would this happen to our son? Once we were taken back, the doctor came in and immediately put us at ease. He explained to us that neuroblastomas that are discovered during pregnancy are totally different than the ones that develop in toddlers and young children. He told us that new research showed neuroblastomas detected in utero often go away on their own.

[Stephanie] The doctor told us that the current thinking among the top researchers was to take a wait-and-see approach and not rush newborns into risky surgery. He answered all our questions. He offered to get me in touch with another mother going through the same thing. He told me not to worry, and I tried to take his advice.

This doctor helped us make a plan. He told me it would be no problem for my regular obstetrician to deliver Austin at the same hospital where I delivered Avery. He said we should bring Austin in 10 days after he was born. He would run some tests and then we could take it from there. For the first time I felt in control.

I made it almost to full term. I delivered a beautiful, 7-pound, 9-ounce boy on Sept. 23, 2009. We took Austin to see the oncologist 10 days later. They gave him a sonogram and an MRI. I cringed as the anesthesiologist put my tiny baby to sleep for the MRI.

[Rich] We worried about the results, planning for the worst but hoping for the best. It turned out the tumor was still there but not substantially bigger than the final prenatal sonogram. Austin’s liver and other organs looked good. The oncologist recommended we wait and monitor the situation with sonograms and blood tests every few months. If tests showed any signs of growth, or if we had any complications, we could reconsider surgery. We talked about it and decided to follow his advice.

[Stephanie] Austin has been so healthy in his first year of life that it’s hard to believe all the stress we went through those first few months. He hasn’t even run a fever. We’ve taken him to the oncologist every three months. The first two appointments, Rich and I went together, so we could support each other in case we got bad news. Even as healthy as he is, I still prepared myself for the worst, telling myself I need to be ready. But the past two times, we’ve gone solo, confident that we’ve beat this thing.

[Rich] It’s been a year now. Aussie’s tumor is still there, but it’s slowly shrinking. We just celebrated his first birthday with family and friends. He was like most every other 1 year old, smearing cake on his face and enjoying the packaging more than the presents.

[Stephanie] Aussie has a contagious laugh. He sounds like a little bird. Every time I hear it, I think about how lucky we are. We know other parents whose children are going through the surgery and chemotherapy we feared. We are truly blessed.

[Stephanie] At Austin’s one-year checkup, the oncologist said it would be our last visit. Aussie’s tumor is gone! It went away all on its own—no surgery, no medication. As always, I was prepared for bad news, but never expected this. I thought this would be something we’d have to monitor for the rest of Austin’s life. Just to make sure, I asked if this was something we’d need to put on his medical release forms when he tries out for basketball in the 7th grade. The doctor said, no, Aussie was totally in the clear. He also showed me the image from the prenatal MRI. You can clearly see the tumor, which looks giant on his tiny growing body. But now it’s gone!

I probably would have cried tears of joy there in the office if I hadn’t been chasing a one- and two-year-old around. All the way home, Austin just kept saying, “Wow, wow, wow,” and I kept thinking the same thing.

The Thalidomide Tragedy: Lessons for Drug Safety and Regulation

Many children in the 1960's, like the kindergartner pictured above, were born with phocomelia as a side effect of the drug thalidomide, resulting in the shortening or absence of limbs. (Photo by Leonard McCombe//Time Life Pictures/Getty Images)

In a post-war era when sleeplessness was prevalent, thalidomide was marketed to a world hooked on tranquilizers and sleeping pills. At the time, one out of seven Americans took them regularly. The demand for sedatives was even higher in some European markets, and the presumed safety of thalidomide, the only non-barbiturate sedative known at the time, gave the drug massive appeal. Sadly, tragedy followed its release, catalyzing the beginnings of the rigorous drug approval and monitoring systems in place at the United States Food and Drug Administration (FDA) today.

Thalidomide first entered the German market in 1957 as an over-the-counter remedy, based on the maker’s safety claims. They advertised their product as “completely safe” for everyone, including mother and child, “even during pregnancy,” as its developers “could not find a dose high enough to kill a rat.” By 1960, thalidomide was marketed in 46 countries, with sales nearly matching those of aspirin.

Around this time, Australian obstetrician Dr. William McBride discovered that the drug also alleviated morning sickness. He started recommending this off-label use of the drug to his pregnant patients, setting a worldwide trend. Prescribing drugs for off-label purposes, or purposes other than those for which the drug was approved, is still a common practice in many countries today, including the U.S. In many cases, these off-label prescriptions are very effective, such as prescribing depression medication to treat chronic pain.

However, this practice can also lead to a more prevalent occurrence of unanticipated, and often serious, adverse drug reactions. In 1961, McBride began to associate this so-called harmless compound with severe birth defects in the babies he delivered. The drug interfered with the babies' normal development, causing many of them to be born with phocomelia, resulting in shortened, absent, or flipper-like limbs. A German newspaper soon reported 161 babies were adversely affected by thalidomide, leading the makers of the drug—who had ignored reports of the birth defects associated with the it—to finally stop distribution within Germany. Other countries followed suit and, by March of 1962, the drug was banned in most countries where it was previously sold.

In July of 1962, president John F. Kennedy and the American press began praising their heroine, FDA inspector Frances Kelsey, who prevented the drug’s approval within the United States despite pressure from the pharmaceutical company and FDA supervisors. Kelsey felt the application for thalidomide contained incomplete and insufficient data on its safety and effectiveness. Among her concerns was the lack of data indicating whether the drug could cross the placenta, which provides nourishment to a developing fetus.

She was also concerned that there were not yet any results available from U.S. clinical trials of the drug. Even if these data where available, however, they may not have been entirely reliable. At the time, clinical trials did not require FDA approval, nor were they subject to oversight. The “clinical trials” of thalidomide involved distributing more than two and a half million tablets of thalidomide to approximately 20,000 patients across the nation—approximately 3,760 women of childbearing age, at least 207 of whom were pregnant. More than one thousand physicians participated in these trials, but few tracked their patients after dispensing the drug.

The tragedy surrounding thalidomide and Kelsey’s wise refusal to approve the drug helped motivate profound changes in the FDA. By passing the Kefauver-Harris Drug Amendments Act in 1962, legislators tightened restrictions surrounding the surveillance and approval process for drugs to be sold in the U.S., requiring that manufacturers prove they are both safe and effective before they are marketed. Now, drug approval can take between eight and twelve years, involving animal testing and tightly regulated human clinical trials.

Despite its harmful side effects, thalidomide is FDA-approved for two uses today—the treatment of inflammation associated with Hansen’s disease (leprosy) and as a chemotherapeutic agent for patients with multiple myeloma, purposes for which it was originally prescribed off-label. Because of its known adverse effects on fetal development, the dispensing of thalidomide is regulated by the System for Thalidomide Education and Prescribing Safety (S.T.E.P.S.) program. The S.T.E.P.S. program, designed by Celgene pharmaceuticals and carried out in pharmacies where thalidomide prescriptions are filled, educates all patients who receive thalidomide about potential risks associated with the drug.

Thalidomide has also been associated with a higher occurrence blood clots and nerve and blood disorders. Northwestern University’s pharmacovigiliance team, Research on Adverse Drug Events And Reports (RADAR), has launched a joint project with the Walgreens pharmacy at Northwestern Memorial Hospital so that these side effects may be understood and monitored, like those affecting fetal development. RADAR, led by Dr. Charles Bennett of the Feinberg School of Medicine, combines the expertise of clinicians, academics, pharmacists, and statisticians to monitor and disseminate information about adverse drug reactions to cancer drugs.

Their project tracks the number of patients who get a blood clot after receiving thalidomide, whether or not the patient received an anticoagulant drug, which are used to help prevent clotting, and if so, which drug was used. Tracking this information will help researchers better identify the incidence and prevention of thalidomide-associated blood clots, allowing the drug to continue to serve as an effective therapy for many patients.

Genetic counseling and testing

People with a strong family history of cancer may want to learn their genetic makeup. This may help the person or other family members plan their health care for the future. Since inherited mutations affect all cells of a person’s body, they can often be found by genetic testing done on blood or saliva (spit) samples. Still, genetic testing is not helpful for everyone, so it’s important to speak with a genetic counselor first to find out if testing might be right for you. For more information, see Understanding Genetic Testing for Cancer.

Cancer in Children and Adolescents

Although cancer in children is rare, it is the leading cause of death by disease past infancy among children in the United States. In 2021, it is estimated that 15,590 children and adolescents ages 0 to 19 will be diagnosed with cancer and 1,780 will die of the disease in the United States (1). Among children ages 0 to 14 years, it is estimated that, in 2021, 10,500 will be diagnosed with cancer and 1,190 will die of the disease (1). Among adolescents ages 15 to 19 years, about 5090 will be diagnosed with cancer and about 590 will die of the disease.

Overall, among children and adolescents (ages 0 to 19) in the United States, the most common types of cancer are leukemias, brain and central nervous system tumors, and lymphomas. Among children (ages 0 to 14 years), the most common types of cancer are leukemias, followed by brain and other central nervous system tumors, lymphomas, neuroblastoma, kidney tumors, and malignant bone tumors (1). Among adolescents (ages 15 to 19 years), the most common types of cancer are brain and other central nervous system tumors and lymphomas, followed by leukemias, thyroid cancer, gonadal (testicular and ovarian) germ cell tumors, and malignant bone tumors (1).

As of January 1, 2018 (the most recent date for which data exist), approximately 483,000 survivors of childhood and adolescent cancer (diagnosed at ages 0 to 19 years) were alive in the United States (2). The number of survivors will continue to increase, given that the incidence of childhood cancer has been rising slightly in recent decades and that survival rates overall are improving.

What is the outlook for children and adolescents with cancer?

The overall outlook for children and adolescents with cancer has improved greatly over the last half-century. In the mid-1970s, 58% of children (ages 0 to 14 years) and 68% of adolescents (ages 15 to 19 years) diagnosed with cancer survived at least 5 years (1). In 2010–2016, 84.1% of children and 85.3% of adolescents diagnosed with cancer survived at least 5 years (3).

Although survival rates for most childhood cancers have improved in recent decades, the improvement has been especially dramatic for a few cancers, particularly acute lymphoblastic leukemia, which is the most common childhood cancer. Improved treatments introduced beginning in the 1960s and 1970s raised the 5-year survival rate for children diagnosed with acute lymphoblastic leukemia at ages 0 to 14 years from 57% in 1975 to 92% in 2012 (4). The 5-year survival rate for children diagnosed with non-Hodgkin lymphoma at ages 0 to 14 years has also increased dramatically, from 43% in 1975 to 91% in 2012 (4).

Because of these survival improvements, in more recent years brain cancer has replaced leukemia as the leading cause of cancer death among children (5).

By contrast, survival rates remain very low for some cancer types, for some age groups, and for some cancers within a site. For example, half of children with diffuse intrinsic pontine glioma (a type of brain tumor) survive less than 1 year from diagnosis (6). Among children with Wilms tumor (a type of kidney cancer), older children (those diagnosed between ages 10 and 16 years) have lower 5-year survival rates than younger children (7). For soft tissue sarcomas, 5-year survival rates in 2008–2014 among children and adolescents ages 0 to 19 years ranged from 65% (rhabdomyosarcoma) to 95% (chondrosarcoma) (8), but children with sarcomas who present with metastatic disease have much lower 5-year survival rates. And the 5-year survival rate for acute lymphoblastic leukemia in 2008–2014 was 91% for children younger than 15 years, compared with 74% for adolescents ages 15 to 19 years (8).

Some evidence suggests that adolescents and young adults with acute lymphoblastic leukemia may have better outcomes if they are treated with pediatric treatment regimens than if they receive adult treatment regimens (9). The improvement in 5-year survival rates for 15- to 19-year-olds with acute lymphoblastic leukemia may reflect greater use of these pediatric treatment regimens.

The cancer mortality rate—the number of deaths due to cancer per 100,000 people per year—among children and adolescents ages 0 to 19 years declined by more than 50% from 1975 to 2017 (3). Specifically, the mortality rate was 5.1 per 100,000 children and adolescents in 1975 and 2.2 per 100,000 children and adolescents in 2017. However, despite the overall decrease in mortality, approximately 1,800 children and adolescents still die of cancer each year in the United States, indicating that new advances and continued research to identify effective treatments are required to further reduce childhood cancer mortality.

Each year in 1997–2017, the cancer death rate dropped the most for 15- to 19-year-olds (a 1.7% drop each year on average), followed by that for 0- to-4-year-olds (a 1.4% drop), 10- to 14-year-olds (a 1.2% drop), and 5- to 9-year-olds (a 1.1% drop) (3).

What are the possible causes of cancer in children?

The causes of most childhood cancers are not known. Up to 10% of all cancers in children are caused by a heritable (germline) mutation (a mutation that can be passed from parents to their children). For example, about 45% of children with retinoblastoma, a cancer of the eye that develops mainly in children, inherited a mutation in a gene called RB1 from a parent (10). Inherited mutations associated with certain familial syndromes, such as Li-Fraumeni syndrome, Beckwith-Wiedemann syndrome, Fanconi anemia syndrome, Noonan syndrome, and von Hippel-Lindau syndrome, also increase the risk of childhood cancer.

Genetic mutations that initiate cancer can also arise during the development of a fetus in the womb. Evidence for this comes from studies of monozygotic (identical) twins in which both twins developed leukemia with an identical leukemia-initiating gene mutation (11).

Children who have Down syndrome, a genetic condition caused by the presence of an extra copy of chromosome 21, are 10 to 20 times more likely to develop leukemia than children without Down syndrome (12). However, only a very small proportion of childhood leukemia is linked to Down syndrome.

Most cancers in children, like those in adults, are thought to develop as a result of mutations in genes that lead to uncontrolled cell growth and eventually cancer. In adults, these gene mutations are often the result of exposure to cancer-causing environmental factors, such as cigarette smoke, asbestos, and ultraviolet radiation from the sun. One study found that melanoma in children and adolescents (ages 11–20 years) has many genomic similarities to melanoma that occurs in adults, including an enrichment of UV-induced mutations (13).

However, environmental causes of childhood cancer have been difficult to identify, partly because cancer in children is rare, and partly because it is difficult to determine what children might have been exposed to early in their development. In fact, most childhood cancers are not thought of as being caused by environmental exposures.

Nevertheless, several environmental exposures have been linked to childhood cancer. One is ionizing radiation, which can lead to the development of leukemia and other cancers in children and adolescents. For example, children and adolescents who were exposed to radiation from the atomic bombs dropped in Japan during the Second World War had an elevated risk of leukemia (14), and children who were exposed to radiation from the Chernobyl nuclear plant accident had an elevated risk for thyroid cancer (15). Children whose mothers had x-rays during pregnancy (that is, children who were exposed before birth) and children who were exposed after birth to diagnostic medical radiation from computed tomography (CT) scans have also been found to have an increased risk of leukemia and brain tumors, and possibly other cancers (16).

A number of other environmental exposures have also been reported to have possible associations with childhood cancer. However, because of challenges in studying these associations, such as recall bias and the difficulty of determining exposure at the relevant time period in a child’s development, it is difficult to draw firm conclusions. Some types of childhood leukemia have been associated with father’s tobacco smoking (17, 18) with exposure to certain pesticides used in and around the home (19) or by parents at their workplace (20, 21) with solvents, which are organic chemicals that are found in some household products and with outdoor air pollution. Studies of childhood brain tumors have suggested possible associations with exposures to pesticides in and around the home (22) and maternal consumption of cured meats (23).

Researchers have also identified factors that may be associated with reduced risk of childhood cancer. For example, maternal consumption of folate has been associated with reduced risks of both leukemia and brain tumors in children (24). And being breastfed and having been exposed to routine childhood infections are both associated with a lowered risk of developing childhood leukemia (25).

What does a child’s cancer diagnosis mean for cancer risk in the rest of the family?

First- and second-degree relatives of a child diagnosed with cancer, particularly if diagnosed before age five, may be at increased risk for developing cancer if there is already a family history of cancer—that is, if the child’s cancer is likely due to an inherited genetic syndrome (26). A clinician may advise as to whether a child could benefit from genetic testing or referral to a medical geneticist for evaluation (26–28).

How do cancers in adolescents and young adults differ from those in younger children?

Cancer occurs more frequently in adolescents and young adults ages 15 to 39 years than in younger children, although incidence in this group is still much lower than in older adults. According to the NCI Surveillance, Epidemiology, and End Results (SEER) program (8), each year in 2011–2015 there were:

  • 16 cancer diagnoses per 100,000 children ages 0 to 14 years
  • 72 cancer diagnoses per 100,000 adolescents and young adults ages 15 to 39 years
  • 953 cancer diagnoses per 100,000 adults aged 40 years or older

The most frequent cancers diagnosed in adolescents and young adults (AYAs) are cancers that are more common among adults than younger children, such as breast cancer, melanoma, and thyroid cancer (29). But certain cancers, such as testicular cancer, are more typical of AYAs than of either younger children or adults (8). However, the incidence of specific cancer types varies widely across the adolescent and young adult age continuum.

Where do children with cancer get treated?

Children who have cancer are often treated at a children’s cancer center, which is a hospital or a unit within a hospital that specializes in diagnosing and treating children and adolescents who have cancer. Most children’s cancer centers treat patients through 20 years of age. The health professionals at these centers have specific training and expertise to provide comprehensive care for children, adolescents, and their families.

Recently, many Adolescent and Young Adult (AYA) cancer programs have been created to address the unique needs of teens and young adults. Areas of focus include long-term survivor care, access to clinical trial enrollment, discussing and preserving future fertility, peer support, and psychosocial support that addresses their personal issues, including finances, education, occupational impacts, and transition to independence.

Children’s cancer centers also participate in clinical trials. The improvements in survival for children with cancer that have occurred over the past half century have been achieved because of treatment advances that were studied and proven to be effective in clinical trials.

More than 90% of children and adolescents who are diagnosed with cancer each year in the United States are cared for at a children’s cancer center that is affiliated with the NCI-supported Children’s Oncology Group (COG). COG is the world’s largest organization that performs clinical research to improve the care and treatment of children and adolescents with cancer. Each year, approximately 4,000 children who are diagnosed with cancer enroll in a COG-sponsored clinical trial. COG trials are sometimes open to individuals aged 29 years or even older when the type of cancer being studied is one that occurs in children, adolescents, and young adults.

Every children’s cancer center that participates in COG has met strict standards of excellence for childhood cancer care. A directory of COG locations is available on their website. Families can ask their pediatrician or family doctor for a referral to a children’s cancer center. Families and health professionals can call NCI's Cancer Information Service at 1–800–4–CANCER ( 1–800–422–6237) to learn more about children’s cancer centers that belong to COG.

If my child is treated at a children’s cancer center, will he or she automatically be part of a clinical trial?

No. Participation in a clinical trial is voluntary, and it is up to each family to decide if clinical trial participation is right for their child.

Can children who have cancer be treated at the National Institutes of Health (NIH) Clinical Center?

Children with cancer may be eligible to be treated in clinical trials at the NIH Clinical Center in Bethesda, Maryland. Because the NIH Clinical Center is a research hospital, only patients who have a specific type or stage of cancer that is under study can be accepted for treatment. In some cases, patients with conditions that are rare or difficult to diagnose may also be accepted for treatment at the Clinical Center. All patients who are treated at the Clinical Center must be referred by a physician.

NCI’s Pediatric Oncology Branch conducts clinical trials for children, adolescents, and young adults with a wide variety of cancers. Patients with newly diagnosed cancer, as well as patients whose cancers have come back after treatment, may be eligible to participate in a clinical trial. Physicians at the Pediatric Oncology Branch can also provide a second opinion on a patient’s diagnosis or treatment plan. To refer a patient to the Pediatric Oncology Branch, the patient’s health care provider should call 301–496–4256 (local) or 1–877–624–4878 (toll-free) weekdays between 8:30 a.m. and 5:00 p.m. ET. Parents can also call these numbers to learn if their child is eligible to participate in a clinical trial.

What should survivors of childhood cancer consider after they complete treatment?

Survivors of childhood cancer need follow-up care and enhanced medical surveillance for the rest of their lives because of the risk of complications related to the disease or its treatment that can last for, or arise, many years after they complete treatment for their cancer. Health problems that develop months or years after treatment has ended are known as late effects.

The specific late effects that a person who was treated for childhood cancer might experience depend on the type and location of his or her cancer, the type of treatment he or she received, and patient-related factors, such as age at diagnosis.

Children who were treated for bone cancer, brain tumors, and Hodgkin lymphoma, or who received radiation to their chest, abdomen, or pelvis, have the highest risk of serious late effects from their cancer treatment, including second cancers, joint replacement, hearing loss, and congestive heart failure (30, 31).

Long-term follow-up analysis of a cohort of survivors of childhood cancer treated between 1970 and 1986 has shown that cancer survivors remain at risk of complications and premature death as they age, with more than half of survivors having experienced a severe or disabling complication or even death by the time they reach age 50 years (32). Children treated in more recent decades may have lower risks of late effects due to modifications in treatment regimens to reduce exposure to radiotherapy and chemotherapy, increased efforts to detect late effects, and improvements in medical care for late effects (33).

It’s important for childhood cancer survivors to have regular medical follow-up examinations so any health problems that occur can be identified and treated as soon as possible. The Children’s Oncology Group (COG) has developed long-term follow-up guidelines for survivors of childhood, adolescent, and young adult cancers.

It is also important to keep a record of the cancer treatment that a child received. This record should include:

  • The type and stage of cancer
  • Date of diagnosis and dates of any relapses
  • Types and dates of imaging tests
  • Contact information for the hospitals and doctors who provided treatment
  • Names and total doses of all chemotherapy drugs used in treatment
  • The parts of the body that were treated with radiation and the total doses of radiation that were given
  • Types and dates of all surgeries
  • Any other cancer treatments received
  • Any serious complications that occurred during treatment and how those complications were treated
  • The date that cancer treatment was completed

The record should be kept in a safe place, and copies of the record should be given to all doctors or other health care providers who are involved with the child’s follow-up care, even as the child grows into adulthood.

Many children’s cancer centers have clinics where survivors of childhood cancer can go for follow-up until they reach their early 20s. Some cancer centers are now creating clinics dedicated to follow-up care for long-term survivors of pediatric and adolescent cancers.

Selected References

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Howlader N, Noone AM, Krapcho M, et al. (eds). SEER Cancer Statistics Review, 1975–2018, National Cancer Institute. Bethesda, MD,, based on November 2020 SEER data submission, posted to the SEER web site, April 2021.

Howlader N, Noone AM, Krapcho M, et al. (eds). SEER Cancer Statistics Review, 1975–2017, National Cancer Institute. Bethesda, MD,, based on November 2019 SEER data submission, posted to the SEER web site, April 2020.

Jemal A, Ward EM, Johnson CJ, et al. Annual Report to the Nation on the status of cancer, 1975–2014, featuring Survival. Journal of the National Cancer Institute 2017 109(9).

Curtin SC, Minino AM, Anderson RN. Declines in cancer death rates among children and adolescents in the United States, 1999–2014. National Center for Health Statistics Data Brief 2016 (257):1–8.

Warren KE. Diffuse intrinsic pontine glioma: poised for progress. Frontiers in Oncology 2012 2:205.

Popov SD, Sebire NJ, Pritchard-Jones K, Vujanić GM. Renal tumors in children aged 10–16 Years: a report from the United Kingdom Children's Cancer and Leukaemia Group. Pediatric and Developmental Pathology 2011 14(3):189–193.

Childhood cancer rates calculated using the Incidence SEER18 Research Database, November 2017 submission (Katrina/Rita Population Adjustment). All cancer site rates are based on the SEER site codes with the exception of medulloblastoma, which used site code C71.6 and International Classification Code of Diseases for Oncology, Third Edition (ICD-O-3) malignant histologic codes 9470/3, 9471/3, and 9474/3.

Ram R, Wolach O, Vidal L, et al. Adolescents and young adults with acute lymphoblastic leukemia have a better outcome when treated with pediatric-inspired regimens: Systematic review and meta-analysis. American Journal of Hematology 2012 87(5):472–478.

Dimaras H, Corson TW, Cobrinik D, et al. Retinoblastoma. Nature Reviews. Disease Primers. 2015 1:15021.

Greaves MF, Maia AT, Wiemels JL, Ford AM. Leukemia in twins: lessons in natural history. Blood 2003 102(7):2321–2333.

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Hsu WL, Preston DL, Soda M, et al. The incidence of leukemia, lymphoma and multiple myeloma among atomic bomb survivors: 1950–2001. Radiation Research 2013 179(3):361–382.

Cardis E, Hatch M. The Chernobyl accident--an epidemiological perspective.Clinical Oncology: A Journal of the Royal College of Radiologists 23(4):251–260.

Pearce MS, Salotti JA, Little MP, et al. Radiation exposure from CT scans in childhood and subsequent risk of leukaemia and brain tumours: a retrospective cohort study. Lancet 2012 380(9840):499–505.

Ji BT, Shu XO, Linet MS, et al. Paternal cigarette smoking and the risk of childhood cancer among offspring of nonsmoking mothers. Journal of the National Cancer Institute 1997 89(3):238–244.

Sorahan T, McKinney PA, Mann JR, et al. Childhood cancer and parental use of tobacco: findings from the inter-regional epidemiological study of childhood cancer (IRESCC). British Journal of Cancer 2001 84(1):141–146.

Bailey HD, Infante-Rivard C, Metayer C, et al. Home pesticide exposures and risk of childhood leukemia: Findings from the childhood leukemia international consortium. International Journal of Cancer 2015 137(11):2644–2663.

Van Maele-Fabry G, Lantin AC, Hoet P, Lison D. Childhood leukaemia and parental occupational exposure to pesticides: a systematic review and meta-analysis. Cancer Causes & Control 2010 21(6):787–809.

Vinson F, Merhi M, Baldi I, Raynal H, Gamet-Payrastre L. Exposure to pesticides and risk of childhood cancer: a meta-analysis of recent epidemiological studies. Occupational and Environmental Medicine 2011 68(9):694–702.

Chen M, Chang CH, Tao L, Lu C. Residential exposure to pesticide during childhood and childhood cancers: A meta-Analysis. Pediatrics 2015 136(4):719–729.

Johnson KJ, Cullen J, Barnholtz-Sloan JS, et al. Childhood brain tumor epidemiology: a brain tumor epidemiology consortium review. Cancer Epidemiology, Biomarkers & Prevention 2014 23(12):2716–2736.

Chiavarini M, Naldini G, Fabiani R. Maternal folate intake and risk of childhood brain and spinal cord tumors: A systematic review and meta-analysis. Neuroepidemiology 2018 51(1–2):82–95.

Amitay EL, Keinan-Boker L. Breastfeeding and childhood leukemia incidence: A meta-analysis and systematic review. JAMA Pediatrics 2015 169(6):e151025.

Curtin K, Smith KR, Fraser A, Pimentel R, Kohlmann W, Schiffman JD. Familial risk of childhood cancer and tumors in the Li-Fraumeni spectrum in the Utah Population Database: implications for genetic evaluation in pediatric practice. International Journal of Cancer 2013 133(10):2444–2453.

Malkin D, Nichols KE, Schiffman JD, Plon SE, Brodeur GM. The future of surveillance in the context of cancer predisposition: Through the murky looking glass. Clinical Cancer Research 2017 23(21):e133–e137.

Barr RD, Ries LA, Lewis DR, et al. Incidence and incidence trends of the most frequent cancers in adolescent and young adult Americans, including "nonmalignant/noninvasive" tumors. Cancer 2016 122(7):1000–1008.

Oeffinger KC, Mertens AC, Sklar CA, et al. Chronic health conditions in adult survivors of childhood cancer. New England Journal of Medicine 2006 355(15):1572–1582.

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