Cancer history on environment-cancer relationship

I am interested to know how environment-cancer relationship knowledge has developed. I know that all began when Muller first proved that mutation could be induced via ionizing radiation, X rays in the case, and hypothesized for the first time the role that this could have on carcinogenesis. Do you know further data and the main or most significant events that leaded from that point until the current state of the art? (like when smoking and cancer were proved related)

(all factors enhancing risk would be included in the query, as human behavioral aspects (such as diet), work environment… )

Actually, "soot wart" was identified by Percival Pott in 1775. It is the first reported occupational cancer (it is a squamous cell carcinoma of the skin of the scrotum). It was shown in 1922 that an active ingredient of coal soot was a carcinogen. I'm not sure of an expansive, technical text on environmental cancers, but you may want to check out "The Emperor of All Maladies: A Biography of Cancer" which covers the origins of man's understanding of cancer starting with the ancient Greeks, progressing to mention Percival Pott, and then moving on to modern day science and medicine. This book won the Pulitzer in nonfiction a few years ago and is well worth your time.

Susan Sontag

Susan Sontag ( / ˈ s ɒ n t æ ɡ / January 16, 1933 – December 28, 2004) was an American writer, filmmaker, philosopher, teacher, and political activist. [2] She mostly wrote essays, but also published novels she published her first major work, the essay "Notes on 'Camp'", in 1964. Her best-known works include the critical works Against Interpretation (1966), Styles of Radical Will (1968), On Photography (1977), and Illness as Metaphor (1978), as well as the fictional works The Way We Live Now (1986), The Volcano Lover (1992), and In America (1999).

Sontag was active in writing and speaking about, or travelling to, areas of conflict, including during the Vietnam War and the Siege of Sarajevo. She wrote extensively about photography, culture and media, AIDS and illness, human rights, and leftist ideology. Her essays and speeches drew controversy, [3] and she has been described as "one of the most influential critics of her generation." [4]

What Is the Relationship Between Mitosis and Cancer?

Mitosis is the process via which cells divide, producing copies of themselves. Cancer is essentially mitosis that is out of control. Cancer cells do not operate in the same way as other cells in the system they occupy, so they replicate and damage surrounding tissues.

When cells divide, the result is generally two identical copies of the original cell. A "parent" cell distributes its genetic material into two "daughter" cells during replication, which then take on the characteristics of the parent cell. Usually, this process works seamlessly however, when Cell Cycle genes mutate within cells, mitosis goes from a controlled process to an uninhibited, reactive event.

Unlike normal cells, which respond to density-dependent inhibition, tumor cells continue to divide, and multiply at an increased rate until all available nutrient supplies are depleted. When tumor cells are benign, they remain at the original site. When they are malignant, however, the tumor quickly becomes invasive: at this point, the mass is known as cancer.

Sometimes, cancerous tumors contain cells capable of triggering the formation of blood vessels specifically designed to create a nutrient supply for the mass. Malignant cells then gain a pathway via which they can travel to other parts of the body. When this occurs, the tumor has metastasised.

What is the Human Microbiome?

Large and diverse populations of bacteria, viruses, and fungi occupy almost every surface of the human body.1 It is estimated that there are nearly 30 trillion bacterial cells living in or on each human.2 That is about one bacterium for every cell in the human body!2 These microbes are collectively known as the microbiome.31 Exposure to microbes first occurs during birth and is later influenced by environmental factors, such as diet and exposure to antibiotics.31 Due to differences in environment, diet, and behavior, the specific types of microbes that make up the microbiome can vary greatly between individuals.1 It is thought that every person’s microbiome is slightly different.4 In fact, work is underway to investigate the use of microbiomes to identify individuals, much like fingerprints.4

Geographical Distinctions

There are also stark geographic differences, with incidence rates varying by as much as thirtyfold between regions. In much of Asia and South and Central America, for example, cervix cancer is the most deadly in females. However, in North America and Europe another kind of gynecological cancer, ovarian cancer, is a more serious threat.

Among males, southern and eastern Africa record the second and third highest rates of oesophageal, or gullet, cancer after China, but western and central regions of Africa have the lowest incidence in the world. Differences in diet may explain this.

Nevertheless, the reasons why many cancers develop remain elusive. Brain cancer, leukemia (blood cancer), and lymphoma (cancer of the lymph glands) are among types that still mystify scientists.

Cancer history on environment-cancer relationship - Biology

Age is the main risk factor for the prevalent diseases of developed countries: cancer, cardiovascular disease and neurodegeneration. The ageing process is deleterious for fitness, but can nonetheless evolve as a consequence of the declining force of natural selection at later ages, attributable to extrinsic hazards to survival: ageing can then occur as a side-effect of accumulation of mutations that lower fitness at later ages, or of natural selection in favour of mutations that increase fitness of the young but at the cost of a higher subsequent rate of ageing. Once thought of as an inexorable, complex and lineage-specific process of accumulation of damage, ageing has turned out to be influenced by mechanisms that show strong evolutionary conservation. Lowered activity of the nutrient-sensing insulin/insulin-like growth factor/Target of Rapamycin signalling network can extend healthy lifespan in yeast, multicellular invertebrates, mice and, possibly, humans. Mitochondrial activity can also promote ageing, while genome maintenance and autophagy can protect against it. We discuss the relationship between evolutionarily conserved mechanisms of ageing and disease, and the associated scientific challenges and opportunities.

Cancer Stem Cells and Treatment

What is the impact of CSCs on treatment?
Current treatments target cancer because the drugs act on cells that are actively dividing. Most of these drugs function by inducing the death (via apoptosis ) of the cancer cells. Cancer stem cells carry mutations that lead to cancer, but they do not necessarily divide quickly. This relatively inactive state would allow them to avoid the effects of cancer treatments which would explain the all too frequent recurrences of cancers. CSCs also efficiently repair DNA damage and avoid apoptosis making them hard targets for today's drugs. This evasion of treatment could be likened to a weed in a garden. Cancer stem cells are like the roots of the weed and the majority of the tumor mass is the leaves and stem of the weed. Removing the visible part of the weed appears to kill it, but the roots underground soon sprout another stem and the weed lives on.12

A potential cancer drug, napabucasin, has been found to target 'stemness.' According to two separate studies, a treatment combining napabucasin with chemotherapy was able to block STAT3 gene transcription in cancer stem cells.13 Napabucasin was shown to kill colorectal stem cells, block their renewal, and kill cancer cells14 Napabucasin could have serious side effects in humans, as it has been shown to cause bone loss in mice.15

NCI Legislative Chronology

February 4, 1927—Senator M. M. Neely, West Virginia, introduced Senate Bill 5589 to authorize a reward for the discovery of a successful cure for cancer. The reward was to be $5 million.

March 7, 1928—Senator M. M. Neely introduced Senate Bill 3554 to authorize the National Academy of Sciences to investigate the means and methods for affording Federal aid in discovering a cure for cancer and for other purposes.

April 23, 1929—Senator W. J. Harris, Georgia, introduced Senate Bill 466 to authorize the Public Health Service and the National Academy of Sciences jointly to investigate the means and methods for affording Federal aid in discovering a cure for cancer and for other purposes.

April 2, 1937—Senator Homer T. Bone, Washington, introduced Senate Bill 2067 authorizing the Surgeon General of the Public Health Service to control and prevent the spread of the disease of cancer, authorizing an annual appropriation of $1 million.

April 29, 1937—Congressman Maury Maverick, Texas, introduced House Resolution 6767 to promote research in the cause, prevention, and methods of diagnosis and treatment of cancer, to provide better facilities for the diagnosis and treatment of cancer, to establish a National Cancer Center in the Public Health Service, and for other purposes. It authorizes an appropriation of $2,400,000 for the first year and $1 million annually thereafter.

August 5, 1937—The National Cancer Institute Act establishes the National Cancer Institute as the federal government’s principal agency for conducting research and training on the cause, diagnosis, and treatment of cancer. The bill also calls upon NCI to assist and promote similar research at other public and private institutions. An appropriation of $700,000 for each fiscal year is authorized. (P.L. 75-244)

March 28, 1938—House Joint Resolution 468, 75th Congress, was passed, "To dedicate the month of April in each year to a voluntary national program for the control of cancer."

July 1, 1944—The Public Health Service Act, P.L. 410, 78th Congress, provided that "The National Cancer Institute shall be a division in the National Institute of Health." The act also revised and consolidated many revisions into a single law. The limit of $700,000 annual appropriation was removed.

December 23, 1971—The National Cancer Act of 1971 provides increased authorities and responsibilities for the NCI Director initiating a National Cancer Program establishing a 3-member President's Cancer Panel and a 23-member National Cancer Advisory Board, the latter replacing the National Advisory Cancer Council authorizing the establishment of 15 new research, training, and demonstration cancer centers establishing cancer control programs as necessary for cooperation with state and other health agencies in the diagnosis, prevention, and treatment of cancer and providing for the collection, analysis, and dissemination of all data useful in the diagnosis, prevention, and treatment of cancer, including the establishment of an international cancer data research bank. (P.L. 92-218)

November 9, 1978—The Community Mental Health Centers Act amends the National Cancer Act to emphasize education and demonstration programs in cancer treatment and prevention, and stipulates that NCI devote more resources to prevention, focusing particularly on environmental, dietary and occupational cancer causes. (P.L. 95-622)

November 4, 1988—The Health Research Extension Act of 1988 provides a two-year extension, which reaffirms the special authorities of NCI and added information dissemination mandates. A representative from the Department of Energy was added to the National Cancer Advisory Board as an ex officio member. (P.L. 100-607)

June 10, 1993—The NIH Revitalization Act of 1993 encourages NCI to expand and intensify its efforts in breast cancer and other women's cancers and authorized increased appropriations. Similar language is included for prostate cancer. (P.L. 103-43)

August 13, 1998—The Stamp Out Breast Cancer Act establishes a special alternative rate of postage up to 25% higher than a regular first-class stamp. 70% of the profits from the sale of the stamp, also referred to as a semipostal, would go to the NIH to fund breast cancer research the remaining 30% would go to the U.S. Department of Defense breast cancer research. (PL 105-41)

July 10, 2000—The Radiation Exposure Compensation Amendments of 1999 allow more workers who handled radioactive material for weapons programs to be eligible to receive federal compensation for radiation-induced illness. (P.L. 106-245)

July 28, 2000—The Semipostal Authorization Act gives the U.S. Postal Service the authority to issue semipostal stamps, which are sold at a premium in order to help provide funding for a particular area of research. The law also extends the Breast Cancer Stamp Act until July 29, 2002. (P.L. 106-253)

January 4, 2002—The Best Pharmaceuticals for Children Act is designed to improve the safety and efficacy of pharmaceuticals for children, by reauthorizing legislation that encourages pediatric drug research by giving drug companies an incentive of six months of additional market exclusivity to test their products for use in children. (P.L. 107-109)

May 14, 2002—The Hematologic Cancer Research Investment and Education Act of 2002 directs the NIH Director, through the NCI Director, to conduct and support research on blood cancers. In addition, the CDC is directed to establish and carry out an information and education program. (P.L. 107-172)

September 10, 2002—The Public Health Security and Bioterrorism Preparedness and Response Act contains a provision instructing Federal agencies to stockpile and distribute potassium iodide (KI) to protect the public from thyroid cancer in the event of a radiation emergency. (P.L. 107-188)

June 30, 2005—The Patient Navigator Outreach and Chronic Disease Prevention Act of 2005 amends the Public Health Service Act to authorize a demonstration grant program to provide patient navigator services to reduce barriers and improve health care outcomes. The bill directs the HHS Secretary to require each recipient of a grant under this section to use the grant to recruit, assign, train, and employ patient navigators who have direct knowledge of the communities they serve to facilitate the care of individuals who have cancer or other chronic diseases. The bill also directs the HHS Secretary to coordinate with, and ensure the participation of, the Indian Health Service, NCI, the Office of Rural Health Policy, and such other offices and agencies as deemed appropriate by the Secretary, regarding the design and evaluation of the demonstration programs. (P.L. 109-18)

November 11, 2005—The 2-Year Extension of Postage Stamp for Breast Cancer Research extends the U.S. Postal Service's authority to issue special postage stamps to help provide funding for breast cancer research through December 31, 2007. (P.L. 109-100)

January 12, 2007—The Gynecologic Cancer Education and Awareness Act of 2005, or "Johanna's Law" directs the HHS Secretary to carry out a national campaign to increase the awareness and knowledge of health care providers and women with respect to gynecologic cancers. (P.L. 109-475)

April 20, 2007—The National Breast and Cervical Cancer Early Detection Program Reauthorization Act of 2007 allows states to apply for federal waivers to spend a greater share of funds on hard-to-reach underserved women. This bill authorizes funding up to $275 million by 2012 $201 million is authorized for 2007. (P.L. 110-18)

September 27, 2007—The FDA Amendments Act of 2007 amends the Federal Food, Drug, and Cosmetic Act to reauthorize the collection of prescription drug user fees for FY2008–FY2012. Requires NIH to expand the clinical trial registry ( and creates a clinical trial results database. (P.L. 110-85)

December 12, 2007—The Breast Cancer Research Stamp Reauthorization Act extends through December 31, 2011, provisions requiring the U.S. Postal Service to issue a special postage stamp which contributes to funding breast cancer research. (P.L. 110-150)

July 29, 2008—The Caroline Pryce Walker Childhood Cancer Act of 2007 amends the Public Health Service Act to advance medical research and treatments into pediatric cancers, ensure patients and families have access to the current treatments and information regarding pediatric cancers, establish a population-based national childhood cancer database, and promote public awareness of pediatric cancers. (P.L. 110-287)

October 8, 2008—The Breast Cancer and Environmental Research Act of 2007 amends the Public Health Service Act to authorize the Director of the National Institute of Environmental Health Sciences to make grants for the development and operation of research centers regarding environmental factors that may be related to the etiology of breast cancer. The bill establishes an Interagency Breast Cancer and Environmental Research Coordinating Committee within HHS. (P.L. 110-354)

February 4, 2009—The Children's Health Insurance Program Reauthorization Act of 2009 increases the tax on cigarettes by 62 cents to $1.01 per pack and raises taxes on other tobacco products, in order to offset the cost of the program expansion. (P.L. 113-3)

February 17, 2009—The American Recovery and Reinvestment Act of 2009 provides $10 billion in additional funding for the NIH of which NCI received $1.3 billion in Recovery Act funds to be distributed during the two-year span of 2009 and 2010. (P.L. 111-5)

June 21, 2009—The Family Smoking Prevention and Tobacco Control Act provides the FDA with the authority to regulate tobacco products and establishes within the FDA, the Center for Tobacco Products to implement this act. The Act allows the Secretary of HHS to restrict the sale or distribution and the advertising or promotion of tobacco products, if appropriate for the protection of the public health, and to the full extent permitted by the First Amendment. (P.L. 111-31)

March 23, 2010—The Patient Protection and Affordable Care Act (HR 3590), the health care reform bill, establishes a private non-profit institute called the Patient-Centered Outcomes Research Institute to conduct comparative clinical effectiveness research, obtain and use data from the Federal government, and establish advisory panels to advise on research priorities, among other provisions. The bill requires NIH to conduct research to develop and validate new screening tests for breast cancer. The bill also requires the NIH Director to establish a Cures Acceleration Network (CAN) program, which shall award grants and contracts to eligible entities to accelerate the development of high need cures and therapies, including the development of medical products, drugs or devices, or biological products. (P.L. 111-148)

March 31, 2010—The Prevent All Cigarette Trafficking Act of 2009 prevents tobacco smuggling, ensures the collection of all tobacco taxes, and includes smokeless tobacco as a regulated substance. The bill amends the federal criminal code to treat cigarettes and smokeless tobacco as non-mailable and prohibit such items from being deposited in or carried through the U.S. mail. (P.L.111-154)

December 23, 2011—The Breast Cancer Research Stamp Reauthorization Act reauthorized provisions requiring the U.S. Postal Service to issue a special postage stamp which contributes to funding breast cancer research, extending them through 2015. (P.L. 112-80)

January 2, 2013—The Recalcitrant Cancer Research Act of 2012 passed as an amendment to the National Defense Authorization Act for Fiscal Year 2013. The legislation calls for NCI to develop a scientific framework for research on two cancers that have a five-year relative survival rate of less than 20 percent, and are estimated to cause the death of at least 30,000 individuals in the United States per year. Pancreatic cancer and lung cancer meet these criteria. (P.L. 112-239)

December 11, 2015­—The Breast Cancer Stamp Reauthorization Act reauthorized the issuance of semipostal stamps for breast cancer research, through 2019. (P.L. 114-19)

December 13, 2016—The 21 st Century Cures Act increases funding for biomedical research, and aims to enhance the speed at which drugs are developed and approved. Key NIH provisions aim to coordinate policies relating to early career investigators, improve loan repayment programs, and streamline procedural requirements for attendance at scientific meetings. The bill reauthorizes the NIH for FY2018-FY2020 and creates a $4.8 billion NIH Innovation Account. This account supports the work of the Beau Biden Cancer Moonshot at a level of $1.8 billion over seven years, as well as the Precision Medicine Initiative, the BRAIN Initiative, and specific regenerative medicine research. The funds in the Account must be appropriated annually.

Where DNA meets daily life

Red hair is a genetically determined trait. And when redheads with Celtic roots move to sun-drenched countries near the equator, their risk of skin cancer dramatically rises. But the risk may not only be tied to the fact that redheads tend to have fair, unpigmented skin that is more susceptible to high doses of ultraviolet light. Some studies suggest that even olive-skinned women with a particular “red hair color” gene face a higher risk of skin cancer.

Red hair and skin cancer: a classic case of gene-environment interaction. What scientists don’t fully understand is why. What is going on in cells with “red hair color” genes that confers the extra risk—a risk that goes beyond the well-documented increase in ultraviolet-induced DNA damage in people who lack UV-absorbing pigment in their skin? And how do these genes in turn influence other biological processes that lead to skin cancer?

That dance between genes and environment is the focus of a burgeoning field of public health research—one that could someday have a big payoff. By revealing the biological underpinnings of disease, it could bring new and improved methods to diagnosis, treatment, and prevention. Ultimately, it could help corroborate and refine—or, perhaps, rewrite—many of today’s standard public health recommendations. “We are not just doing basic science. We are addressing important public health problems from a fresh perspective—using genomic and mechanistic studies,” says Quan Lu, Mark and Catherine Winkler Assistant Professor of Lung Biology in the Departments of Environmental Health and of Molecular Metabolism.

Gene-environment studies describe the complex ecology of disease. If smoking is the most common cause of lung cancer, why do only 10 to 20 percent of heavy smokers develop the disease? Why do most patients initially do well on asthma medications, while a fraction eventually fail to respond to the drugs? Why are rates of breast cancer high in the United States, compared to other parts of the world—though, even in the U.S., most women do not develop the disease?

Public health scientists are in a unique position to answer these questions because of their access to large population-based cohort studies. These studies, replete with lifestyle and demographic data, include the Nurses’ Health Studies, the Health Professionals Follow-up Study, the Physicians’ Health Study, and the Normative Aging Study—all efforts in which HSPH faculty have had long affiliations. “At the School, we’re in a great position, because our data sets are drawn from studies that have been collecting detailed information about exposures for 30 years,” says Peter Kraft, associate professor of epidemiology.

Redefining “Genes” and “Environment”
In gene-environment studies, scientists are not just interested in inherited genetic mutations. They are also examining what turns genes on and off. And they are looking at “epigenetics”: changes in protein­­­s—the molecules synthesized by genes and involved in virtually all cell functions—caused not by alterations in the DNA code, but by shifts in the cells during biologically sensitive periods (an epigenetic cause of vaginal and cervical cancer, for example, is exposure in the womb to the chemical DES).

Likewise, researchers are expanding the definition of “environment” beyond conventional meanings such as air pollution or radiation exposure. They are exploring how genes are influenced by anything to which the body is exposed: diet, exercise, drugs, bacteria, UV sunlight, and workplace hazards, to name a few.

In fact, it is only by taking environment into account in their studies that researchers can identify the genes that interact with environment.

Recent reports in the New York Times and elsewhere have noted that the Human Genome Project—the 13-year effort to identify all of the approximately 20,000-25,000 genes in human DNA—hasn’t delivered on once-promised preventions or cures. The genome-wide association studies, or GWAS, spawned by the Project have largely not turned up links between common gene variants and greatly elevated risk for major diseases such as breast or prostate cancer, heart disease, or type 2 diabetes. Put another way, these common genes do not predict the risk of developing disease any better than a family history or lifestyle information.

But that may be because the studies only looked at genes—not at the environments that could have influenced those genes. Today, research groups are going back and incorporating data from those same individuals—data such as behaviors, personal characteristics, height, weight, diet, etc.—to see if the genetic pattern varies according to environmental exposures. If it does, then that could point a spotlight on genes associated with the disease.

Discarding Old Theories
Gene-environment research reflects a broader change in the scientific landscape. No longer do scientists assume that single genes cause single diseases. Except for classic single-gene conditions such as Huntington’s disease—in which everyone who carries the defective gene and lives long enough will develop Huntington’s devastating neurological symptoms—most diseases are the upshot of both genes and environment, with the activities of genes greatly modified by environmental exposures. Moreover, genes appear to work in concert with other genes to raise (or lower) the chance that, under certain environmental triggers, a person harboring those genes could develop a disease.

As gene-environment analyses get more fine-grained, what we think of as one disease may turn out to be several diseases, with different underlying causes and treatments. Diabetes, for example, can be triggered by obesity—but also by exposure to arsenic. The first condition responds to insulin and weight loss the second does not. According to Lu, “The idea will be to design, not only disease-specific, but also subdisease-specific therapies.”

Genes Determine Drug Response
Indeed, some of the clearest examples of gene-environment interaction are in pharmacogenetics. A patient’s genetic profile can help predict whether that person will respond to certain medications, or face the chance that the drug will be toxic or ineffective.

Gene-environment studies will also help scientists sharpen their estimates of disease risk. Initially, scientists had assumed that genes and environment had a synergistic relationship—with genes and environment interacting in a way that was more than the sum of their separate risks. But according to David Hunter, Dean for Academic Affairs and Vincent L. Gregory Professor in Cancer Prevention in the Departments of Epidemiology and Nutrition, “Most disease risks just add—they don’t multiply in a synergistic, jackpot sort of way. You’re worse off if you’re exposed to the adverse environment and to the adverse genetics. But you’re not spectacularly worse off. They add. But together, they can still add up to substantial increases in risk. The implication is that if you’re genetically exposed, there’s even more reason for you not to be exposed to the environmental factor.”

Lifestyle Trumps Genes in Breast Cancer
In a March 2010 paper in the New England Journal of Medicine, Hunter and his colleagues showed that, although a set of common gene variants were clearly associated with the risk of breast cancer—and predicted breast cancer risk as well as, or better than, the method that doctors often use, which is based on a patient’s demographic and lifestyle profile—these latter risk factors still played out at every level of genetic risk. In other words, no matter what you inherit in terms of common gene variants, maintaining a healthy weight after menopause, limiting alcohol intake, and being prudent about hormone replacement therapy remain important ways to reduce the threat.

Genes to Policy
Gene-and-environment research could well shape public policy and medical practice. Understanding more about the mechanisms of disease will undoubtedly lead to new treatments. It could also bolster existing public health wisdom about prevention. “Our work may reinforce the idea that cockroaches or air pollution contribute significantly to asthma—because we have the genetic mechanisms to show it,” says Lu.

Policy Quandaries
Gene-environment research could also introduce policy quandaries. The more scientists identify and fine-tune the genetic factors behind disease or drug response, the more doctors will want to screen individuals for gene variants in order to tailor medical care. Such personalized medicine may well lead to higher health care costs. According to Hunter, “There’s every chance that this genetic knowledge, rather than making medicine more rational and saving health care costs, will drive greater use of screening or prophylactic therapies.”

If not communicated well, the findings from gene-environment research could even backfire. “If you found a set of genes that made people highly resistant to the effect of smoking on lung cancer—and again, that’s a hypothetical—it’s unlikely that those same genes would make people resistant to the other bad effects of smoking, like heart disease. So it wouldn’t change public health advice one iota,” says Hunter. “If you tell people they’re genetically more susceptible to a particular disease, they may be more motivated to adopt healthy practices. But people who are less susceptible might mistakenly ignore these. It could be a net negative.”

Which means that, paradoxically, modern genomics may underscore old-fashioned, broad-brush, public health advice, says David Christiani, Elkan Blout Professor of Environmental Genetics in the Departments of Environmental Health and Epidemiology. Christiani found a common gene variant that made Shanghai cotton textile workers more vulnerable to lung disease. The practical implication of that discovery, Christiani argues, is not to screen out workers who harbor the gene, but to impose stricter environmental standards overall. “Protecting the most vulnerable among the population protects everyone better,” he says. “For most disease risk, you can control the environment better—because that’s what’s controllable. You’re not going to genetically engineer disease out of the population.”

“Lung cancer and diabetes are two good examples of retaining current recommendations,” adds Kraft. “You shouldn’t smoke and you should maintain a healthy weight. Regardless of your genes, that’s great advice.” As the era of public health genomics unfolds, we may have even stronger backing for today’s common wisdom—and new evidence for other ways to protect the health of populations.

—Madeline Drexler is editor of the Review. Illustration by Celia Johnson. Photos by Kent Dayton.

Treatment for HPV or HPV-related diseases

There’s no treatment for the virus itself, but there are treatments for the cell changes that HPV can cause.

Cancer is easiest to treat when it’s found early – while it’s small and before it has spread. Some cancer screening tests can find early cell changes caused by HPV, and these changes can be treated before they even become cancer.

Visible genital warts can be removed with prescribed medicines. They can also be treated by a health care provider.