Physical Carcinogenesis

Carcinogenesis is defined as the process of cancer growth. Specifically, the term refers to the process by which normal cells in the body mutate into cancer cells. In order for carcinogenesis to occur, damages in healthy cell DNA must occur. For this reason, carcinogenesis is often tied to genetics. However, exposure to certain chemicals and other hazardous materials can also cause cell damage that can lead to cancer.

Factors That Contribute to Carcinogenesis

While the factors that contribute to cancer growth are complex and still being studied by the research community, a number of contributing factors have been identified that increase a cell’s risk for carcinogenesis. These factors include genetics, environmental exposure and age. Regardless of the instigating cause of cancer growth, proliferation is dependent on the ability of the cancer cells to:

  • Grow quickly and inappropriately
  • Avoid cell death via the body’s defense systems
  • Stimulate their microenvironment
  • Spread to new areas of the body

Based on research, the biological contributing factors that foster carcinogenesis include:

  • Errors in gene expression due to faulty chromatin structure
  • Improper signal transduction between cells
  • Unhealthy hormone exposure
  • Improper metabolism of fatty acid
  • Damaged DNA or repair responses

The Importance of Proto-Oncogenes

Proto-oncogenes are a specific subcategory of genes that are responsible for inducing cell growth. A series of mutations in this key gene category is typically where carcinogenesis begins. Due to one or several of the contributing factors listed above, these proto-oncogenes become damaged in a way that accelerates cell growth. This, in turn, provides the rapid growth necessary for cancer cells to flourish, grow and spread throughout the body at such a rate that the natural immune system cannot adequately defend itself.

Damage to tumor suppressor genes often works in tandem with damaged proto-oncogenes to create cancer. Tumor suppressor genes are designed to clean up any DNA damage that may occur during cell replication. When damage to these tumor suppressors occurs, DNA damage proliferates, which can lead to mutations that ultimately give rise to cancer cells.

Other Instigators of Cancer

Mutation of proto-oncogenes and tumor suppressor genes are thought to be the most common cause of carcinogenesis. However, there are other non-mutagenic effects that also are believed to cause cancer. For example, an increase in estrogen in the body is thought to increase the rate of cell mitosis without causing gene mutation. This increase in mitosis proliferates cell growth much in the same way as damaged proto-oncogenes. Excessive consumption of alcohol can also stimulate mitosis.

To a lesser degree, bacteria and viruses have also been known to spur carcinogenesis. For example, HPV, Hepatitis B and EBV are all known illnesses that can directly cause cancer. It is believed that the reason for this is the virus’ ability to promote cell proliferation by inserting a portion of its own DNA into healthy human cells.

Difference Between Benign and Malignant Tumors

There are three stages of carcinogenesis – initiation, promotion and progression. Initiation results when a cell experiences damaged DNA. Promotion exacerbates cell damage and growth by altering gene expression, suppressing an immune response and enhancing cell division. While in the promotion stage, tumor cells are said to be benign. This means that they are non-cancerous, yet still unhealthy and growing at an abnormal rate.

Once the damaged cells begin to exchange DNA between chromosomes, express oncogenes and exhibit additional mutations, the progression stage of carcinogenesis is achieved. It is in this third stage that malignant tumors begin to grow.

Resource:

http://www.niehs.nih.gov/research/atniehs/labs/escbl/

Lung cancer and veterans

Veterans often develop cancer as a result of exposure to hazardous materials – even when the exposure happened decades ago. The herbicide Agent Orange was used in Vietnam and it is acknowledged to cause prostate and respiratory cancers. The Department of Veterans Affairs even states that any respiratory cancer in a veterans known to have served in an Agent Orange area automatically qualifies for benefits.

Lung cancer is also caused by exposure to asbestos, depleted uranium, and other materials that many servicemen encountered. Contrary to popular thinking, there are many causes of lung cancer beside tobacco.

There are two main types of lung cancer, small-cell lung cancer and non-small-cell lung cancer. The types have different staging classifications.

About 10 to 15 percent of lung cancers are small-cell. Small-cell lung cancer is categorized as either limited stage or extensive stage. In the limited stage, the cancer is found in one lung and the surrounding lymph nodes in that lung only. In the extensive stage, the cancer has spread into both lungs or other organs in the body.

Small-cell lung cancer tends to progress from the limited to the extensive stage fairly early, forming large tumors and entering other organs rather quickly. For this reason, surgery is often not an option for treatment for small-cell lung cancer. However, chemotherapy is often employed as a treatment.

Non-small-cell lung cancer makes up over 80 percent of all lung cancers. Within non-small-cell lung cancer are the subtypes adenocarcinoma, squamous cell carcinoma, and large cell carcinoma.

Non-small-cell lung cancer is categorized into four stages. The higher the number, the more advanced the cancer. Most lung cancers are diagnosed in Stage 3 or Stage 4.

Non-small-cell lung cancer can be treated by surgery, radiation, and chemotherapy. Doctors decide on a treatment plan based on the stage of the cancer, and the age and overall health of the patient.

If you think you could get lung cancer, be sure to get screened. The earlier the cancer is diagnosed, the better your chances will be.

Can Quitting Smoking Easily Be a Symptom of Lung Cancer?

An article in the most recent issue of the Journal of Thoracic Oncology detailed a study on patients who quit smoking with ease. The study showed that patients whose experience in quitting smoking had few or no troubles also developed lung cancer within three years of quitting. The study subjects quit smoking well before they exhibited any sings of the disease, which has convinced researchers that the comparative easiness of how the patients were able to quit could also be a symptom of lung cancer itself.

Researchers at the Thomas Jefferson University Medical Center in Philadelphia have hypothesized that active lung cancer cells release a compound that counteracts the body’s dependence on nicotine, the active ingredient in tobacco. Since one of the primary obstacles that smokers come across when attempting to quit smoking is nicotine addiction, the hardest part of quitting becomes much easier, albeit at a severe cost to the patient’s health.

The study looked at the behavior 115 former smokers who were later diagnosed with lung cancer. Out of those 115, 55 had gone through some type of program to quit smoking, such as nicotine gums or patches, well before they were diagnosed with the disease, with 31 reporting that they quit with ease. The data revealed that patients who had stopped smoking with very little or no difficulty showed symptoms of lung cancer in just over two years.

Dr. Barbara Campling and her team of researchers conducted the tests with patients at the Philadelphia Veterans Hospital. Dr. Campling and her group ascertained the level of the patient’s nicotine addiction through an interview and psychological test. The data from those tests showed that the patients who said they quit with ease were just as addicted to nicotine as those who either quit with difficulty or continued to smoke.

Dr. Campling also pointed out that her team’s findings might refute much of the popular belief behind smoking cessation and lung cancer. Many doctors previously believed that smokers eventually quit due to the visible symptoms of lung cancer, including heavy coughing and other respiratory issues, which made the task of inhaling the smoke more difficult.

The findings of this new study, despite the limited number of participants, have opened up other ideas on how to detect lung cancer in smokers. The news may lead to smokers who suddenly lose their cravings for nicotine to visit a doctor and determine if they are undergoing the early stages of lung cancer. As with most cancers, early detection is a key to any possible recovery.

The study may also lead to other potential applications for smoking cessation programs. If scientists can isolate the agent that induces the patients in the study to quit smoking immediately and painlessly, such a discovery could lead to new forms of therapy to help smokers quit the habit much easier.

Dr. Campling also suggests that smokers do not take the findings as a justification for continuing to smoke. She said that a smoker who does not consider quitting based on her study has “the absolutely wrong interpretation” of the findings.

Sources:
http://topnews.net.nz/reports/212505-ease-quitting-linked-lung-cancer
http://www.philly.com/philly/entertainment/20110307_If_quitting_comes_easy.html
http://www.washingtonpost.com/wp-dyn/content/article/2011/03/07/AR2011030703659.html

Heavy Cigarette Smoking On the Decline

A recent report from researchers at the University of California at San Diego has revealed that the habit of smoking at least one pack (20 cigarettes) a day has severely declined over the last fifty years. Investigators observed that the rate of decline was particularly noteworthy in California, where lung cancer rates also fell in proportion to the reduction in smoking rates. The data and the corresponding interpretation of the study were printed in the Journal of the American Medical Association’s March 2011 issue.

The UCSD study showed how much smoking has declined since the early 1960s. According to reports, more than fifty percent of all adult smokers in the US smoked at least one pack per day. That number fell to just over forty percent by 2007. “Moderate” smoking (10 to 20 cigarettes a day) rates also fell. In California, the number of moderate smokers fell from 11.1 percent of all adults in 1965, down to 3.4 percent in 2007. In other states, the number fell from 10.5 percent of all adults down to 5.4 percent.

The study credits much of the decline to smoking education programs. In 1964, the US Surgeon General released the first major findings on the correlation between cigarette smoking and lung cancer. Two years later, the Food and Drug Administration required mandatory warning labels on all cigarette packaging. Today, most cigarette packs and cartons carry warning labels, including warnings about how smoking can complicate pregnancy and lead to low birth rates in pregnant women who smoke.

Another factor attributed to the reduction in smoking rates is the development in new technologies to combat nicotine addiction. One of the primary reasons that smokers find quitting so difficult is the intense nicotine addiction that smoking brings. The invention of nicotine patches, lozenges and gums as part of a smoking cessation program has helped millions of smokers quit the habit over the last twenty years.

In addition to federal mandates requiring the addition of warning labels to cigarette packaging, many state and municipal jurisdictions created anti-smoking laws and ordinances. Several states added higher taxes to cigarettes, with California among the first to enact such statutes. Also, many cities passed local laws prohibiting smoking in bars, restaurants and public buildings.

Public awareness campaigns, such as those conducted by the American Heart Association, the American Lung Association and the American Cancer Society, also helped bring the issues of cigarette smoking to the attention of the American public. The campaigns highlighted many of the dangers that surround cigarette smoking, including lung cancer, throat cancer and emphysema.

As California took the lead in many of the anti-smoking efforts, the study also showed how lung cancer incidence rates declined in the state well before other states saw the same results. Deaths from lung cancer peaked in 1987 in California, with 109 per 100,000. The death rate fell to 77 per 100,000 in 2007. In other states, the lung cancer death rate peaked in 1993 at 117 per 100,000 and fell to 102 per 100,000 in 2007.

Sources:
http://www.npr.org/blogs/health/2011/03/16/134597676/heavy-smoking-is-fast-becoming-history?ps=sh_sthdl
http://www.wtma.com/rssItem.asp?feedid=116&itemid=29645079
http://health.usnews.com/health-news/managing-your-healthcare/articles/2011/03/15/heavy-smoking-declines-in-us
http://www.webmd.com/smoking-cessation/news/20110315/heavy-smokers-us-dwindling
http://www.cnn.com/2011/HEALTH/03/15/pack.smokers.now.rare/index.html
http://www.medicalnewstoday.com/articles/219085.php
http://www.latimes.com/health/boostershots/la-heb-california-smoking-20110316,0,5345363.story
http://en.wikipedia.org/wiki/Tobacco_packaging_warning_messages#United_States_of_America

Lung Cancer Rates Increase Among British Women

A new report by the group Cancer Research UK compares lung cancer rates in the British population from 1975 to 2008. The report showed that the number of women over sixty years of age diagnosed with lung cancer jumped from 5,700 in 1975 to 15,100 in 2008, an increase of nearly 165 percent in just over thirty years.

Also, the number of women overall diagnosed with lung cancer increased by 125 percent, from 7,800 in 1975 to 17,500 in 2008. By comparison, the number of men over sixty diagnosed with the disease actually fell, from 23,400 in 1975 to 15,100 in 2008.

The report cites the increase in the number of women taking up smoking in the 1960s and 1970s as the reason for the sharp increase. Statistics have shown that between 80 and 90 percent of all instances of lung cancer are tied to smoking.

Dr. Stephen Spiro, a spokesman for the British Lung Foundation, said that lung cancer has surpassed breast cancer as the leading cause of cancer deaths for women in Britain and several European nations. Dr. Spiro praised the efforts of government officials to raise the public’s awareness of the dangers of smoking, but also cited the fact that up to ten million adult Britons, about 20 percent of the population, still smoke.

Jean King, the director of tobacco control for Cancer Research UK, said that the group would continue to support smoking cessation programs. Also, Cancer Research UK is attempting to have advertisements for cigarettes covered or removed from stores that young people might frequent. Ms. King said that the advertising ban would “protect young people from being recruited into an addiction that kills half of all long term smokers”.

Sources:
http://www.mirror.co.uk/news/top-stories/2011/03/07/lung-cancer-rates-in-women-over-60-have-almost-trebled-in-past-40-years-115875-22971496/
http://www.cafonline.org/Default.aspx?page=19967
http://www.bbc.co.uk/news/health-12651455

Massachusetts Helps Vets Quit Smoking

State health officials in Massachusetts are developing measures to help the state’s military veterans quit smoking.  The new campaign is the second effort launched since 2008 to help veterans with this growing health problem.  Massachusetts Lieutenant Governor Tim Murray released a statement praising “the brave men and women” in uniform and said that the campaign would help to “provide (veterans) with the opportunity to live long, healthy lives”.

A report from the office of Governor Deval Patrick showed that nearly one-fourth of all Massachusetts veterans smoke cigarettes.  The US Centers for Disease Control and Prevention in Atlanta estimates that less than one-sixth of all adults in the Bay State smoke.  A related report from the Institute of Medicine showed that nearly one in three people on active military duty smoke, with the number rising to half or more among those veterans who have been deployed to war zones in Iraq and Afghanistan.

Coleman Nee, a veteran of the US Marine Corps during Operation Desert Storm in 1991, is now the Massachusetts Secretary of Veterans’ Services.  Mr. Nee also spoke out about the anti-smoking campaign, saying that smoking among veterans is “a very serious problem”.  He said that smoking is an issue for veterans’ services agencies as well as public health groups.  He called the addiction to smoking among service members “a real shame”.

Mr. Nee recalled that, during his time in the Marine Corps, he and other service personnel would receive cigarettes and smokeless tobacco as part of their care packages from home, a tradition that started back in World War I.  He remarked that this practice has since stopped; especially in light of the numerous health problems that smoking is now understood to cause.

A report from the state public health office revealed that cigarette smoking is the number-one cause of preventable disease and death in Massachusetts.  The report also estimates that health care costs for smokers add up to over $4.3 billion annually.

The public awareness campaign for veterans includes a toll-free number that offers support and information on smoking cessation programs.  When the first campaign started in 2008, thousands of veterans called the support hotline and obtained nicotine patches to help them quit the habit.  Massachusetts State Representative James E. Valle, chairman of the Joint Committee on Veterans and Federal Affairs, said that the program shows the state’s commitment to “helping those who have served” in uniform to lead healthier lives.

The moves to help veterans quit smoking come in light of a study commissioned by the Department of Defense in 2009.  The study examined the feasibility of banning smoking among all service personnel within the next decade.  All military bases prohibit smoking indoors, but the study also considers banning the sale of tobacco products on bases, as well as stopping troops in the field from smoking.

However, some military personnel are opposed to any ban on smoking.  Many see smoking as a stress reliever, especially during the heat of battle.  The Defense Department study also found that bases generate millions of dollars from tobacco sales, most of which goes toward covering the costs of programs for dependents and for recreation.

Sources:
http://www.wwlp.com/dpp/news/massachusetts/veterans-receive-help-to-stop-smoking
http://www.boston.com/news/local/massachusetts/articles/2011/03/08/veterans_get_help_to_quit_smoking/
http://articles.cnn.com/2009-07-12/us/military.smoking.ban_1_smokeless-tobacco-tobacco-sales-pancreatic?_s=PM:US

Scientists Find Potential New Skin Cancer Treatments

Scientists at Fred Hutchinson Cancer Research Center in Seattle have found a new method for the treatment for a common form of skin cancer. Researchers at the laboratory, under the direction of Dr. Valeri Vasioukhin, have detected that a protein, known as alpha-catenin, that functions acts as a suppressive agent for squamous cell carcinoma tumors. The research team has also discovered the process by which this protein keeps tumor cell growth in line.

Dr. Vasioukhin’s team studied mice that were genetically engineered not to create the alpha-catenin protein, which is typically found in hair follicles. The scientists noted that the mice without the protein developed squamous cell carcinoma tumors at a faster rate than the control group. Dr. Vasioukhin noted that the cells in the alpha-catenin-deficient mice grew at such a rapid rate that “they become very crowded in the Petri dish”.

The rapid rates of cell growth and proliferation are some of the primary characteristics of cancer cells. Dr. Vasioukhin also said that the fact that the mice without the protein experienced such accelerated rates of cell growth “is an important event in cancer development.” The research team found that alpha-catenin also limits the production of another protein, labeled Yap1. Scientists believe that the Yap1 protein acts as a triggering agent for cells to become malignant.

Dr. Vasioukhin also remarked on the connection between alpha-catenin and Yap1. He noted that, in the mice with alpha-catenin deficiencies, the Yap1 protein was activated. “Therefore, Yap1 is likely to be an excellent target for the treatment of patients with squamous cell carcinoma,” he said. If further tests are successful in isolating the Yap1 protein, future research efforts may be devoted to developing a treatment for squamous cell carcinoma patients based on the alpha-catenin protein.

What is squamous cell carcinoma?

Squamous cell carcinoma is the second-most common form of skin cancer, behind basal cell carcinoma and ahead of melanoma.  According to reports from public health officials, more than 700,000 cases of squamous cell carcinoma are diagnosed each year. The disease affects areas of the skin that receive more exposure to the sun’s harmful ultraviolet rays, including the face, arms, neck and legs.

Treatments for the disease range from topical chemotherapy and radiation therapy to surgical removal of the tumors. Dr. Ian Frazer, an Australian cancer researcher who helped develop the human papilloma virus (HPV) vaccine, is also developing a vaccine to protect patients from squamous cell carcinoma. The vaccine is currently undergoing trials and may be ready for the mass market by 2020.

Sources:
http://www.eurekalert.org/pub_releases/2011-05/fhcr-sdn051611.php
http://en.wikipedia.org/wiki/Squamous_cell_carcinoma
http://www.cosmosmagazine.com/news/2327/skin-cancer-vaccine-within-reach
http://www.imperfectparent.com/topics/2011/05/20/advances-in-skin-cancer-treatment-and-detection/

Vaccine Stops Cancer Before It Starts

The biotechnology company OncoPep is developing a vaccine against a deadly form of cancer before it becomes evident in patients at risk to contract the disease.  The vaccine is designed to prevent the onset of multiple myeloma, a type of cancer that attacks the bone marrow and forms tumors inside the bone.  The disease also strikes the immune system, increasing the production of antibodies and leading to pain and excess bleeding.

The vaccine represents a new step in the growing field of immunotherapy. Scientists who research immunotherapy treatments for various cancers develop methods for the body’s own immune system to combat cancer.  Immunotherapy research had led to the creation of vaccines that can prevent cancer, such as the human papillomavirus (HPV) vaccine that prevents cervical cancer in women. The field has also produced vaccines by programming antibodies to fight cancer as they would fight infections or other diseases.

The myeloma vaccine fits in an intermediate stage in cancer treatment. The primary treatment group would consist of patients who have a preliminary, pre-cancer stage of the disease, known as smoldering multiple myeloma (SMM).  Patients with SMM have abnormal growth rates in the plasma cells that create antibodies, but do not have the tumors and other symptoms that come with the full onset of the disease.

A team of researchers at the Dana Farber Cancer Institute in Boston developed a method to administer a vaccine made up of a mix of protein molecules called peptides.  The peptides contain protein molecules that myeloma tumors require for sustained life and growth.  As the antibodies attack the peptides, they also attack the myeloma cells. The immune system then robs the cancer cells of the proteins they need to survive.

Just as with blood types, doctors have classified patients into different types of immune systems, called “human leukocyte antigen (HLA) types”.  Doctors commonly use HLA typing to match donors and recipients in bone marrow transplants.  Researchers on the myeloma vaccine will target the treatment at patients with the most common HLA type, known as HLA type A2. Doris Peterkin, CEO of OncoPep, said that the peptides were more likely to trigger the needed antibodies in patience with the most common HLA type, and would be more effective in preventing SMM from becoming full myeloma.

As promising as the preliminary results have been, the road to a vaccine for multiple myeloma is still a long one.  Although patients with SMM develop full myeloma in almost 80 percent of all cases, only 10 percent of those cases progress to that stage each year.  OncoPep and the research team will still need to collect data for several years on the effectiveness of the vaccine before it will be ready for the wider marketplace.

Dr. Kenneth Anderson, one of the research team leaders who developed the vaccine, said that he hopes it could be used as a preventative measure for patients with SMM, who currently do not have treatment options available until the disease becomes full-blown myeloma.  “The idea (behind the vaccine) would be to prevent the development of an active cancer, ” Dr. Anderson said.

Sources:
http://www.technologyreview.com/printer_friendly_article.aspx?id=37520
http://www.fiercevaccines.com/story/oncopep-vax-aims-stop-multiple-meyloma-it-starts/2011-05-05
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001609/

Breast Cancer Drug May Help Fight Lung Cancer

A new study from researchers at the University of Geneva shows that the breast cancer drug Tamoxifen may also be useful in combating lung cancer. The study found that women who were undergoing treatment for breast cancer, with Tamoxifen as part of their chemotherapy routines, also showed a reduced death rate from lung cancer. The research team examined data from women who received Tamoxifen from 1980 to 2003 and found that the death rate from lung cancer in those patients was eighty-seven percent lower than those who did not take the drug.

Tamoxifen has been used for decades to suppress the production of estrogen, a female sex hormone. Previous research efforts have tied the production of estrogen to breast cancer. Recent studies have also linked hormone replacement therapy, often prescribed to post-menopausal women, to an increased incidence of lung cancer. One of the premises of the Geneva study was to learn if suppressing hormones could be used as a therapy to treat lung cancer.

The study data did not show a decrease rate in the appearance of lung cancer in women who took Tamoxifen, but the results did show a remarkable reduction in the mortality rate from the disease. Dr. Elisabetta Rapiti, the study’s team leader, said that the data shows clear signs, “that there is a hormonal influence on lung cancer”. She also cited earlier findings that showed that lung cancer cells have receptors for estrogen and progesterone, another female sex hormone, which suggests that the mutated cells could feed off the hormones.

Oliver Childs, the senior science information officer at the British research facility Cancer Research UK, told reporters that it was “possible” that Tamoxifen and other anti-estrogen drugs could also have a positive effect on lung cancer patients. However, he also said that the results from the Geneva study were inconclusive since “the number of women who developed lung cancer (in the study) was small”.

In Dr. Rapiti’s study, out of more than six thousand patient records examined, only forty of the women showed signs of lung cancer. Less than half of the Geneva study patients underwent treatment with Tamoxifen or other hormone suppressants, and only one-third of the patients had ever smoked. The study data shows that nearly as many smokers used Tamoxifen as underwent other kinds of chemotherapy for their breast cancer.

The study authors also mentioned that the data was incomplete in places, including how the breast cancer diagnosis affected the women’s smoking behaviors. They also mentioned that they often lacked specific information on the types and dosages of anti-estrogen therapies the women received during their chemotherapy treatments.

Mr. Childs said that “large-scale clinical trials” would be necessary to determine how Tamoxifen could be used as a potential weapon against lung cancer. Dr. Rapiti also mentioned “prospective studies” to examine the findings further. She also said that, if any new studies confirm the earlier findings, it “could have substantial implications for clinical practice” in the treatment of lung cancer.

Sources: http://www.bbc.co.uk/news/health-12243206 http://www.medpagetoday.com/HematologyOncology/LungCancer/24487 http://www.financialexpress.com/news/Breast-cancer-drug-may-also-cut-lung-cancer-deaths–Study/741687/

Scientists Attempt to Widen Range of Targeted Cancer Drugs

The development of new chemotherapy drugs that target cancerous tumor cells – while leaving healthy cells alone – has been a breakthrough in the cancer treatment field. However, these treatments have been shown to work only on a select few patients. Even when they do work, the tumor can create a resistance to the drugs, leaving the patient with fewer options. Several scientific research teams are working on new drugs that will work with a wider range of patients and target tumors before they can develop a resistance to the treatments.

The main component in the research behind these new cancer drugs comes from a deeper knowledge of how cancer cells come into being, grow, multiply and spread throughout the body.  One study at the Massachusetts Institute of Technology examines lung cancer cells and how scientists can synthesize drugs that can target the tumors.  The treatments can also be modified to help the patient as they proceed through the chemotherapy routines.

The MIT study takes a close look at a class of drugs known as “epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors”. Tyrosine kinase is a protein that functions as an “on/off” switch for many cell functions. When the proteins that regulate cell growth are permanently set in the “on” position, the cells can grow quickly and in uncontrolled ways, a common occurrence in cancer cells. Tyrosine kinase inhibitors act to slow down or stop the wild cell growth and stabilize or reduce the size of lung cancer tumors.

EGFR inhibitors are effective in less than 40 percent of all lung cancer patients. The drug’s effectiveness varies widely based on the patient’s medical history, smoking habits, race, gender and ethnicity. Dr. Philip Sharp, Professor at the Koch Institute for Integrative Cancer Research at MIT, said that laboratories around the world have “hundreds of drugs” that are in various stages of testing and development. “To personalize cancer care, we must interpret changes in (tumors) to predict the correct drug combination to use.”

Another factor in customizing cancer treatments is that some patients carry a mutation in the gene for EGFR, which makes the drugs more effective. The MIT study examined the differences between those patients and patients that did not respond to the drug. MIT researcher Doug Lauffenburger, along with a team of researchers, developed mathematical models to simulate the behavior of different types of cancer cells. The models revealed that the cancer cells that responded to the drug had a slower uptake of EGFR than the less responsive tumors.

While these methods require further verification, scientists are hopeful that the findings can lead to a possible screening test for lung cancer patients to determine the effectiveness of EGFR inhibitors in individual cases. Lauffenburger and his team also learned that the EGFR inhibitors could be more effective in certain cases when combined with another class of chemotherapy drug known as MEK inhibitors, which are often used to treat melanoma. In terms of tailoring drug combinations to individual patients, Dr. Sharp remarked that these findings “indicate that this is beginning to become possible.”

Sources: Technology Review, Medscape.com