Showing posts with label Cancer. Show all posts
Showing posts with label Cancer. Show all posts

December 1, 2016

Man Cured of Bladder Cancer with Testosterone Experimental Therapy





 

A man with advanced prostate cancer that didn’t seem to be treated has been “cured” by a new experimental therapy.

The new treatment involved shocking tumours to death using testosterone.

Other very ill men involved in the trial saw astonishing results, with tumours being seen to shrink and the progress of the disease stopping in its tracks.

Overall, most of the people involved in the trial seemed to undergo positive results. Scientists tested that by looking at levels of Prostate Specific Antigen (PSA), a blood marker used to monitor prostate cancer – and found that it fell in most of the 47 people involved in the study.

 
And one individual had so little of the market in his body – and no trace of the disease – that doctors said he appears to be cured after 22 cycles of the treatment.

The trial saw the men complete at least three cycles of what is called bipolar androgen therapy, or BAT. That sees their bodies get flooded with testosterone and then starved of it.

Until now, the male hormone had thought to help spur prostate cancer on. And so scientists have traditionally looked to treat it by cutting off the supply of testosterone.

 
Mouth cancer rates up 68% – and unhealthy lifestyles are to blame
But the new study comes off the back of lab experiments that have seen cancer cells get suppressed or even killed by blasts of the same hormone.

Professor Sam Denmeade, from Johns Hopkins University School of Medicine in Baltimore, US, who led the new study, said: "We think the results are unexpected and exciting.

"We are still in the early stages of figuring out how this works and how to incorporate it into the treatment paradigm for prostate cancer.

"Thus far we have observed dramatic PSA response in a subset of men; PSA levels declined in about 40% of men and in about 30% of men levels fell by more than 50%.

"Some men also have objective responses with a decrease in the size of measurable disease, mostly in lymph nodes. Many of the men have stable disease that has not progressed for more than 12 months.

"I think we may have cured one man whose PSA dropped to zero after three months and has remained so now for 22 cycles. His disease has all disappeared."

Early findings from the on-going Restore study were presented at the EORTC-NCI-AACR symposium on Molecular Targets and Cancer Therapeutics in Munich, Germany.

All the patients had spreading cancer that was resistant to treatment with two of the latest hormone therapy drugs, abiraterone and enzalutamide.

The men received high dose injections of testosterone once every 28 days. At the same time, they were given a drug that stopped testosterone being produced naturally by the testicles.

"Our goal is to shock the cancer cells by exposing them rapidly to very high followed by very low levels of testosterone in the blood," said Prof Denmeade.

Six of the men tested positive for a protein called AR-V7 that may be associated with resistance to enzalutamide.

After BAT treatment, no sign of the protein was seen in the blood of all six. Two of the men had declines in PSA level of 50% or more.

The therapy appears to be well-tolerated by the patients, one man experiencing an increase in pain and another having a problem with urine retention.

Prof Denmeade said it was still not clear how the treatment worked, but it appeared to involve cell signalling and part of the process of cell division. Large doses of testosterone also seemed to cause prostate cancer cells to make breaks in their DNA.

Cancer cells stopped dividing and turned "senescent", meaning they "become like old men who sit around and tell stories but don't make much trouble", said the professor.

He cautioned that the therapy was still highly experimental and only suitable for men not suffering painful symptoms.

"Testosterone treatment can definitely worsen pain in men with prostate cancer who have pain from their disease," he said.

A multi-centre randomised US trial called Transformer is now comparing BAT with enzalutamide in men who have become resistant to abiraterone. It aims to recruit a total of 180 participants.

Prof Denmeade said: "If we find testosterone is superior then we would hope to move on to larger trials. Our problem is this is not a drug that is owned by a pharmaceutical company; it is generic testosterone. So moving forward is going to be difficult due to issues with finding funds to run a bigger trial."

Each year around 47,000 men are diagnosed with prostate cancer in the UK and 11,000 die from the disease.

Dr Matt Hobbs, deputy director of research at the charity Prostate Cancer UK, said: "Drugs that reduce the levels of testosterone (androgen deprivation therapy) are an effective treatment for thousands of men with advanced prostate cancer.

"However, at some point the cancer evolves and those drugs stop working. This research is intriguing because it offers a hint that - somewhat unexpectedly - for some men whose cancers have reached that 'hormone-resistant' stage it may be possible to kill or stop growth of the cancer cells by actually overloading them with testosterone.

"Many exciting new lines of attack against prostate cancer are emerging of which this is one.

“However, this is early stage research and further studies are needed in order to understand exactly how intriguing developments like this work and to test the findings more robustly in large clinical trials."


Press Association

May 18, 2016

Study: HIV Cancer Patients Less Likely to be Treated


 
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ATLANTA -A new study finds HIV-infected patients with cancer in the United States appear to be less likely to receive cancer treatment, regardless of insurance and other existing health conditions. The study, by researchers at the University of Utah, National Cancer Institute and the American Cancer Society, appears early online in Cancer.

Cancer is an increasingly common cause of morbidity and mortality among individuals infected with the human immunodeficiency virus (HIV). In the United States, cancer incidence rates in this population have increased since the introduction of highly active antiretroviral therapy (HAART). Cancer is now the second most common cause of death among HIV-infected individuals, after AIDS-related deaths.

While previous studies have shown that cancer patients who are infected with HIV are less likely to receive cancer treatment compared with HIV-uninfected individuals, whether that was due to insurance status and other conditions was largely unstudied. For the new study, researchers led by Gita Suneja, MD, MSHP, from the Department of Radiation Oncology at the University of Utah used the National Cancer Data Base to study non-elderly adults diagnosed with ten common cancers from 2003 to 2011. They examined associations between HIV status and lack of cancer treatment, taking into account insurance status and comorbidities.

After adjusting for those two known predictors of lack of treatment, the disparity remained for all cancers studied, except anal cancer. HIV-infected patients were more likely to lack cancer treatment for cancers of the head and neck (relative risk [RR] = 1.48); upper gastrointestinal tract (RR = 2.62); colorectum (RR = 1.70); lung (RR = 2.46); breast (RR = 2.14); cervix (RR = 2.81); prostate (RR = 2.16); Hodgkin lymphoma (RR = 1.92); and diffuse large B-cell lymphoma (RR = 1.82).

The authors say factors that predicted a lack of cancer treatment among HIV-infected individuals varied by tumor type (solid tumor vs lymphoma), but black race and a lack of private insurance (e.g.: having Medicaid, Medicare or no insurance) were found to be predictors for both groups. However, even among privately insured cancer patients, HIV-infected cancer patients are less likely to receive cancer directed treatment compared to HIV-uninfected patients.

The study says several factors may contribute to the finding. HIV-infected patients have historically been excluded from cancer clinical trials, thereby limiting the applicability of clinical trial results for this population. Cancer treatment guidelines specific to HIV-infected patients are not available for most cancer types. Clinicians may lack experience treating HIV infected patients with cancer. Furthermore, the psychosocial and economic challenges associated with the dual management of cancer and HIV treatment may make adherence to treatment a challenge.

"...cancer care providers and policy makers need to devote special attention to the HIV-infected patient population to understand and address the factors driving differential cancer treatment," write the authors. "Cancer treatment not only extends survival from cancer, but also can improve quality of life, even for patients with advanced stage disease. The observed disparity is of particular importance given the extended survival of HIV infected patients treated with antiretroviral therapy and the rising number of cancer cases."

###

The study was a collaboration between the University of Utah School of Medicine Department of Radiation Oncology, American Cancer Society Intramural Research, Emory University Epidemiology, and the National Cancer Institute Division of Cancer Epidemiology and Genetics.

Article: Disparities in Cancer Treatment among Patients Infected with the Human Immunodeficiency Virus, CANCER; published early online May 17, 2016 DOI: 10.1002/cncr.30052
eurek

alert.org

November 6, 2015

On Organic Diet and No Family Hist of Cancer but Still gets Stomach Cancer? Organic Salt?



                                                                       

There’s plastic in your salt, Organic Salt.
That’s the finding of a new study published in the journal Environmental Science & Technology. 
When researchers analyzed fifteen brands of common table salt bought at supermarkets across China, they found among the grains of seasoning micro-sized particles of the common water bottle plastic polyethylene terephthalate, as well as polyethylene, cellophane, and a wide variety of other plastics.
The highest level of plastic contamination was found in salt sourced from the ocean: The researchers measured more than 1,200 particles of plastic per lb of sea salt. The team, led by Huahong Shi of East China Normal University also found tiny particles of plastic in salt sourced from briny lakes, briny wells, and salt mines, although at lower levels—between 15 and 800 particles/ lb.
Where’s all that plastic coming from? Microbeads, for one — those tiny bits of plastic in your face wash that go down the drain and into the water table, where they eventually end up in the ocean, and then your stomach. That’s not good because microplastics soak up cancer-causing and endocrine-disrupting pollutants in the water and deposit them in your body.
This study looked specifically at salt sold in Chinese markets, but is it possible that salt sold in the U.S. is contaminated with microplastics as well? Definitely, according to Sherri Mason, professor at SUNY Fredonia, and an expert on microplastics. “Plastics have become such a ubiquitous contaminant, I doubt it matters whether you look for plastic in sea salt on Chinese or American supermarket shelves,” she told Scientific American.
How big a problem is this, and what’s the conscientious consumer to do? Well, the concentration of plastics in salt is still less than it is in shellfish, so it probably shouldn’t be the biggest concern on your plate. Besides that, salt is both essential for life and fairly easy on the environment, compared to most things we eat, so don’t go cold turkey on it just yet. So what’s the solution? You can start by ditching the microbeads: The less plastic that ends up in the ocean, the less that ends up in your gut.

August 12, 2015

Ex President Jimmy Carter has Cancer


                                                                         



Former U.S. President Jimmy Carter said on Wednesday that recent liver surgery revealed he had cancer that had spread to other parts of his body.

"I will be rearranging my schedule as necessary so I can undergo treatment by physicians at Emory Healthcare," Carter, 90, said in a statement. "A more complete public statement will be made when facts are known, possibly next week."

Carter, a Democrat, served as the 39th president from 1977 to 1981 after defeating Republican incumbent Gerald Ford. He was defeated for re-election in 1980 by Republican Ronald Reagan.

The Carter Center in Atlanta said last week that he had undergone elective surgery at Emory University Hospital to remove a small mass in his liver.

It added that the operation had proceeded without issues and that the prognosis was excellent for a full recovery.

Carter cut short a trip to Guyana in May after feeling unwell and returned to Atlanta. He had traveled to the South American country to observe national elections. At the time, the center said only that Carter had departed after "not feeling well."

Reuters
 

May 25, 2015

Ejaculation Reduces Chances of Prostate cancer




Good news, men: you may be able to decrease your risk for prostate cancer by ejaculating — frequently, according to research presented here at American Urological Association 2015 Annual Meeting.
The frothy advice is not new but is now backed up by the "strongest evidence to date" on the subject, according to lead author Jennifer Rider, ScD, MPH, an epidemiologist at the Harvard T.H. Chan School of Public Health in Boston.
"There is no modifiable risk factor for developing prostate cancer," Dr Rider told Medscape Medical News. "It would be exciting to tell men that there was a way to modify their risk."
However, she noted that these are observational data and urged caution when "interpreting them."
The results are "fascinating," said Jesse Sammon, MD, a urologist at the Henry Ford Hospital in Detroit, who attended Dr Rider's presentation. "It was the highlight of the session on cancer epidemiology; the moderator called it the 'study most likely to be tweeted'."
These are "incredibly high-quality data," said Dr Sammon, who was not involved with the study.
The data come from nearly 32,000 men in the prospective Health Professionals Follow-up Study, who now have been followed for 18 years.
During the study period, 3839 men have been diagnosed with incident prostate cancer, 384 cases of which were lethal.
At recruitment in 1992, all participating men were asked to report their average monthly frequency of ejaculation from the ages of 20 to 29 years and 40 to 49 years, and during the previous year. A lifetime average was then computed from these reports.
After potential confounders were controlled for, the risk for prostate cancer was 20% lower in men who ejaculated at least 21 times a month than in men who ejaculated 4 to 7 times a month. The 20% risk reduction was seen at ages 20 to 29 and 40 to 49, and for the lifetime average (P trend < .0001 for all).
At ages 40 to 49, men most (38.0%) reported 8 to 12 ejaculations per month; only 8.8% reported at least 21 ejaculations per month.
"We shouldn't dwell on the exact numbers of ejaculation, but instead should focus on the dose–response relation," Dr Rider advised.
She summarized: "Safe sexual activity could be good for prostate health."
Notably, there was no association between ejaculation frequency and the risk for high-grade, advanced, or lethal disease, she reported. The reason for this exception is not known.
These results are an update of the last major report from the Health Professionals Follow-up Study, which was published about 10 years ago (JAMA2004;291:1578-1586). At that time, investigators concluded that "high ejaculation frequency may possibly be associated with a lower risk of total and organ-confined prostate cancer," as reported by Medscape Medical News.
Many other studies have likewise reported that ejaculation frequency might be tied to prostate cancer risk, with more orgasms being protective.
But these new data have three outstanding strengths, Dr Rider said.
First, the study is prospective, whereas most other studies have been retrospective, and the data are long term. Second, the study involves the largest cohort to date. And third, the study has specific information on ejaculation, she explained.
Whereas previous studies have tended to rely on "proxies" for ejaculation, such as age at marriage, number of children, and number of sex partners, the Health Professionals Follow-up Study investigators were bold; they explicitly asked about ejaculations from sexual intercourse, masturbation, and nocturnal emissions.
The average age of the men in the study was about 59 years, and they had undergone an average of five PSA tests by 2008. Most of the men were married, but the men who reported at least 21 ejaculations per month at ages 40 to 49 were more likely to be divorced than less robust ejaculators (11.8% vs 4% - 7%).
American Urological Association (AUA) 2015 Annual Meeting: Abstract PD6-07. Presented May 15, 2015.

January 7, 2014

The Best Treatment of Pancreatic Cancer





The best treatment for pancreatic cancer depends on how far it has spread, or its stage. The stages of pancreatic cancer are easy to understand. What is difficult  is attempting to stage pancreatic cancer without resorting to major surgery. In practice, doctors choose pancreatic cancer treatments based upon imaging studies , surgical findings, and an individual’s general state of well being. 
Stages of Pancreatic Cancer
Stage is a term used in cancer treatment to describe the extent of spread of the cancer. The stages of pancreatic cancer are used to guide treatment and to classify patients for clinical trials. The stages of pancreatic cancer are:
  • Stage 0: No spread. Pancreatic cancer is limited to a single layer of cells in the pancreas. The pancreatic cancer is not visible on imaging tests or even to the naked eye.
  • Stage I: Local growth. Pancreatic cancer is limited to the pancreas, but has grown to less than 2 centimeters across (stage IA) or greater than 2 centimeters (stage IB).
  • Stage II: Local spread. Pancreatic cancer has grown outside the pancreas, or has spread to nearby lymph nodes.
  • Stage III: Wider spread. The tumor has expanded into nearby major blood vessels or nerves but has not metastasized.
  • Stage IV: Confirmed spread. Pancreatic cancer has spread to distant organs.
Determining pancreatic cancer's stage is often tricky. Imaging tests like CT scans and ultrasound provide some information, but knowing exactly how far pancreatic cancer has spread usually requires surgery.
Since surgery has risks, doctors first determine whether pancreatic cancer appears to be removable by surgery (resectable). Pancreatic cancer is then described as follows:
  • Resectable: On imaging tests, pancreatic cancer hasn't spread (or at least not far), and a surgeon feels it might all be removable. About 10% of pancreatic cancers are considered resectable when first diagnosed.
  • Locally advanced (unresectable): Pancreatic cancer has grown into major blood vessels on imaging tests, so the tumor can't safely be removed by surgery.
  • Metastatic: Pancreatic cancer has clearly spread to other organs, so surgery cannot remove the cancer.
If pancreatic cancer is resectable, surgery followed by chemotherapy or radiation or both may extend survival.

Treating Resectable Pancreatic Cancer

People whose pancreatic cancer is considered resectable may undergo one of three surgeries:
Whipple procedure (pancreaticoduodenectomy): A surgeon removes the head of the pancreas, parts of the stomach and small intestine, some lymph nodes, the gallbladder, and the common bile duct. The remaining organs are reconnected in a new way to allow digestion. The Whipple procedure is a difficult and complicated surgery. Surgeons and hospitals that do the most operations have the best results.
About half the time, once a surgeon sees inside the abdomen, pancreatic cancer that was thought to be resectable turns out to have spread, and thus be unresectable. The Whipple procedure is not completed in these cases.

Treating Resectable Pancreatic Cancer continued...

Distal pancreatectomy: The tail and/or body of the pancreas are removed, but not the head. This surgery is uncommon for pancreatic cancer because most tumors arising outside the head of the pancreas within the body or tail are unresectable.
Total pancreatectomy: The entire pancreas is surgically removed. Although once considered useful, this operation is uncommon today.
Chemotherapy or radiation therapy or both can also be used in conjunction with surgery for resectable and unresectable pancreatic cancer in order to:
  • Shrink pancreatic cancer before surgery, improving the chances of resection (neoadjuvant therapy)
  • Prevent or delay pancreatic cancer from returning after surgery (adjuvant therapy)
Chemotherapy includes cancer drugs that travel through the whole body. Chemotherapy ("chemo") kills pancreatic cancer cells in the main tumor as well as those that have spread widely. Either of three chemotherapy drugs can be used for pancreatic cancer:
Both 5-FU and gemcitabine are given into the veins during regular visits to an oncologist (cancer doctor).  An oral drug, capecitabine, may be substituted for 5-FU, especially with radiation.
In radiation therapy, a machine beams high-energy X-rays to the pancreas to kill pancreatic cancer cells. Radiation therapy is done during a series of daily treatments, usually over a period of weeks.
Both radiation therapy and chemotherapy damage some normal cells, along with cancer cells. Side effects can include nausea, vomiting, appetite loss, weight loss, and fatigue as well as toxicity to the blood cells. Symptoms usually cease within a few weeks after radiation therapy is complete.

Treating Locally Advanced (Unresectable) Pancreatic Cancer

In locally advanced pancreatic cancer, surgery can't remove the entire tumor. Since surgery to remove only part of the pancreatic cancer has been shown not to help, nonsurgical therapies are best.
Treatment consists of chemotherapy with or without radiation therapy. Either 5-FU or gemcitabine can extend life in people with locally advanced pancreatic cancer.

Treating Metastatic Pancreatic Cancer

In metastatic pancreatic cancer, surgery is used only for symptom control, such as for pain, jaundice, or gastric outlet obstruction.. Radiation may be used for symptom relief as well.  
Gemcitabine is the single most active drug for treating metastatic pancreas cancer. Many studies have been performed to improve on the results of gemcitabine. The latest study,demonstrated that a 4 drug regimen, known as FOLFIRINOX (5-FU/leucovorin/oxaliplatin/irinotecan), is superior to gemcitabine. However due to toxicities, this therapy should be reserved for persons with good activity levels. Other combinations include gemcitabine with erlotinib, gemcitabine with capecitabine gemcitabine with cisplatin, gemcitabine with nab-paclitaxel. .
If an individual progresses on gemcitabine, usual regimens include oxaliplatin with 5-FU or capecitabine or cisplatin with 5-FU or capecitabine. However, efficacy of these regimens is limited.

Palliative Treatment for Pancreatic Cancer

As pancreatic cancer progresses, the No. 1 priority of treatment will shift from extending life to alleviating symptoms, especially pain. Numerous treatments can help protect against the discomfort from advanced pancreatic cancer:
  • Procedures like bile duct stents can relieve jaundice, thus reducing  itching and loss of appetite associated with bile obstruction.
  • Opiod analgesics can help relieve pain.
  • Antidepressants and counseling can help treat depression common in advanced pancreatic cancer.

Clinical Trials for Pancreatic Cancer

New pancreatic cancer treatments are constantly being tested in clinical trials. You can find out about clinical trials for the latest treatments for pancreatic cancer on the web sites of the American Cancer Society or the National Cancer Institute.

January 6, 2014

‘Pringles’ Cancer in a Can

 


Are you aware of the dangerous cancer-causing chemical that is present in almost every bottle or bag of potato chips? Pringles certainly contain this dangerous substance, but they are far from being the only culprit. Although acrylamide is found in essentially all potato chips, it is widely considered to be a harmful, cancer-causing chemical, which makes potato chips one of the most toxic processed foods on the market.

The Story Behind Acrylamide

Pringles.svgAcrylamide develops when carbohydrate-rich foods are cooked at high temperatures (anything above 212°F (100°C). Whether a potato is baked, fried, or roasted, acrylamide will be produced. Many of our standard carbohydrates can be slightly toxic when cooked, including potatoes, and grains. But the levels of acrylamide you would get from naturally cooked whole foods will never be as elevated as junk food.
Pringles chips.JPGFor instance, potato chips and French fries seem to be the worst sources of acrylamide. In fact, a study by the Environmental Law Foundation found that every single chip product that they tested exceeded the legal limit for acrylamide by at least 39 times. Some brands had as much as 910 times the legal limits of acrylamide.
HEATOX was a study that examined the dangers of heat-induced compounds. The report shows that acrylamide is not alone, unfortunately. There are actually over 800 compounds formed by heat, 52 of which have the potential to be dangerous carcinogens. That means that there are plenty of reasons besides acrylamide to avoid cooking your food at high temperatures! For instance, heterocylic amines (HCAs), polycylic aromatic hydrocarbons (PAHs), and advanced glycation end products (AGEs) all pose a serious threat to your health.
The bad news is that researchers currently don’t have an effective strategy for completely cutting acrylamide out of our food. In fact, even using all of our best technology, we are only capable of reducing acrylamide in our food products by 40%, according to HEATOX’s report. That still leaves a lot of cancer-causing chemicals in our diet!
Since you aren’t able to completely eliminate your exposure to acrylamide, it is crucial to take the steps you can in order to decrease your risk of cancer. Interestingly enough, home-cooked food is less likely to contain extremely high levels of acrylamide, so taking the time to prepare your own food is a good start towards reducing acrylamide in your diet!
The main method of decreasing your intake of acrylamide is to mostly consume raw or minimally processed foods. If you don’t cook your food, you never allow acrylamide to form! Raw fruits and vegetables are your healthiest option. There is a widespread movement towards eating raw foods, so you can easily find plenty of tasty recipes that don’t require you to cook your food.
If you aren’t quite ready to cut out that much cooked food, focus on eliminating your intake of obvious problems, such as donuts, sodas, French fries, and, of course, potato chips.
What are your favorite recipes for a raw-food diet? Share your tips in the comments!

 dailyhealthpost

My Cancer is Alive and Im Dying

The advance has sparked new hope that someday doctors may be able to test a host of cancer-killing drugs on a person's own tumor cells in the lab, before returning to the patient with a therapy that is likely to be a good match. Half a century ago, the story goes, a person was far more likely to die from heart disease. Now cancer is on the verge of overtaking it as the No. 1 cause of death.
Troubling as this sounds, the comparison is unfair. Cancer is, by far, the harder problem — a condition deeply ingrained in the nature of evolution and multicellular life. Given that obstacle, cancer researchers are fighting and even winning smaller battles: reducing the death toll from childhood cancers and preventing — and sometimes curing — cancers that strike people in their prime. But when it comes to diseases of the elderly, there can be no decisive victory. This is, in the end, a zero-sum game.
The rhetoric about the war on cancer implies that with enough money and determination, science might reduce cancer mortality as dramatically as it has with other leading killers — one more notch in medicine’s belt. But what, then, would we die from? Heart disease and cancer are primarily diseases of aging. Fewer people succumbing to one means more people living long enough to die from the other.
The newest cancer report, which came out in mid-December, put the best possible face on things. If one accounts for the advancing age of the population — with the graying of the baby boomers, death itself is on the rise — cancer mortality has actually been decreasing bit by bit in recent decades. But the decline has been modest compared with other threats.
graph from the Centers for Disease Control and Prevention tells the story. There are two lines representing the age-adjusted mortality rate from heart disease and from cancer. In 1958 when the diagram begins, the line for heart disease is decisively on top. But it plunges by 68 percent while cancer declines so slowly — by only about 10 percent — that the slope appears far less significant.
Measuring from 1990, when tobacco had finished the worst of its damage and cancer deaths were peaking, the difference is somewhat less pronounced: a decline of 44 percent for heart disease and 20 percent for cancer. But as the collision course continues, cancer seems insistent on becoming the one left standing — death’s final resort. (The wild card in the equation is death from complications of Alzheimer’s disease, which has been advancing year after year.)
Though not exactly consoling, the fact that we have reached this standoff is a kind of success. A century ago average life expectancy at birth was in the low to mid-50s. Now it is almost 79, and if you make it to 65 you’re likely to live into your mid-80s. The median age of cancer death is 72. We live long enough for it to get us.
The diseases that once killed earlier in life — bubonic plaguesmallpoxinfluenza, tuberculosis — were easier obstacles. For each there was a single infectious agent, a precise cause that could be confronted. Even AIDS is being managed more and more as a chronic condition.
Progress against heart disease has been slower. But the toll has been steadily reduced, or pushed further into the future, with diet, exercise and medicines that help control blood pressure and cholesterol. When difficulties do arise they can often be treated as mechanical problems — clogged piping, worn-out valves — for which there may be a temporary fix.
Because of these interventions, people between 55 and 84 are increasingly more likely to die from cancer than from heart disease. For those who live beyond that age, the tables reverse, with heart disease gaining the upper hand. But year by year, as more failing hearts can be repaired or replaced, cancer has been slowly closing the gap.
For the oldest among us, the two killers are fighting to a draw. But there are reasons to believe that cancer will remain the most resistant. It is not so much a disease as a phenomenon, the result of a basic evolutionary compromise. As a body lives and grows, its cells are constantly dividing, copying their DNA — this vast genetic library — and bequeathing it to the daughter cells. They in turn pass it to their own progeny: copies of copies of copies. Along the way, errors inevitably occur. Some are caused by carcinogens but most are random misprints.
Over the eons, cells have developed complex mechanisms that identify and correct many of the glitches. But the process is not perfect, nor can it ever be. Mutations are the engine of evolution. Without them we never would have evolved. The trade-off is that every so often a certain combination will give an individual cell too much power. It begins to evolve independently of the rest of the body. Like a new species thriving in an ecosystem, it grows into a cancerous tumor. For that there can be no easy fix.
These microscopic rebellions have been happening for at least half a billion years, since the advent of complex multicellular life — collectives of cells that must work together, holding back, as best each can, the natural tendency to proliferate. Those that do not — the cancer cells — are doing, in a Darwinian sense, what they are supposed to do: mutating, evolving and increasing in fitness compared with their neighbors, the better behaved cells of the body. And these are left at a competitive disadvantage, shackled by a compulsion to obey the rules. 
As people age their cells amass more potentially cancerous mutations. Given a long enough life, cancer will eventually kill you — unless you die first of something else. That would be true even in a world free from carcinogens and equipped with the most powerful medical technology.
Faced with this inevitability, there have been encouraging reductions in the death toll from childhood cancer, with mortality falling by more than half since 1975. For older people, some early-stage cancers — those that have not learned to colonize other parts of the body — can be cured with a combination of chemicals, radiation therapy and surgery. Others can be held in check for years, sometimes indefinitely. But the most virulent cancers have evolved such wily subterfuges (a survival instinct of their own) that they usually prevail. Progress is often measured in a few extra months of life.
OVER all, the most encouraging gains are coming from prevention. Worldwide, some 15 to 20 percent of cancers are believed to be caused by infectious agents. With improvements in refrigeration and public sanitation,stomach cancer, which is linked to Helicobacter pylori bacteria, has been significantly reduced, especially in more developed parts of the world. Vaccines against human papilloma virus have the potential of nearly eliminating cervical cancer.
Where antismoking campaigns are successful, lung cancer, which has accounted for almost 30 percent of cancer deaths in the United States, is steadily diminishing. More progress can be made with improvements in screening and by reducing the incidence ofobesity, a metabolic imbalance that, along with diabetes, gives cancer an edge.
Surprisingly, only a small percentage of cancers have been traced to the thousands of synthetic chemicals that industry has added to the environment. As regulations are further tightened, cancer rates are being reduced a little more.
Most of the progress has been in richer countries. With enough political will the effort can be taken to poorer parts of the world. In the United States, racial disparities in cancer rates must be addressed. But there is a long way to go. For most cancers the only identifiable cause is entropy, the random genetic mutations that are an inevitable part of multicellular life.
Advances in the science will continue. For some cancers, new immune system therapies that bolster the body’s own defenses have shown glints of promise. Genomic scans determining a cancer’s precise genetic signature, nano robots that repair and reverse cellular damage — there are always new possibilities to explore.
Maybe someday some of us will live to be 200. But barring an elixir for immortality, a body will come to a point where it has outwitted every peril life has thrown at it. And for each added year, more mutations will have accumulated. If the heart holds out, then waiting at the end will be cancer.

George Johnson is a former reporter and editor at The New York Times and the author of “The Cancer Chronicles.”
A version of this news analysis appears in print on January 5, 2014, on page SR1 of the New York edition with the headline: Why Everyone Seems to Have Cancer.

June 27, 2013

Soon Coming To A Hospital Near You } NO MORE CHEMO

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There’s a revolution occurring in cancertreatment, and it could mean the end of chemotherapy.
When it comes to taming tumors, the strategy has always been fairly straightforward. Remove the offending and abnormal growth by any means, in the most effective way possible. And the standard treatments used today reflect this single-minded approach — surgery physically cuts out malignant lesions, chemotherapy agents dissolve them from within, and radiation seeks and destroys abnormally dividing cells.
  The report was only the latest to emerge since 2001, whenimatinib, or Gleevec, the first drug to veer away from the take-all-comers approach on which cancer therapies have been built, accomplished similar improvements in survival for patients with chronic myeloid leukemia and gastrointestinal stromal tumor (GIST).
There is no denying that such methods work; deaths from cancer have dropped by around 20% in the U.S. over the past two decades. But as effective as they are, these interventions can be just as brutal on the patient as they are on a tumor. So researchers were especially excited by a pair of studies published in the New England Journal of Medicine last week that showed a new type of anticancer drug, which works in an entirely different way from chemotherapy, helped leukemia patients tally up to an 83% survival rate after being treated for two years.
Could the end of chemotherapy be near?
“It’s a question we are all asking,” says Dr. Martin Tallman, chief of the leukemia service at Memorial Sloan-Kettering Cancer Center. “I think we are definitely moving farther and farther away from chemotherapy, and more toward molecularly targeted therapy.”
It’s the difference between carpet bombing and “smart bomb” strategies for leveling an enemy — in this case a fast-growing mass of cells that can strangle and starve surrounding normal tissues. Targeted therapies, as they are called, are aimed at specific pathways that tumor cells use to thrive, blocking them in the same way that monkeying with a car’s ignition, or its fuel intake, can keep it from running properly. The advantage of such precise strategies is that they leave healthy cells alone, which for patients means fewer side effects and complications.
 “The field is moving toward using the right drugs at the right time in the right patients,” says Dr. George Demetri, senior vice president of experimental therapeutics at the Dana-Farber Cancer Institute. “We’re moving toward a more precise understanding of cancer, and being able to tailor therapies toward an individual’s cancer.”
In the case of the NEJM studies, researchers were able to target an active receptor on immune cells responsible for enticing them to grow out of control, blocking the protein and essentially shutting down two different types of leukemia tumors.
 Already, patients diagnosed with GIST can avoid chemotherapy altogether, thanks to Gleevec. “No patient diagnosed with GIST should be getting chemotherapy today,” says Demetri. Patients who develop certain types of lung cancer or melanoma caused by a cancer-promoting mutation known as BRAF are also starting to replace toxic chemotherapy agents with new, more precise medications designed to thwart the BRAF pathway. And a study presented at the most recent meeting of the American Society of Clinical Oncology showed for the first time that a chemotherapy-free regimen led to a higher survival rate after two years than traditional chemotherapy for acute promyelocytic leukemia, a cancer of the bone marrow. Working in the doctors’ — and patients’ — favor is the fact that cancers aren’t monolithic entities composed of the same abnormal cell copied thousands of times over. Individual tumors may be composed of different types of aberrant cells, possessing a variety of mutations that are susceptible to different drugs. And this cast of cells can be ever changing over the course of an individual patient’s battle with the disease.
The refined approach does have a weakness, however. Cancer cells, like bacteria and viruses, are wily enough to bypass roadblocks to their survival, and often mutate to overcome the effects of targeted drugs. That’s the case for a small percentage of patients on Gleevec. But even that shortcoming isn’t insurmountable. With growing knowledge about the molecular processes that drive tumor biology, researchers are able to design medications that thwart cancer cells’ attempts to bypass medications. It’s all about staying one or two steps ahead of the cancer, and already, researchers are testing drugs that address Gleevec resistance and hoping to widen the resistance gap. “The field is moving so fast that there are new drugs already being developed to tackle new resistant clones,” says Tallman. “[Resistance] is a concern, yes, but it doesn’t negate our excitement about the future.”
While such heterogeneity and unpredictability could, on one hand, make tumors too daunting to tackle, they also represent an opportunity to employ an entirely new way of fighting tumors. Traditionally, if a tumor developed resistance to a chemotherapy agent, doctors would have abandoned it completely and moved on to another drug or another treatment strategy. But now they are able to biopsy tumors and perform more sophisticated genetic and molecular tests that help them to decide, for example, that the bulk of a tumor remains susceptible to a targeted therapy while only a small portion has become resistant. They can then either remove the resistant portion surgically or add another targeted therapy to tackle just that portion while keeping the patient on the original regimen that will still treat the remainder of his cancer. “That’s a new concept,” says Demetri. “That didn’t exist before targeted therapies.”
 For patients, these types of creative strategies could mean gentler, more tolerable cancer treatments, and more years of living cancer-free. Combinations of drugs may become the norm, much as they have become the standard for treating HIV infections. So far, says Dr. Scott Kopetz, associate professor of gastrointestinal oncology at MD Anderson Cancer Center, refined targeted-therapy cocktails appear to work best for blood-cell and immune-cell cancers like chronic leukemias that tend to be more homogenous from the start, making them susceptible to the newer drugs. Solid tumors such as those in the breast, prostate and lung generally contain a wider variety of genetically different cells even at diagnosis, which makes them more challenging — although not impossible — to treat with targeted drugs. “Where there is a lot of genetic heterogeneity, such as in most solid tumors, there is more headwind we have to fight against, more opportunities for rapid resistance to develop,” says Kopetz.
That means that for the time being, chemotherapy may remain part of the cancer doctor’s arsenal — and even these agents are being revamped to cause fewer side effects. New ways of encasing the toxin in fat-based bubbles or linking it to nanoparticles that deliver the drug just to the tumors while bouncing off healthy cells are making regimens more tolerable.
Increasingly, though, chemotherapy may become the treatment of last resort, rather than the first wave, as some basic truths about cancer are being knocked down and rewritten. For instance, it may not be as helpful to treat cancers by where they originate — in the breast or prostate or lung — but rather by the processes that fuel them. That’s why a targeted drug developed to treat melanomas is now used to suppress lung cancers, and why genetic and molecular analyses of tumors are becoming more critical to match the right medications to the right cancers.
“Many, many fundamental concepts in cancer are being challenged now based on new information,” says Tallman. “Of course that is leading to major shifts, paradigm shifts in treatment approaches and ultimately, I think, better care [for] patients and better outcomes.”

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