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For years medicine has viewed cancer as a "malignant seed" and looked for ways to kill these seeds before they spread throughout the body (metastasis). This past week two provocative articles stresses that we should also look at the "environments" that the cancer cells grow in - that some environments in the person nourish and encourage the growth of cancer, while other environments suppress the growth of cancer and don't allow its spread.

This is a very different approach to cancer, but it also makes sense. Studies find that small cancers can just sit there harmlessly or regress on their own - even breast and prostate cancers, but it raises the questions: Why? Why do they regress or are suppressed in some people, but grow malignantly in others? What is different about those people and their bodies?

Researchers are starting to do research along these lines - that is, looking at the environment that cancer may or may not grow in. Yesterday's post discussed amazing research showing that cancer tumors are continuously shedding cancer cells in a person's body, but only in some people do they actually take root and grow. It's as if some people have environments that encourage growth of cancer, while other people have environments that do not.

Today's article, besides discussing the micro-environment in which cancer grows, also discusses the role of inflammation in cancer and how things causing inflammation (e.g., smoking, inactivity, poor diet) are also associated with cancer. So some micro-environments are good for cancer, and some are not. Some of the research I've posted in the past has tried to see if influencing the person's environment with "lots of exercise and activity"(here and here), or vitamin D levels in the body, or a person's diet somehow prevents or keeps cancer in check. From Nautilus:

The Problem with the Mutation-Centric View of Cancer

To better understand and treat cancer, physicians need to stop oversimplifying its causes. Cancer results not solely from genetic mutations but by adapting to and thriving in micro-environments in the body. That’s the point of view of James DeGregori, a professor in the Department of Biochemistry and Molecular Genetics at the University of Colorado School of Medicine.... In our conversation, DeGregori expanded on how a renewed focus on micro-environments and Darwinian evolutionary pressures can benefit cancer research.

How should we study the origins of cancer? My lab has been researching the origins of cancers for the last 15 to 17 years. We’re trying to understand cancer from an evolutionary viewpoint, understanding how it evolves. A lot of people think about cancer from an evolutionary viewpoint. But what sets us apart is that we’ve really come to understand cancer by the context these cells find themselves in.

What’s an example of such a context? While other people will think about aging as the time for mutations to cause advantageous events [for cancer] in cells, we see aging as a very different process. It’s not about the time you get mutations—you get many mutations when you’re young. It’s the tissue environment for the cells that changes dramatically as we age. Those new tissue environments basically stimulate the evolution. So the evolution isn’t a process that’s limited by the mutation so much as a process that is limited by micro-environment changes.

Instead of just attacking the cancer, we should be altering the micro-environment to disfavor the cancer. What we’ve shown is that you could take the same oncogenic mutation and put it into young cells in a young environment and it’s not advantageous [for cancer]. It doesn’t cause expansions and it doesn’t cause the cancer. You make that same mutation in old tissue and it can be adaptive for cancer.

When we’re young, our tissues are relatively constant and well maintained. If you look at the tissues of a 20-year-old and a 35-year-old, or maybe even a 40-year-old, you wouldn’t notice much of a difference. It’s not like we age linearly. It’s only after 45 or 50 that we start to really go downhill. Then that downhill accelerates. As those changes happen, our tissues are no longer presenting that same environment to our cells. What I argue is that we evolve stem cells, or the cells that are continuously making our tissues, to be well adapted to the youthful environment and not to be well adapted to an aged environment.

I’ve been criticized as putting forward a straw man because, essentially, they don’t really talk about micro-environment. But to me that’s the whole point—there’s a major factor that should be considered, and I would say not just “should.” You can’t really model cancer without it and yet they’re not taking it into account. In other words, the difference between a smoker and a nonsmoker isn’t just that the smoker has more mutations. The difference is the smoker’s lung—and I’m sure you’ve seen pictures of the charred blackened lungs of a smoker—and that presents a completely different environment for cells with mutations.

How can your ideas change the way doctors treat cancer? Mostly we now target the cancer cells. That’s changing somewhat. Immune therapies are in some ways targeting the environment. It’s almost like a predator strategy. Instead of just attacking the cancer, we should be altering the micro-environment to disfavor the cancer. If you just attack the cancer, you immediately select for resistance, which is what they see in the clinic so often. You can get a person into remission, but it’s keeping them in remission that’s the hard part. Cancer that comes back is inevitably worse than the cancer you started with.

.... If we can understand what factor about a smoker’s lung, or an old person’s lung, leads to more cancer, then we could modulate that factor to basically prevent the cancers from occurring in the first place. If it’s inflammation, for all we know maybe there are even dietary interventions that will reduce inflammation in the lungs. All the things we know that are associated with cancer are also associated with increased inflammation. Everything we know that basically leads to longer, healthier lives, is known to modulate inflammation. Exercise reduces it. Good diet reduces it. Not smoking, not exposing yourself to too much sun.

 Cancer cells. Credit:Wikipedia, National Cancer Institute

Image result for cancer cells wikipedia For years medicine has viewed cancer as a "malignant seed" and looked for ways to kill these seeds before they spread throughout the body (metastasis). This past week two provocative articles about new research stresses that we should also look at the "soil" that the cancer "seeds" grow in - that some "soils" or environments in the person nourish and encourage the growth of cancer, while other environments suppress the growth of cancer and don't allow its spread.

This is a very different approach to cancer, but it also makes sense. Studies find that small cancers can regress on their own - even breast and prostate cancers, but it raises the questions: Why? Why do they regress or are suppressed in some people, but grow malignantly in others? What is different about those people and their bodies?

Researchers are starting to do research along these lines - that is, looking at the environment or "soil" that cancer may or may not grow in. Amazing research shows that cancer tumors are continuously shedding cancer cells in a person's body, but only in some people do they actually take root and grow. It's as if some people have ecosystems that encourage growth of cancer, while other people have ecosystems that do not.

Of course Gilbert Welch's research is discussed - that many people have tiny cancers that are just sitting there without growing (here, here, here). And how early diagnosis of cancer is not really changing the percentage of deaths from many cancers (overdiagnosis). Some of the research I've posted in the past has tried to see if influencing the person's environment with "lots of exercise and activity" somehow keeps cancer in check (here and here), or vitamin D levels in the body, or a person's diet. Do go read the whole fascinating article. Excerpts from New Yorker:

Cancer’s Invasion Equation

We aren’t particularly adept at predicting whether a specific patient’s cancer will become metastatic or not. Metastasis can seem “like a random act of violence,” Daniel Hayes, a breast oncologist at the University of Michigan, told me when we spoke at the asco meeting in Chicago. “Because we’re not very good at telling whether breast-cancer patients will have metastasis, we tend to treat them with chemotherapy as if they all have potential metastasis.” Only some fraction of patients who receive toxic chemotherapy will really benefit from it, but we don’t know which fraction. And so, unable to say whether any particular patient will benefit, we have no choice but to overtreat.

There are deep roots to the idea that a cancer’s metastases depend on local habitats. In 1889, an English doctor named Stephen Paget set out to understand cancer’s “primary growth and the situation of the secondary growths derived from it.” .... But when Paget collected the case files of seven hundred and thirty-five women who had died of breast cancer, he found a bizarre pattern of metastatic spread. The metastases didn’t appear to spread centrifugally; they appeared in discrete, anatomically distant sites. And the pattern of spread was far from random: cancers had a strange and strong preference for particular organs. Of the three hundred-odd metastases, Paget found two hundred and forty-one in the liver, seventeen in the spleen, and seventy in the lungs. Enormous, empty, uncolonized steppes—anatomical landmasses untouched by metastasis—stretched out in between.

Why was the liver so hospitable to metastasis, while the spleen, which had similarities in blood supply, size, and proximity, seemed relatively resistant? As Paget probed deeper, he found that cancerous growth even favored particular sites within organ systems. Bones were a frequent site of metastasis in breast cancer—but not every bone was equally susceptible. “Who has ever seen the bones of the hands or the feet attacked by secondary cancer?” he asked. Paget coined the phrase “seed and soil” to describe the phenomenon. The seed was the cancer cell; the soil was the local ecosystem where it flourished, or failed to. Paget’s study concentrated on patterns of metastasis within a person’s body. The propensity of one organ to become colonized while another was spared seemed to depend on the nature or the location of the organ—on local ecologies. Yet the logic of the seed-and-soil model ultimately raises the question of global ecologies: why does one person’s body have susceptible niches and not another’s? .... Paget’s way of framing the issue—metastasis as the result of a pathological relationship between a cancer cell and its environment—lay dormant for more than a century.

In 2001, Joan Massagué, a cancer biologist at New York’s Memorial Sloan Kettering Cancer Center, came upon a scientific paper that radically changed his thinking about metastasis..... He had spent years studying cell biology, elucidating mechanisms of gene regulation that might prime breast cells to travel to the bone instead of to the brain. Then came a crucial piece of evidence, buried in an obscure journal and published nearly three decades earlier. Researchers at the National Institutes of Health had implanted a sac of breast-cancer cells into the ovarian pedicle of a female rat. The cells grew to form a bean-size tumor. The researchers then cannulated a large vein that was draining the tumor and siphoned blood from the vein every few hours in order to count the number of cancer cells that the tumor was shedding.

The results baffled the investigators. On average, they found, the tumor was sloughing off twenty thousand cancer cells into every millilitre of blood—roughly three million cells per gram of tumor every twenty-four hours. In the course of a day, the tumor molted nearly a tenth of its weight. Later studies, performed with more sophisticated methods and with animal tumors that had arisen more “naturally,” confirmed that tumors continually shed cells into circulation. (The rate of shedding from localized human tumors is harder to study; but available research tends to confirm the general phenomenon.)

But if primary human tumors shed cells continually, and if every cell is capable of forming visible metastasis, then every patient should have countless visible metastatic deposits all over his or her body.” Anna Guzello’s breast tumor should have stippled her brain, bones, and liver with mets. Why, then, did she have no visible evidence of disease anywhere else in her body? The real conundrum wasn’t why metastases occur in some cancer patients but why metastases don’t occur in all of them.

“The only way I could explain the scarcity of metastasis,” Massagué said, “was to imagine that an enormous wave of cellular death or cellular dormancy must restrict metastasis. Either the cells shed by the tumor are killed, or they stop dividing, becoming dormant. When tumor cells enter the circulation, they must perish almost immediately, and in vast numbers. Only a few reach their destination organ, such as the brain or the bone.” Once they do, they face the additional problem of surviving in unfamiliar and possibly hostile terrain. Massagué inferred that those few survivors must lie in a state of dormancy. “A visible, clinical metastasis—the kind that we can detect with cat scans or MRIs—must only occur once a dormant cell has been reactivated and begins to divide,” he said. Malignancy wasn’t simply about cells spreading; it was also about staying—and flourishing—once they had done so.

.... Rather than viewing invasiveness as a quality intrinsic to a cancer, researchers needed to consider invasiveness as a pathological relationship between an organism and an environment. “Together, cancer cells and host cells form an ecosystem,” Pienta reminded the audience. “Initially, the cancer cells are an invasive species to a new niche or environment. Eventually, the cancer-cell-host-cell interactions create a new environment.” Ask not just what the cancer is doing to you, Pienta was saying. Ask what you are doing to the cancer.

Evidence suggested, for example, that most men with prostate cancer would never experience metastasis. What made others susceptible? The usual approach, Welch knew, would be to look for markers in their cancer cells—to find patterns of gene activation, say, that made some of them dangerous. And the characteristics of those cells were plainly crucial. Pienta was arguing, though, that this approach was far too narrow. At least part of the answer might lie in the ecological relationship between a cancer and its host—between seed and soil. .....Once we think of diseases in terms of ecosystems, then, we’re obliged to ask why someone didn’t get sick

Image result for cancer cells wikipedia Cancer cells. Credit: Wikipedia, National Cancer Institute

 Two recent studies link low vitamin D levels with more aggressive cancers: aggressive prostate cancer in men and more aggressive breast cancers (in mice and women). Researchers generally advise people to take 1000 to 2000 international units per day of vitamin D3 to maintain normal blood levels of of more than 30 nanograms/milliliter. The best source of vitamin D is sunlight, which is why vitamin D is frequently called the sunshine vitamin.

From Science Daily:  Low vitamin D predicts aggressive prostate cancer

A new study provides a major link between low levels of vitamin D and aggressive prostate cancer. Northwestern Medicine research showed deficient vitamin D blood levels in men can predict aggressive prostate cancer identified at the time of surgery.

"Vitamin D deficiency may predict aggressive prostate cancer as a biomarker," said lead investigator Dr. Adam Murphy, an assistant professor of urology at Northwestern University Feinberg School of Medicine and a Northwestern Medicine urologist. "Men with dark skin, low vitamin D intake or low sun exposure should be tested for vitamin D deficiency when they are diagnosed with an elevated PSA or prostate cancer. Then a deficiency should be corrected with supplements."

Aggressive prostate cancer is defined by whether the cancer has migrated outside of the prostate and by a high Gleason score. A low Gleason score means the cancer tissue is similar to normal prostate tissue and less likely to spread; a high one means the cancer tissue is very different from normal and more likely to spread. The study was part of a larger ongoing study of 1,760 men in the Chicago area examining vitamin D and prostate cancer. The current study included 190 men, average age of 64, who underwent a radical prostatectomy to remove their prostate from 2009 to 2014.

Of that group, 87 men had aggressive prostate cancer. Those with aggressive cancer had a median level of 22.7 nanograms per milliliter of vitamin D, significantly below the normal level of more than 30 nanograms/milliliter. The average D level in Chicago during the winter is about 25 nanograms/milliliter, Murphy noted....The Institute of Medicine recommends 600 international units of D per day, but Murphy recommends Chicago residents get 1,000 to 2,000 international units per day.

From Medical Xpress:  Vitamin D deficiency contributes to spread of breast cancer in mice, study finds

Breast tumors in laboratory mice deficient in vitamin D grow faster and are more likely to metastasize than tumors in mice with adequate levels of vitamin D, according to a preliminary study by researchers at the Stanford University School of Medicine.The research highlights a direct link between circulating vitamin D levels and the expression of a gene called ID1, known to be associated with tumor growth and breast cancer metastasis.

The finding builds upon several previous studies suggesting that low levels of vitamin D not only increase a person's risk of developing breast cancer, but are also correlated with more-aggressive tumors and worse prognoses. Although the research was conducted primarily in mice and on mouse cells, the researchers found in a study of 34 breast cancer patients that levels of circulating vitamin D were inversely correlated with the expression levels of ID1 protein in their tumors, and they confirmed that a vitamin D metabolite directly controls the expression of the ID1 gene in a human breast cancer cell line.

Once ingested or made by the body, vitamin D is converted through a series of steps into its active form, calcitriol. Calcitriol binds to a protein in cells called the vitamin D receptor, which then enters the cell's nucleus to control the expression of a variety of genes, including those involved in calcium absorption and bone health.

In the new study, Williams and Aggarwal investigated whether vitamin D levels affected the metastatic ability of mouse breast cancer cells implanted into the mammary fat pad of laboratory mice. One group of 10 mice was first fed a diet lacking in the vitamin for 10 weeks; the other 10 received a normal dose in their food. Mice fed a diet deficient in vitamin D developed palpable tumors an average of seven days sooner than their peers, and after six weeks of growth those tumors were significantly larger in size than those in animals with adequate vitamin D levels.

A report by 3 prominent specialists (including Gilbert Welch - who has been discussed in earlier posts) about trends in metastatic breast and prostate cancer came out today in the New England Journal of Medicine. The biggest finding was that mammograms have not cut the rate of metastatic breast cancer. Mammography screening is based on the hope that cancer that is detected in an early, localized phase can then be treated more easily and that it would reduce the numbers of metastastic cancers (that spread to lymph nodes and to more distant organs) that eventually kill. However, this has not happened.The incidence of metastatic breast cancer has been stable since 1975, and the average age of diagnosis among women older than 40 is still 63.7 years . The authors theorize that "breast cancer is a systemic disease by the time it's detectable". From Medical Xpress:

Study: Mammograms haven't cut rate of advanced breast cancer

A new report raises fresh questions about the value of mammograms. The rate of cancers that have already spread far beyond the breast when they are discovered has stayed stable for decades, suggesting that screening and early detection are not preventing the most dangerous forms of the disease. The report, in Thursday's New England Journal of Medicine, is by three prominent cancer specialists and is based on federal statistics going back to the 1970s.

"We're undergoing what I think for the public is a very confusing debate" about screening, but it's really "a course correction" prompted by more awareness of its risks and benefits to various groups of women, said Dr. H. Gilbert Welch, a health policy expert at Dartmouth Medical School. "All they heard for years was, 'there are only benefits.'" He is the lead author of the report, co-written with Dr. David Gorski of Wayne State University School of Medicine in Detroit and Dr. Peter Albertsen of the University of Connecticut Health Center in Farmington.

"Screening offers hope that cancer can be detected in an early, localized phase when it's more amenable to treatment," they write, but that assumes that cancer starts in one place, grows and then spreads. If that was always true, screening would reduce the rate of advanced cancers. And that has not happened. The rate of breast cancers detected at an advanced stage has been stable since 1975, despite wide use of mammography since the 1980s. The average age of women diagnosed with cancer also has remained around 63, another sign cancers are not being found sooner.

The trends suggest that some breast cancers are already "systemic" or widely spread from the start, and that finding them sooner has limited impact. "Screening mammography has been unable to identify those bad cancers, destined to become metastatic, at an earlier stage. That doesn't say mammography doesn't help less aggressive cancers," but those are less likely to prove deadly, Welch said.

Dr. Barnett Kramer, a screening expert at the National Cancer Institute, said the report shows the limitations of mammography. "I wouldn't want to say it has had no effect but it certainly has not lived up to the anticipated effect," he said. For every tumor detected early because of mammography, "you would hope to see ... an equal reduction in metastatic disease, and that has not occurred."

The situation is very different with prostate cancer. The rate of advanced cases of that disease has been cut in half since screening with PSA blood tests came into wide use around 1988, and the average age at which men are diagnosed has fallen—from 72 to 70, the authors write. However, this does not prove PSA testing is good. Shifting the stage at which a disease is diagnosed is "only the first step for successful screening," which also has to save lives to be worthwhile, Welch said. "Just because you find something earlier doesn't mean you can change its course."

Again, Kramer agreed. Prostate screening, "when put to a definitive test, did not show a clear reduction in prostate cancer mortality" in large, rigorously done trials, he said. The government task force recommends against PSA testing, and says its risks outweigh its benefits for most men.

"Screening is a close call," Welch said. "My guess is few people are helped" by prostate or breast cancer screening while many are harmed by false alarms that trigger unnecessary tests and treatments, he said.

The original report, which also includes a discussion on prostate cancer and the PSA test, in the New England Journal of Medicine:  Trends in Metastatic Breast and Prostate Cancer — Lessons in Cancer Dynamics

The issue of overdiagnosis and overtreatment has recently been in the news, especially when discussing breast cancer, prostate cancer, and thyroid cancer. Meaning too much unnecessary treatment with harms, when the best approach would have been to do nothing, as studies have suggested or actually shown. Now here is an article in Medscape suggesting that rather than be quick to operate or treat, the best approach for nearly 70% of prostate cancers may be just "watching".

The U.S. Preventive Task Force, which analyzes the value of screening tests, in May 2012 recommended AGAINST routine prostate-specific antigen (PSA)-based screening for prostate cancer for all age groups. According to them, studies do not show that benefits of routine screening of asymptomatic prostate cancer and the resulting treatment outweigh the harms of treatment (e.g., surgical complications including death from surgery, erectile dysfunction, urinary incontinence, bowel dysfunction, and bladder dysfunction), or that prostate cancer treatment even reduces mortality (deaths). They point out that: "There is convincing evidence that PSA-based screening programs result in the detection of many cases of asymptomatic prostate cancer. There is also convincing evidence that a substantial percentage of men who have asymptomatic cancer detected by PSA screening have a tumor that either will not progress or will progress so slowly that it would have remained asymptomatic for the man's lifetime. The terms "overdiagnosis" or "pseudo-disease" are used to describe both situations." (NOTE: others have argued against this recommendation)

When reading the full Medscape article, it was pointed out that in the study being discussed, one person who was offered active surveillance but declined and was treated with an immediate radical prostatectomy, still died of metastatic prostate cancer. This was an example of a case where when the disease is truly aggressive, it may have spread "like a bird" throughout the body (in Dr. H. Gilbert Welch's terms in his books Overdiagnosed and Less Medicine, More Health) from the very beginning, and may be unstoppable no matter what is done. I have also noticed reading other prostate cancer studies that a certain percentage of prostate cancers regress from the point of diagnosis (the PSA test and biopsy). In other words, researchers are finding that cancer can have different paths: regresses, stays the same, grows slowly (and can be treated when symptoms appear), or grows very quickly and is so aggressive and unstoppable that it goes through the body "like a bird". And we don't know which will be the aggressive ones when we first find them, thus the controversies over what to do: screen or not?, and treat or not? From Medscape:

Nearly 70% of US Prostate Cancers Could Be Watched

More than two-thirds (68%) of all prostate cancers in the United States qualify for active surveillance, according to a study published in the September issue of the Journal of Urology. And if a more stringent definition of surveillance eligibility is used, 44% of cases would be candidates for monitoring instead of immediate treatment, say senior author Ian M. Thompson III, MD, from the University of Texas Health Science Center at San Antonio, and colleagues. These "target" figures are especially credible because they come from a population-based study funded by the National Cancer Institute, and the 3828 participants from Texas undergo regular prostate-specific antigen (PSA) testing.

Of the 320 men in the cohort who developed prostate cancer from 2000 to 2012, 281 had data that were sufficient to allow scoring on very detailed surveillance scorecard.Disease characteristics, such as a high Gleason score, rendered 131 of the 320 men ineligible for active surveillance. But 123 of the men (44%) met a conservative set of criteria and were eligible for surveillance.These "lowest-risk" patients had a PSA density below 15%, fewer than three cores involved with cancer, a Gleason score of 6 or less, and cancer involving 50% of biopsy volume or less. Another 64 men (24%) were eligible when a more expansive set of criteria was used. These "higher-risk" men had fewer than five cores with Gleason 3 + 3 cancer and only one core of Gleason 3 + 4 cancer with up to 15% of the core involved with the Gleason 3 + 4 disease.

When the two groups were combined, 187 patients (68%) were eligible for active surveillance. Predictably, the number of men who actually chose active surveillance was much lower. From 2000 to 2007, 11% of the men diagnosed with prostate cancer opted for surveillance. From 2007 to 2012, 35% of the men opted for surveillance.

Active surveillance should be offered to "an expanded population of well-informed men who may value preserving function above a small risk of disease progression," write Marc Dall'Era, MD, from the University of California, Davis, and Peter Carroll, MD, from the University of California, San Francisco, in an accompanying editorialIn other words, the approach is not just for the lowest-risk cases, they opine.They explain that "the risks of adverse disease-specific outcomes will likely be higher with the inclusion of men with more intermediate-risk features." However, the "absolute risk may still be low," they write.

Perhaps even more important, the study authors observe, is that if the well-documented phenomenon of upgrading or upstaging "truly translated to subsequent consequential outcomes," then "far greater" rates of disease progression, metastases, and death would have been reported in other series of patients. And that has not happened.

 The pair also point to the current study as proof that active surveillance is a reasonable approach, not just for "very-low-risk" disease, but for low- and intermediate-risk prostate cancer, too.

Notably, two of the 320 patients in the Texas cohort either experienced metastatic disease or died of prostate cancer.One of these patients met the expanded criteria and was eligible for active surveillance. "While this could argue against active surveillance, it is notable that this patient underwent radical prostatectomy immediately following diagnosis," the authors explain. The other patient, who was ineligible for surveillance under either definition, was treated definitively but experienced disease progression.     

The prostate gland is located beneath a man's bladder.    Credit: Alila Medical Media | Shutterstock

  In the past few months there has been a lot of discussion about early screening tests for cancer (when there are no symptoms)  versus diagnostic tests (testing once symptoms appear), especially for prostate cancer and breast cancer. Because unfortunately screening also has harms - it is not without significant risks. So the following 2 articles discussing breast cancer are real eye openers. The first article discusses a large study that found that no matter how early the screening and no matter how tiny the cancer and extensive the treatment (e.g, mastectomy of both breasts), in a certain percentage of women the cancer will reappear in a deadly fashion and eventually kill about 3.3% even though they are treated early. The Medscape article points out that it is thought that 28% of early stage breast cancers will progress or reappear as deadly metastatic cancer (even years later) no matter the treatment.

As Dr. Welch has pointed out in his book Overdiagnosis and Less Medicine, More Health - these aggressive cancers are like "birds" - they fly away throughout the body and are deadly no matter when they are diagnosed. A certain percentage of tiny cancers regress (disappear) on their own, others just sit there doing nothing, others grow very slowly (and can be treated successfully when symptoms appear), and then there are those that are so very aggressive that they go throughout the body from the beginning (the birds). And we don't know which will be the aggressive ones when we first find them. So sad..... Meanwhile try to eat healthy foods, get enough sleep, lose weight if overweight, live a healthy lifestyle (don't smoke or drink to excess), and get plenty of exercise in hopes of cancer prevention. I also like to think that each week eating some turmeric (in foods), broccoli famiy foods, olive oil, and berries may also help. Do go read the full original articles. From NY Times:

Early-Stage Breast Condition May Not Require Cancer Treatment

As many as 60,000 American women each year are told they have a very early stage of breast cancer — Stage 0, as it is commonly known — a possible precursor to what could be a deadly tumor. And almost every one of the women has either a lumpectomy or a mastectomy, and often a double mastectomy, removing a healthy breast as well. Yet it now appears that treatment may make no difference in their outcomes. Patients with this condition had close to the same likelihood of dying of breast cancer as women in the general population, and the few who died did so despite treatment, not for lack of it, researchers reported Thursday in JAMA Oncology. 

Their conclusions were based on the most extensive collection of data ever analyzed on the condition, known as ductal carcinoma in situ, or D.C.I.S.: 100,000 women followed for 20 years. The findings are likely to fan debate about whether tens of thousands of patients are undergoing unnecessary and sometimes disfiguring treatments for premalignant conditions that are unlikely to develop into life-threatening cancers.

Diagnoses of D.C.I.S., involving abnormal cells confined to the milk ducts of the breast, have soared in recent decades. They now account for as much as a quarter of cancer diagnoses made with mammography, as radiologists find smaller and smaller lesions. But the new data on outcomes raises provocative questions: Is D.C.I.S. cancer, a precursor to the disease or just a risk factor for some women? Is there any reason for most patients with the diagnosis to receive brutal therapies? If treatment does not make a difference, should women even be told they have the condition?

A majority of the 100,000 patients in the database the researchers used, from a national cancer registry, had lumpectomies, and nearly all the rest had mastectomies, the new study found. Their chance of dying of breast cancer in the two decades after treatment was 3.3 percent, no matter which procedure they had, about the same as an average woman’s chance of dying of breast cancer, said Dr. Laura J. Esserman, a breast cancer surgeon and researcher at the University of California, San Francisco, who wrote an editorial accompanying the study.

The data showed that some patients were at higher risk: those younger than 40, black women, and those whose abnormal cells had molecular markers found in advanced cancers with poorer prognoses. D.C.I.S. has long been regarded as a precursor to potentially deadly invasive cancers, analogous to colon polyps that can turn into colon cancer, said Dr. Steven A. Narod, the lead author of the paper and a researcher at Women’s College Research Institute in Toronto. The treatment strategy has been to get rid of the tiny specks of abnormal breast cells, just as doctors get rid of colon polyps when they see them in a colonoscopy.

But if that understanding of the condition had played out as expected, women who had an entire breast removed, or even both breasts as a sort of double precaution, should have been protected from invasive breast cancer. Instead, the findings showed, they had the same risk as those who had a lumpectomy. Almost no women went untreated, so it is not clear if as a group, they did worse. But some women who died of breast cancer ended up with the disease throughout their body without ever having it recur in their breast — many, in fact, had no breast because they had had a mastectomy. Those very rare fatal cases of D.C.I.S. followed by fatal breast cancer, Dr. Narod concluded, had most likely already spread at the time of detection. As for the rest, he said, they were never going to spread anyway.

Dr. Esserman said that if deadly breast cancers started out as D.C.I.S., the incidence of invasive breast cancers should have plummeted with rising detection rates. That has not happened, even though in the pre-mammography era, before about 1980, the number of women found to have D.C.I.S. was only in the hundreds. Nearly 240,000 women receive diagnoses of invasive breast cancer each year.

Those facts lead Dr. Narod to a blunt view. After a surgeon has removed the aberrant cells for the biopsy, he said, “I think the best way to treat D.C.I.S. is to do nothing." ... Others drew back from that advice.

From Medscape:  The Mystery of a Common Breast Cancer Statistic

A commonly cited breast cancer statistic — that 30% of all early-stage breast cancers will progress, despite treatment, to deadly metastatic disease — appears to have no strong contemporary evidence to back it up. Nonetheless, the statistic appears widely...."It is estimated that 20% to 30% of all breast cancer cases will become metastatic," said the MBCN in response, repeating a statistic from its own website.

The primary source for this declaration is a 2005 CME review on metastatic disease published in the Oncologist by prominent medical oncologist Joyce O'Shaughnessy, MD, from Baylor University in Houston."Despite advances in the treatment of breast cancer, approximately 30% of women initially diagnosed with earlier stages of breast cancer eventually develop recurrent advanced or metastatic disease," Dr O'Shaughnessy wrote.

According to the National Cancer Institute (NCI), the definition of early-stage breast cancer is that which has not spread beyond the breast or the axillary lymph nodes. The range includes stage I, stage IIA, stage IIB, and stage IIIA disease....According to experts, early breast cancers are known to metastasize at 20 years or beyond.


Dr Brawley worked with two ACS epidemiologists to examine the issue. They looked at breast-cancer-specific mortality (as identified on death certificates) in 12 health districts in the United States from 2008 to 2012. They were surprised by the finding: "28% of the women who died of breast cancer during that time period had localized disease at diagnosis," said Dr Brawley. The result was unexpected. "We all thought 30% was too high," said Dr Brawley.

(NOTE: Photo credit: Wikipedia Commons of Edouard Manet- Blond Woman With Bare Breasts.)