Cancer Today Coverage From the San Antonio Breast Cancer Symposium

For 35 years, the mission of the San Antonio Breast Cancer Symposium (SABCS) has been to provide a forum for researchers, health care professionals and patient advocates to share the most recent updates and cutting-edge information about breast cancer research.

The symposium, held every year in San Antonio, Texas, is the largest breast cancer research conference, boasting thousands of attendees from more than 100 countries.

SABCS is hosted by four prestigious and highly respected institutions: the Cancer Therapy and Research Center (CTRC) at University of Texas Health Science Center at San Antonio, the American Association for Cancer Research (AACR) and Baylor College of Medicine. The driving force behind this collaboration is the shared mission of these four organizations to advance progress in breast cancer research.

From Dec. 4–8, Cancer Today contributing writer Melissa Weber will be covering the exciting new research and innovations being discussed at the symposium. Check back here each day for her coverage of the latest in breast cancer research and treatment.

Weber is an Austin, Texas–based freelance writer and editor specializing in health and medicine. Her work has been published by many national publications and nonprofits, including Cancer Today.

Check out the Cancer Today website daily for important news and information about breast cancer research presented at this esteemed symposium. Also, don’t forget to follow Cancer Today on Twitter @CancerTodaymag and Facebook.

From San Antonio, Away We Go

Posted: Dec. 7, 2012 – 4:20 p.m. CT

Tamoxifen is better when taken for 10 years, not five. Research showing HER2-mutated breast cancers can be crushed by an experimental drug. A study revealing a manageable cause to the mental haze plaguing so many patients.

It’s been a busy, busy week in San Antonio.

Of the nearly 1,100 studies presented, either during the general sessions or along the rows of poster boards, and 42 scientific presentations, some may change the way patients are treated today while others are not yet ready for primetime.

The San Antonio Breast Cancer Symposium, which began in 1978 with 141 attendees from a handful of states, welcomed more than 7,300 oncologists, researchers, statisticians, nurses, survivors and patient advocates from around the world this year.

I was talking to one of those survivors the other day.

Diagnosed with breast cancer in 1994, Sandi Stanford soon started attending the annual symposium. But the reason she attends has changed over the years.

“At the beginning, I came so that I could find out for myself what’s out there – what do I need to know, are there other people like me. Today, I’m here for the researchers and the advocates,” said Stanford, president of the San Antonio-based nonprofit Alamo Breast Cancer Foundation.

“I’m so amazed at the detail of research that I’m awestruck. Look at what they’ve done and look at what advocates have done to get breast cancer in the forefront,” Stanford said.

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Drugs to Treat HER2-positive Breast Cancer May Also Work Against Some Tumors Testing Negative for HER2

Posted: Dec. 7, 2012 – 4:00 p.m. CT

Look, I know: You don’t need to be told that when it comes to drugs that only work against breast cancers with too much HER2, it’s a big deal when someone discovers that the drugs can also dismantle a cancer that tests negative for high amounts of HER2.

But let’s humor everyone else, shall we?

HER2 is a gene that produces a protein by the same name. In about 20 percent of breast cancers, there are too many copies of the HER2 gene making too much HER2 protein. This overload of HER2 protein fuels the growth of breast cancer – a subtype labeled HER2-positive breast cancer. Drugs like Herceptin (trastuzumab) and Tykerb (lapatinib) block HER2 and are staples in the clinic.

The possible game-changer we’re talking about now is still in Petri dishes and mice. But, even so, the study’s lead researcher Ron Bose called the lab results “dramatic.”

An experimental HER2-targeted drug called neratinib halted breast cancer cell growth and even killed cancer cells in tissue samples from patients with so-called activating HER2 mutations, the driving force behind 1 to 2 percent of breast cancers, Bose reported Friday at the San Antonio Breast Cancer Symposium. The results were simultaneously published online by Cancer Discovery, a journal of the American Association for Cancer Research.

“The findings could mean the pool of patients eligible for HER2-targeted drugs may soon get a little bigger,” Bose said.

“I know that going from 20 percent to about 22 percent doesn’t sound like a whole lot, but breast cancer strikes 230,000 women each year in the U.S. That could mean helping 4,000 more women every year,” said Bose, assistant professor in the division of oncology at the Washington University School of Medicine and the Siteman Cancer Center in St. Louis, Mo.

Bose and his colleagues peered into the DNA of breast cancer cells from nearly 1,500 patients and found 25 HER2-mutant cancers. Of the 13 HER2 mutations tested in the lab, about 75 percent were activating mutations that spurred cancer growth. Keep in mind, these mutations aren’t inherited. They’re only found in cancer cells, not a woman’s normal cells.

All except two cancers with an activating HER2 mutation responded to Herceptin and Tykerb. But neratinib proved deadly to every cancer with an activating HER2 mutation.

“It’s a good day when researchers learn something new about breast cancer,” said Jody Schoger, who was diagnosed with HER2-negative breast cancer in 1998, the same year Herceptin became the first drug approved for HER2-positive disease. “We used to think HER2 was just an on or off switch, but now we’re getting into the complexities of what can flip that switch,” said Schoger, 58, of The Woodlands, Texas.

Finding a HER2 mutation lurking inside a breast tumor takes a process called DNA sequencing. Tests currently used in the pathology lab only look for HER2 overexpression. That’s a big problem since nearly all the HER2 mutations Bose found were in patients whose tumors tested negative for HER2 overexpression.

“But all roads are leading to Rome here. Both mutations and overexpression turn on HER2, and patients with either may benefit from the same drugs,” Bose said.

And he’s not wasting any time. Bose is now recruiting women for a phase II study testing neratinib in HER2-mutant metastatic breast cancer.

“Another piece of the breast cancer puzzle was just fit into place,” said C. Kent Osborne, director of the Lester and Sue Smith Breast Cancer Center at Baylor College of Medicine in Houston.

“There are going to be these mutations that are perhaps contributing to the cancer, but they’re pretty rare in the population. But that’s important for that particular patient to know,” Osborne said during a press conference at the meeting. Osborne was not involved in the study.

“HER2 mutations may actually be more common in women with advanced breast cancer,” Osborne said. “I will bet that when Dr. Bose and others begin to look at metastatic cancer that is presumably resistant to the treatment patients got earlier in their disease, they’re going to find a greater percentage of these [HER2] mutations,” he said.

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Fatigue May Be The Reason Behind Chemobrain

Posted: Dec. 7, 2012 – 3:40 p.m. CT

Maybe you’ve walked into a room only to forget why you went in there in the first place. Or maybe you’ve lost your train of thought mid-sentence. It’s more common than you think: As many as one in three cancer survivors experience the mental fog better known as chemobrain.

But chemotherapy may have little to do with it, researchers said Friday at the San Antonio Breast Cancer Symposium (SABCS). The culprit may actually be fatigue. Here’s why: Breast cancer patients experienced cognition problems before treatment even started.

“When people are fatigued, their brains aren’t functioning as well. It takes more effort to function, and then they get more fatigued. It’s a downward spiral,” said Bernadine Cimprich, the study’s lead researcher and associate professor emerita at the University of Michigan School of Nursing in Ann Arbor.

Cimprich started by separating women into three groups. One group awaited post-surgery chemotherapy, while another was about to start radiation. A third group of women – the control group – did not have breast cancer.

Before treatment and again one month after treatment, the women answered questions about their fatigue level. They also spent an hour or so pushing a “yes” or “no” button in response to progressively harder memory questions while a functional MRI machine took pictures of their brains. Called a verbal working memory task, the test allowed researchers to measure activation in an area of the brain that supports working memory.

Turns out, the more fatigued breast cancer patients were, the less the memory area of their brains lit up and the more they experienced cognition problems, both before treatment and over time. The mind fog hit chemotherapy patients the worst. “There was something about anticipating chemotherapy that suggested there was an added anxiety. The anxiety and worry were linked to fatigue,” said Cimprich, who presented the findings at SABCS.

Sandy Castillo fell into a mental haze as soon as she started chemotherapy three years ago. “I’d be in the middle of a full-on conversation and then the words and thoughts would just vanish,” said Castillo, 43, of Houston. “The other big issue was sheer confusion because I could not focus on one thing long enough to finish it. It was exhausting.”

Castillo said she often felt stupid and even guilty that she couldn’t pick up the mental pieces.

The good news is, fatigue and anxiety can be managed. Strategies like yoga, mindfulness and cognitive behavioral therapy all work, Cimprich said.

Nevertheless, doctors here are thrilled to finally have a way to help patients.

“I’ve wondered in my own practice whether just the stress of having been diagnosed with cancer and the anticipation of the treatment and the concern of if I’m going to live or die may contribute [to cognitive problems],” said C. Kent Osborne, director of the Lester and Sue Smith Breast Cancer Center at Baylor College of Medicine in Houston. Osborne was not involved in the study.

This isn’t the final word on the matter. A single study isn’t enough, Cimprich cautioned. Other studies must be done to see if the findings stick.

Even so, Cimprich is confident “chemobrain” is a limiting term that ends up excluding breast cancer patients receiving radiation therapy who also experience problems with thinking.

“If you’re suffering from this, you know it becomes so frustrating. If we can reduce some of the factors that contribute to it, we can help people function better,” she said.

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Researchers Find Achilles’ Heel in Triple-Negative Breast Cancer

Posted: Dec. 7, 2012 – 1:05 p.m. CT

Triple-negative breast cancer cells were dying right before his eyes. Those stubborn cancer cells that have branded triple-negative breast cancer as “hard-to-treat” were no more. At the San Antonio Breast Cancer Symposium on Thursday, researcher Kapil Bhalla told a captive audience how he did it.

Triple-negative breast cancers with a BRCA1 mutation are more sensitive than those without the mutation to the chemotherapy drug cisplatin and experimental drugs called PARP inhibitors. So the idea in Bhalla’s lab was to create a “BRCAness” in cancer cells that did not have a BRCA1 mutation. In other words, make the cancer think it is vulnerable and then exploit it.

It worked.

Bhalla and his co-investigators used a class of drugs called histone deacetylase inhibitors – HDAC inhibitors for short – to turn off BRCA1, a protein that springs into action when damaged DNA is in need of repair. With BRCA1 knocked out, researchers delivered the next blow to a backup repair protein called PARP. Without a way to patch up damaged DNA, the cancer cells died. Researchers also tested a HDAC inhibitor with cisplatin, with the same cancer cell-killing effect.

“The HDAC inhibitor is helping PARP be more lethal. And the beauty is that even the HDAC inhibitor is causing further DNA damage,” said Bhalla, chief of personalized cancer medicine at the University of Kansas Cancer Center in Kansas City.

Think of the cancer cell as a table. You knock out one of its legs – BRCA1 in this case – and you’ve still got a standing, albeit wobbly, table. But knock out another leg – PARP – and the table collapses. And voila, a dead cancer cell.

The HDAC inhibitors used in the study were panobinostat and vorinostat, a drug already approved under the brand name Zolinza to treat cutaneous T-cell lymphoma. The experimental PARP inhibitor is called veliparib.

Triple-negative breast cancer gets its name from what it doesn’t have, specifically those desirable drug targets HER2 and hormone receptors. The countless molecular switches that power triple-negative tumors to grow and survive have long left researchers stumped, forcing doctors to rely solely on chemotherapy drugs to fight the disease.

Bhalla said the new drug combination is ready for clinical trials. “Even though we didn’t test it this way, in patients, you would use all three drugs: a HDAC inhibitor, PARP inhibitor and cisplatin,” he said.

Carlos Arteaga, associate director for clinical research and director of the Breast Cancer Program at Vanderbilt-Ingram Cancer Center in Nashville, Tenn., agreed the combo is ready to test in patients. Problem is, we still don’t know who the odds favor, he said.

“This study suggests there’s something we can combine with PARP inhibitors, but it doesn’t necessarily tell us which triple-negative tumors are sensitive to the combination,” said Arteaga, who was not involved in the study.

It’ll take homework, Arteaga said. “I would hope a researcher would collect tissue samples and then look for things that make sense based on this preclinical data.”

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For Triple-Negative Breast Cancer, Being Young May Be a Good Thing

Posted: Dec. 7, 2012 – 8:20 a.m. CT

Good news for young women with triple-negative breast cancer: You’re not only more likely to respond to pre-surgery chemotherapy than your older counterparts, but a response also ups your odds for keeping the disease in check.

“Age matters. It is a biological marker, possibly for chemosensitivity,” said Sibylle Loibl, who presented her research findings Thursday at the San Antonio Breast Cancer Symposium.

Nearly a third of triple-negative patients older than 35 who received chemotherapy before surgery had a pCR, short for pathological complete response. That means there was no cancer in the breast or lymph nodes at the time of surgery. In the 35-and-under group, almost half had a pCR.

Not bad, but what about survival?

Triple-negative patients who achieved a pCR were 82 percent more likely to be free of their disease after five years compared to triple-negative patients whose cancers were still lingering at the time of surgery.

“For patients with triple-negative breast cancer who experience a pathological complete response from neoadjuvant (pre-surgery) chemotherapy, the prognosis is excellent,” said Loibl, an associate professor at the University of Frankfurt in Germany. Triple-negative breast cancer is an aggressive form of the disease that accounts for about 15 percent of all breast cancers in the United States.

Ghecemy Lopez was diagnosed almost two years ago with triple-negative breast cancer. She was 30. “I thought if I’m ever going to get this disease, it’s going to be when I’m an old person, when I have grandchildren. Not right now,” said Lopez, of Los Angeles, Calif.

Her doctors didn’t think she needed chemotherapy before surgery. After all, her tumor was small, only 1.6 centimeters. But two and a half weeks later, a lumpectomy to remove the tumor revealed it had quickly grown by a third of its original size to 2.1 centimeters. Doctor’s orders were four rounds of post-surgery chemotherapy.

“You already feel like you have a heavy rock on your back. But then you hear that if the chemo doesn’t work, that’s it, you have no other treatment options. That was scary,” Lopez said.

It worked. She’s now cancer-free.

Women 35 and younger also responded well to chemo before surgery if they had hormone receptor-positive, HER2-negative breast cancer, also called luminal A breast cancer. But the time they spent cancer-free fell short of statistical significance because so few women fit into this rare group, Loibl said.

The researchers analyzed data from eight German studies that included nearly 9,000 women with operable or locally advanced breast cancer who were treated with neoadjuvant chemotherapy. The goal of neoadjuvant chemotherapy is to shrink a breast tumor enough that it can be removed with less extensive surgery.

Back in the U.S., the findings won’t change practice because doctors are already treating most young women with chemotherapy before surgery, said Carlos Arteaga, associate director for clinical research and director of the Breast Cancer Program at Vanderbilt-Ingram Cancer Center in Nashville, Tenn.

“We always err on the side of more treatment with young women,” said Arteaga, who was not involved in the study. “I find this presentation reassuring of what we’re doing already.”

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Racial Gap in Breast Cancer Still Exists, But Patient Navigation May Help Close It

Posted: Dec. 6, 2012 – 11:45 a.m. CT

At big cancer meetings like the one here in San Antonio, the news is almost always good. A new scientific discovery here, a better treatment option there.

But at a special session Wednesday morning came a reality check: black women are 41 percent more likely to die of breast cancer than white women. For Latinas, the risk of dying is 22 percent higher than for white women.

“Regardless of your race or ethnicity, those are really eye-opening numbers,” said epidemiologist Krystal Sexton. “With all the advances we’ve made, we really need to start focusing on making survival more equal for everybody.”

Sexton, an assistant professor of medicine at Baylor College of Medicine in Houston, spoke about disparities in breast cancer at a special session hosted by the American Association for Cancer Research and the Alamo Breast Cancer Foundation. The session coincided with the 2012 CTRC-AACR San Antonio Breast Cancer Symposium.

Sitting in the audience was Barbara Segarra-Vazquez, a nine-year breast cancer survivor from San Juan, Puerto Rico.

“I’m one of the lucky persons in this journey because I had excellent health insurance,” said Segarra-Vazquez, a professor at the University of Puerto Rico. “Every day I meet people who cannot afford their deductible or who have to wait months to see a specialist. The outcome of cancer should not depend on your social status or where you live. It’s very sad and very unfair.”

Sexton admitted the “race gap” in cancer often has more to do with socioeconomic status and geographic differences than race itself. And various attempts have been made to overcome barriers to diagnosis and care. The first one to really work is patient navigation, Sexton said.

Think of a patient navigator as your personalized GPS for all things cancer, everything from setting up mammography appointments to steering you through the maze of diagnosis, treatment and the what-the-heck-happens-now realm of cancer survivorship.

“It’s nice to have someone make sure you’re in the right place at the right time, doing the right thing, seeing the right doctor, getting the right treatment,” Sexton said.

The American Cancer Society already offers services through its Patient Navigator Program at more than 130 locations nationwide. Susan G. Komen for the Cure and the Lance Armstrong Foundation have also funded patient navigation programs, Sexton said. And starting in 2015, patient navigation services will be required at the more than 1,500 community hospitals accredited by the American College of Surgeon Commission on Cancer, a consortium of professional organizations that sets standards for quality cancer care.

Sexton’s final slide offered a bit of hope for what patient navigation can do. Two bars sat horizontally on a graph. One showed that 39 percent of women treated at a hospital in Harlem 30 or 40 years ago lived at least five years. The other bar showed the survival stat for women who were shepherded through a screening and patient navigation program at the same hospital in the late 1990s: 70 percent were still alive after five years. Sexton quickly pointed out, however, that better treatments may have also contributed to the dramatic bump.

Indeed, a recent study found no difference in survival and cautioned that “while patient navigation programs have spread throughout the country, their impact upon cancer outcomes is understudied.”

So stay tuned.

As president of the board of directors for the Puerto Rico affiliate of Komen, Segarra-Vazquez hands out community grants for free mammograms and other big needs. “We are trying to give people information and give them opportunities. Every year, people are less afraid of breast cancer,” she said.

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Not All Women, Particularly Blacks, Are Getting Modern Lymph Node Surgery

Posted Dec. 5, 2012 – 3:50 p.m. CT

Let’s start with the good news first. More women with early breast cancer are taking advantage of a safer procedure to investigate whether cancer cells have spread to the lymph nodes. It’s just as effective as surgery to remove many or all of the nodes under the arm.

Now the bad news: Not everyone is getting this less-invasive surgery. Especially if they’re black.

It’s called a sentinel lymph node biopsy. A decade ago, only about 58 percent of white women and 45 percent of black women eligible for the procedure got it. Fast forward to 2007—right around the time the new technique replaced a 100-year-old surgery called axillary lymph node dissection—and 83 percent of white patients and 70 percent of black patients were receiving the new and improved approach.

Better, but not great.

When researchers looked at the data curves, they found that the uptake of sentinel lymph node biopsies in black women lagged about two to three years behind white women, said Dalliah Mashon Black, the study’s lead investigator who presented the findings on Wednesday at the 2012 CTRC-AACR San Antonio Breast Cancer Symposium. She said the explanations may be rooted in where patients live—possibly black communities not having the same nearby access to hospitals that offer the modern procedure—or doctors sticking with what they know. Income levels might also play a role, she said.

Researchers crunched the numbers from a national database of Medicare patients who were treated for node-negative breast cancer between 2002 and 2007.

Here’s what they found: In regions with lower levels of income and education, as well as fewer surgeons, fewer sentinel lymph node biopsies are performed among all races. Researchers haven’t broken the geographic data down by race, but Black said doing so is next on their list.

Black, an assistant professor of surgery in the department of surgical oncology at MD Anderson Cancer Center in Houston, also expects to have updated Medicare data by next spring that will allow her to look at whether the disparity trend persists through 2010.

But for now, what are the available data telling us?

Peter Ravdin, director of the Breast Health Clinic at the Cancer Therapy and Research Center at The University of Texas Health Science Center at San Antonio, said the findings show a constant improvement in the number of women getting the new procedure. White patients just happened to start making the switch first, he said.

“The question really is, what’s the interplay between economics, regionalism and race? Depending on what the strong variables are, you might take different approaches to addressing the barriers,” said Ravdin, who was not involved in the study.

For now, Ravdin suggests patients ask their doctors about the option of sentinel lymph node biopsy. “It should be part of the surgical decision-making process,” he said.

With sentinel lymph node biopsy, surgeons remove one or two of the tiny bean-shaped nodes that are most likely to contain cancer. Axillary node dissection, on the other hand, is far messier. There are more possible complications from removing 10, 20 or sometimes 40 lymph nodes from under the arm—like possible infections and bleeding, for starters. There’s also a higher risk for lymphedema, a sometimes painful swelling of the arm that can impact a woman’s quality of life for the long term.

Indeed, in Black’s study, 18 percent of black patients and 12 percent of white patients developed lymphedema following an axillary node dissection. With sentinel lymph node biopsy, the risk dropped to about 9 percent and 7 percent for black and white patients, respectively.

“If a black patient received the correct [staging] surgery—sentinel lymph node biopsy—she had a lymphedema rate similar to white patients,” Black said. This was even after researchers controlled for variables like obesity, a risk factor for lymphedema.

Axillary node dissection is still recommended over sentinel lymph node biopsy in women with stage 3 cancers and those receiving a mastectomy, partial breast radiation or chemotherapy before surgery.

Nevertheless, with innovation comes change. “We need to think of better and more creative ways of disseminating these new practice guidelines to health care providers and their communities so that all patients can benefit from improvements,” Black said.

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Advocates Gather to Hear Highlights of Breast Cancer Research From 2012

Posted Dec. 5, 2012 – 3:45 p.m. CT

In the fight against breast cancer, 2012 was a very promising year.

Two new drugs were approved, with possibly a third coming late next year. We got our first complete look at the genetic changes driving breast cancer. And thanks to a guideline change from the National Comprehensive Cancer Network, some women are being spared extensive lymph node surgery that sometimes has long-term consequences.

“It was a blockbuster year,” said Ann Partridge, the medical oncologist and clinical researcher who handpicked the latest and greatest news to share with 75 people—mostly breast cancer survivors—who gathered Wednesday morning in San Antonio. The special session, hosted by the American Association for Cancer Research and the Alamo Breast Cancer Foundation, coincided with the 2012 CTRC-AACR San Antonio Breast Cancer Symposium.

“Any time you have two drug approvals in one year, it’s a big year,” said Partridge, director of the Adult Cancer Survivorship Program at the Dana-Farber Cancer Institute in Boston.

In June, the Food and Drug Administration green-lit Perjeta (pertuzumab) for HER2-positive breast cancer. About a month later, the agency approved Afinitor (everolimus) for hormone-sensitive tumors. Now, a third powerful new drug called T-DM1 is poised for approval.

The buzz surrounding T-DM1 has been intensifying since June. That’s when news broke at the American Society of Clinical Oncology’s annual meeting that T-DM1 could put the brakes on worsening metastatic breast cancer for almost 10 months—a three-month improvement over the popular drug combo Tykerb (lapatinib) and Xeloda (capecitabine). Plus, it was safer.

T-DM1 is specifically for HER2-positive breast cancer and it’s made of two parts: a potent toxin attached to an antibody. DM1 is the toxic chemotherapy and the antibody drug is Herceptin, generically known as trastuzumab. Together, they work as a Trojan horse, Partridge said.

“T-DM1 sneaks chemotherapy into cancer cells that are HER2-positive, without damaging the rest of the body. It makes a very toxic chemotherapy very tolerable,” she said. Possible side effects of T-DM1 include diarrhea, nausea, fatigue and sometimes severely low platelet counts.

In November, the Food and Drug Administration announced it would expedite the review of T-DM1, also called trastuzumab emtansine. The agency will make its decision by Feb. 26, 2013.

There are more studies already under way for T-DM1, Partridge said, including one that combines the drug with the newly approved Perjeta.

Other big headlines covered by Partridge:

TAKING AN AX TO THE KNIFE: Some patients can now skip the extensive surgery where surgeons remove all the lymph nodes under the arm, the first place breast cancer is likely to spread.

New research prompted the National Comprehensive Cancer Network, an alliance of the country’s top cancer centers, to change its breast cancer guidelines in 2012. No longer must women have all their underarm lymph nodes removed if only one or two test positive for cancer. Now, these women can avoid so-called axillary lymph node dissection as long as the tumor is no bigger than 5 centimeters and the treatment plan includes lumpectomy, radiation and no pre-surgery chemotherapy.

“The new guidelines are changing the care of women today,” Partridge said.

This change, she said, will result in fewer breast cancer survivors developing lymphedema, a chronic swelling of the arm. The condition requires long-term management that can take a toll on a woman’s quality of life. A recent study found that about 35 percent of women who receive axillary lymph node dissection develop lymphedema, compared to roughly 5 percent who receive a sentinel lymph node biopsy to remove only a few nodes.

CLEVER MOVES: This year also gave us our first complete look at the genetic changes driving breast cancer—insight that could help researchers craft a more clever approach to treating breast cancer in the future.

“The better you understand breast cancer, the better you can pick it apart and attack it. This was a big step,” Partridge said of the research, reported in October in the journal Nature. “But we have more to do.”

Among those listening to Partridge discuss the year’s breast cancer headlines Wednesday was Ginny Mason, who has become a fixture at the San Antonio symposium. This year marks her 10th time here, which is 10 times more than she ever expected.

Mason had been given a year to live after being diagnosed in 1994 with inflammatory breast cancer. Now she’s the executive director of the Inflammatory Breast Cancer Research Foundation. “I just turned 60 in October and I don’t think I ever expected to live that long,” Mason said.

“I try to wrap my brain around everything that’s happened since that diagnosis,” she continued. “All the things that you didn’t know you were going to get the chance to experience.

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For Tamoxifen, Longer Is Better

Posted: Dec. 5, 2012 – 2:00 p.m. CT

Breast cancer experts and survivors are downright delighted with a study dubbed ATLAS that could be the start of better odds for the thousands of women taking tamoxifen. Consider these numbers: a 25 percent lower chance of breast cancer coming back, and a 29 percent lower chance of dying from the disease.

That’s what researchers found when women with estrogen receptor-positive breast cancer were given 10 years of tamoxifen — the go-to treatment for many breast cancer patients — rather than the standard five years of the estrogen-blocking drug.

What the typical tamoxifen regimen can do for patients isn’t too shabby. Research published in 2011 showed that women who take tamoxifen for five years reduce their risk of dying from breast cancer by almost a third over the 15 years after diagnosis compared to women who don’t.

And when women stick with tamoxifen for an entire decade?

“We’ve now shown that extending tamoxifen use to 10 years reduces the risk of breast cancer death by about half. Cancer treatments don’t tend to have effects that big,” said Richard Gray, a professor of medical statistics at the University of Oxford in the U.K. and a co-investigator on the ATLAS (Adjuvant Tamoxifen – Longer Against Shorter) study.

Results were reported Wednesday at the 2012 CTRC-AACR San Antonio Breast Cancer Symposium and simultaneously published online in The Lancet.

It’s those first five years when the risk of breast cancer’s return is at its peak. But the risk is still pretty high when survivors reach five, even 10 years out, said Peter Ravdin, director of the Breast Health Clinic at the Cancer Therapy and Research Center at The University of Texas Health Science Center at San Antonio. “The idea was that after five years, any cancer that was left behind would perhaps be resistant to tamoxifen and it wouldn’t make any difference to use it longer,” said Ravdin, who was not involved in the study.

Not so, found ATLAS.

The researchers looked at 6,846 women with estrogen receptor-positive breast cancer from the U.S. and 35 other countries. Most women in the study were postmenopausal and all had already taken five years of tamoxifen. Half stopped the drug at five years, while the other half took tamoxifen for five more years.

Breast cancer returned in 617 women who took tamoxifen for a decade compared to 711 recurrences in women who stopped tamoxifen after five years. Fewer women died from a recurrence if they received 10 years of tamoxifen: 331 deaths compared to 397 deaths.

Lori Marx-Rubiner, who was not involved with the ATLAS study, took five years of tamoxifen after chemotherapy and surgery to treat stage 2 hormone receptor-positive breast cancer. She took what she thought was her last dose in 2007, only to find out last year that the cancer was back and it had spread to her bones.

“I’m happy for whoever comes after this study,” said Marx-Rubiner, 46, of Los Angeles, Calif. “It will always be an outstanding question for me: Should I have stayed on tamoxifen? But I also don’t find it helpful to dwell in that place of what ifs.”

Now she’s back on tamoxifen. “I’ll take it until it stops working,” she said.

Then there was the question of safety. Would more of the drug cause more of its side effects, most notably the risk of endometrial cancer? It did, but the uptick was barely 2 percent. “The benefits are about 10 times the risks,” Gray said.

Bottom line: For women nearing the end of their five years’ worth of tamoxifen, asking their doctor how much another five years would drop their recurrence risk isn’t a bad idea. “It’s going to influence treatment,” Ravdin said. “I think most women will continue taking tamoxifen.”

Ravdin said postmenopausal women taking a class of hormone drugs called aromatase inhibitors to prevent recurrence could have success with a longer treatment, too, but more research is still needed.

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Breast Cancer Research Takes Center Stage at SABCS

Posted: Dec. 4, 2012 – 11:00 a.m. CT

The nation’s largest scientific breast cancer meeting is now under way in San Antonio.

Roughly 8,000 are expected to attend the 2012 CTRC-AACR San Antonio Breast Cancer Symposium (SABCS), now in its 35th year. An international crowd of clinicians, researchers, nurses, patient advocates and other health professionals will gather from today through Saturday to hear the latest advances in the treatment of breast cancer and the translational and basic sciences that are leading to a better understanding of the disease.

The conference is sponsored by the American Association for Cancer Research (AACR), the Cancer Therapy and Research Center (CTRC) at University of Texas Health Science Center at San Antonio and Baylor College of Medicine.

“Much of the progress in breast cancer research is presented and discussed at this meeting every year,” said Judy Garber, past president of the AACR and director of the Center for Cancer Genetics and Prevention at Dana-Farber Cancer Institute in Boston. In recent years, Garber has seen a push to highlight more basic science discoveries alongside breakthroughs in the clinic.

“These days, treatment is increasingly scientifically based. So at a meeting like this, you get to learn not only about the results of the studies showing clinical progress, but also the basis of where the next progress will come from,” she added.

For the next few days, San Antonio will also be the meeting place for breast cancer survivors. Women from around the globe receive scholarships to attend the symposium from the San Antonio-based nonprofit Alamo Breast Cancer Foundation, which has brought 528 patient advocates to SABCS since 1998.

The nonprofit holds nightly “Hot Topics Mentor Sessions” where mentor physicians and scientists take the day’s research highlights and put them into perspective for patients. The Alamo Breast Cancer Foundation president and 18-year breast cancer survivor Sandi Stanford remembers barely 25 people filling the room during one of the first Mentor Sessions. In 2011, more than 300 people packed the room each night.

“For the patient advocates and survivors, it’s a setting where they can truly understand the science. They leave the Mentor Sessions with the confidence to go back home and talk to their oncologists,” Stanford said. Mentor Sessions will be held Dec. 5-7 from 5:30-7:30 p.m.

On the science side, offering a sneak peek at what’s hot at this year’s SABCS is symposium co-director Peter Ravdin, director of the Breast Health Clinic at UT Health Science Center:

• ATLAS trial: Is 10 years of tamoxifen better than the standard five years at preventing recurrence?

• CONFIRM trial: Does doubling the dose of Faslodex (fulvestrant) improve survival in advanced breast cancer?

• LEA study: Does adding Avastin (bevacizumab) improve the effectiveness of endocrine therapy for advanced breast cancer?

• UK START trial: How does a larger daily dose of radiation therapy over three weeks compare to a smaller daily dose over five weeks?

• HERA trial and PHARE trial: Is longer or shorter use of Herceptin (trastuzumab) as good as or better than the standard one year?

• Cognition and fatigue study: Is fatigue the real culprit behind cognitive problems in breast cancer patients?

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