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Cancer, Research, Science, Stanford News

Organs in a dish help pinpoint cancer-causing mutations

Organs in a dish help pinpoint cancer-causing mutations

bodyTiny ‘organs in a dish’ are providing a way for researchers like cancer researcher Calvin Kuo, MD, PhD, to more readily study the effect of specific, cancer-associated mutations. Unlike the traditional research approach of growing and studying sheets of identical cells on plastic, Kuo’s approach mimics the shape, structure and tissue organization of a three-dimensional organ. The work of Kuo and his lab members was published Sunday in Nature Medicine. As Kuo explained in an e-mail to me:

We have developed a method to grow many different, normal organs outside of the body, in something like a petri dish. We call this an “organoid” system in which we can grow colons, or stomachs, or pancreases as little balls of cells. We can then introduce the DNA for potential cancer genes at will into the organoids and see if these genes induce cancerous characteristics. Using this system, we have accomplished the first conversion of normal colon, stomach or pancreas tissue to cancer in a petri dish.  Then, we can rapidly decipher whether genes that are mutated in a given patient’s tumor are truly causing the cancer.  In our initial studies, we have already found surprising results in which presumed cancer-causing genes were actually not, whereas cancerous properties actually resided in previously unsuspected genes.

Previously, Kuo has shown that, although the organoids are tiny, they can act like the real thing. For example, the colon organoids contract in a synchronized fashion that mimics the normal process of digestion. Now the researchers are thinking of new ways to use the organoids to help patients. As Kuo described:

Additionally, we would like to use the organoids for drug testing purposes to determine which current cancer drugs work against which mutations. This information could help physicians to give cancer patients only those drugs likely to be effective against their particular tumor mutations, which would save time, economic resources, and ultimately lives.

The possibilities don’t end there, said Kuo:

Finally, we would like to extend our colon organoid technologies to directly grow tumor samples from individual patients. We could thus direct the treating oncologist to only prescribe those therapies for which we had prior evidence “in the dish” of a tumor response.

Previously: In animal study, cancer drug appears helpful for diabetes and Intestinal cell cultures keep the research moving
Photo by William Creswell

Cancer, Fertility, Parenting, Pregnancy, Women's Health

A cancer survivor discusses the importance of considering fertility preservation prior to treatment

pregnancy_testBack in 1998, Joyce Reinecke, JD, was on a cross-country business trip when her increasing fatigue and lightheadedness resulted in her being admitted to the emergency room and the discovery that she had tumors in her stomach, one of which was necrotic and bleeding causing her to be severely anemic. She was diagnosed with leiomyosarcoma, and the tumors, as well as all of the surrounding lymph nodes, were surgically removed. Before she was discharged from the hospital an oncology fellow casually mentioned to Reinecke that since she was scheduled to start chemotherapy she might want to consider options to preserve her fertility.

At the time, Reinecke and her husband hadn’t considered how her treatment would affect their future plans to have a family. The couple eventually decided to complete a round of in vitro fertilization and work with an agency to select a gestational carrier. Their twin daughters were born in February 2000. Reinecke, executive director of the Alliance for Fertility Preservation, shared her patient perspective during a keynote speech at the Family Building After Cancer: Fertility Preservation and Future Options Symposium held at Stanford earlier this month.

To continue the conversation, I reached out to Reinecke about the issue of fertility and cancer survivorship. In the following Q&A, she discusses advancements in the field, why patients need to be proactive in sharing their wishes to have a family with providers, and questions to consider prior to treatment.

What motivated you to focus your career on expanding patient and provider awareness of fertility preservation?

When my girls were around two, I received several inquiries from family acquaintances who had young adults in their lives who were newly diagnosed with cancer. These people had reached out to my parents, to try to understand more about what I had done, where I had gone, etc. in order to preserve my fertility. In speaking to others and hearing about their challenges in finding fertility information and services, I started to really feel that something about the status quo was not right. These patients/family members had learned about possible infertility because they knew of my story, not because their doctors had discussed it with them. This really emphasized to me that my situation – learning about my possible infertility in a very ad hoc way – was not unique, not unusual, but the norm, and perhaps, lucky.

I began doing research around the issue, to see what was out there, what information was available online, etc. I found very little, but I did stumble upon information that Fertile Hope was having a fundraiser. I was in complete shock that a new nonprofit focused on this very issue existed, not to mention that it was based in New York. I went to the fundraiser, signed up to volunteer, met with Lindsay Beck, and signed on as Employee #2. The rest is history.

A past study shows that less than half of U.S. physicians are following the American Society of Clinical Oncology’s guidelines suggesting all patients of childbearing age be informed about fertility preservation. How can patients make sure they get the necessary information about their fertility options prior to treatment?

This question is tricky, because I feel like the onus for initiating this discussion has to be on the provider. Newly diagnosed patients are overwhelmed with all sorts of medical information and decisions to make, not to mention the emotional distress of the diagnosis. Also, patients don’t know what they don’t know. Sometimes providers mistakenly believe a patient isn’t interested in fertility preservation because they don’t ask about it. However, providers have to remember that newly diagnosed young adults probably have very little understanding about how chemotherapy and radiation work – unless they have a cancer that has a direct impact on their reproductive system they probably have no inkling that their fertility is at stake.

That being said, patients need to advocate in their own interest (or enlist a family member to help them do this if they cannot during this difficult time). That means communicating their wishes and values about future parenthood with their providers. That means asking the right questions: Will I be able to have children in a few years? Ever? What can I do about it? It might also mean being able to challenge their doctor’s disapproval or ask that treatment be pushed back [so the patient has time to] bank sperm or eggs. Which is sometimes hard to do.

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Applied Biotechnology, Cancer, Genetics, otolaryngology, Research, Stanford News

Stanford researchers identify genes that cause disfiguring jaw tumor

Stanford researchers identify genes that cause disfiguring jaw tumor

jawPatients with the rare jaw tumor ameloblastoma have few treatment choices. Radiation and drugs have failed to stop this slow-growing cancer, leaving jaw removal as the only option. The surgery also takes out facial nerves and blood vessels, and so patients need reconstructive surgery and rehabilitation just to smile and chew again.

In a new study, published in Nature Genetics, Stanford researchers discovered two gene mutations that cause this tumor. Their findings point to FDA-approved drugs that are effective against these mutations in other types of cancer.

To find the mutations, the researchers sequenced mRNA – messages copied from genes that tell the cell how to make proteins – from slices of preserved tumor. In 80% of the samples, they found a mutation in either the SMO or the BRAF gene. Interestingly, the SMO mutations occurred predominantly in the upper jaw, while BRAF mutations were found mainly in the lower jaw.

From our press release:

“These genes are essential for delivering signals of growth and development, particularly in developing organs,” said Robert West, MD, PhD, associate professor of pathology at Stanford and a senior author on the study. “But it’s increasingly apparent that they are often mutated in cancers.”

Perhaps most promising, researchers found that there are already FDA-approved drugs for cancers with mutations in the same developmental pathway. A drug called vemurafenib is toxic to ameloblastoma cell cultures that harbor a BRAF mutation, they found. This drug is effective against melanomas that carry the same mutant gene. Researchers also found that a compound called arsenic trioxide, an approved anti-leukemia drug, is affective at blocking the mutant SMO protein.

West and his colleagues, A. Cain McClary, MD, a co-author and chief pathology resident at Stanford Hospital, and A. Dimitrios Colevas, MD, an associate professor of oncology at Stanford, have already submitted an application to the biotech company Genentech, which manufactures the most popular brand of vemurafenib. Their pilot study would test whether the drug could shrink tumors in people with ameloblastomas.

Also from the release:

Throughout this project, McClary has engaged with an ameloblastoma Facebook group to hear members’ stories and to learn about what a patient goes through during the initial surgery and subsequent facial reconstruction. He plans to conduct a webinar with the group, and can’t wait to share his findings with them.

“It’s a great motivator,” he said about his involvement with the group. “Our face is a special place. I couldn’t imagine not smiling.”

Patricia Waldron is a science writing intern in the medical school’s Office of Communication & Public Affairs.

Previously: Gene panel screens for dozens of cancer-associated mutations, say Stanford researchers
Photo by Gray’s Anatomy Plates/Wikimedia Commons

Cancer, Research, Science, Stanford News

Listening in on the Ras pathway identifies new target for cancer therapy

Listening in on the Ras pathway identifies new target for cancer therapy

2843144877_fd9593fdca_zEavesdropping on conversations among proteins is one way for researchers to understand how cells make decisions to divide or die, to move or to stay put, to respond to or ignore the insistent signals from a neighboring cell. Often these messages are passed from protein to protein within the cell, like a molecular game of “telephone”, via the transfer of small chemical tags like phosphate groups. These tags regulate the activity of a protein and affect how it interacts with other, downstream partners.

Understanding these messaging pathways  is even more important when they become corrupted. As a result, cells can divide uncontrollably or (in the case of immune cells) launch attacks on other, harmless bystander cells or tissues.

Many of the message trails, called pathways, are governed by one or two loudmouths. One, known as the Ras family of proteins, is critically important to cell growth. In fact, the three Ras genes are among the most frequently mutated class of genes in human cancers. But it’s been very difficult to find effective ways to gag the Ras genes and their troublesome proteins. Recently, the National Cancer Institute pegged the molecule for special attention with its Ras Program, meant to encourage researchers to develop new, innovative ways to curb either the activity of the mutant Ras proteins or to inhibit the Ras pathway in other ways.

Now, cancer biologist Julien Sage, PhD, and biologist Or Gozani, MD, PhD, have identified a new signaling protein that works on another protein participant in the Ras pathway. Unlike the phosphate groups often passed from protein to protein in our example, this pathway relies instead on the transfer of what’s known as a methyl group from one protein to another. Their work was published (subscription required) yesterday in Nature. Sage explained the research to me in an e-mail:

A large number of human cancers are driven by activation of the Ras pathway, including pancreatic cancer and a subset of lung cancers. This observation has led to the development of small molecule inhibitors that target kinases (enzymes that add phosphate groups to other proteins) in the Ras signaling network. However, these drugs can be toxic and resistance can occur fairly rapidly. In this study, we found that the SMYD3 methyltransferase (an enzyme that adds methyl groups to other proteins) directly regulates the Ras pathway by adding a methyl group to a Ras pathway member (MAP3K2). In the absence of SMYD3, the Ras pathway is less active.

The researchers found that blocking SMYD3 expression in laboratory mice slowed the development of pancreatic and lung cancers when Ras genes were mutated. They also found that it had an important impact when the animals with cancers were treated with experimental Ras inhibitors. As Gozani explained:

Importantly, mice mutant for SMYD3 are completely viable but the dose of Ras pathway inhibitors required to inhibit pancreatic cancer growth is lower in SMYD3 mutant mice than in control mice. These experiments identify SMYD3 as a novel regulator of Ras signaling, one of the central oncogenic pathways in humans, and suggest that inhibitors targeting the  methytransferase activity of SMYD3 may be combined with Ras pathway inhibitors to achieve lower toxicity and higher efficacy.

In other words, it might be possible to achieve greater therapeutic effect for some of these deadly cancers by hitting the Ras pathway twice. According to both Sage and Gozani:

 This work establishes SMYD3 as a bona fide therapeutic target for pharmacologic intervention to treat some of the most deadly human cancers and argues that enzymes with similar functions might regulate crucial cellular pathways.

Previously: Big data = big finds: Clinical trial for deadly lung cancer launched by Stanford study
Photo by Ben Smith

Cancer, Patient Care, Stanford News, Videos

When a rash isn’t just a rash: A patient’s battle with mycosis fungoides

Paul Raffer, MD, is a doctor, accustomed to avoiding the kind of leap that non-physicians often make by assuming common symptoms are something far more serious. So he saw the rash that appeared on his body a few years ago as nothing to worry about. The irony, of course, is that the rash turned out to be something quite serious: mycosis fungoides, a form of blood cancer that shows itself in the skin. It’s a common form of cutaneous lymphoma but it is considered rare, appearing at a rate of 3.6 cases per million people each year.

Raffer’s belief that the rash was benign changed, as he told me for this story, when that rash spread over his entire body and began to itch continuously. “I stopped being able to sleep. My skin started flaking and peeling. I also started getting very thick plaques, with lesions all over my back, my abdomen and my arms. But the worst part was the itchiness. And there was nothing that worked very well to control it.”

Because mycosis fungoides is rare, specialists are not plentiful. But what encouraged Raffer, who lives in Arizona, was when his doctor instructed him: “Go to Stanford. See Dr. Youn Kim. If not one of the world’s experts, she is certainly the West Coast guru for what you have.”

Once Raffer was evaluated at the Stanford Multidisciplinary Cutaneous Lymphoma Clinic, he received another blow: His condition was at Stage IV. (Mycocis fungoides can progress quite slowly, but Raffer’s had advanced to an aggressive form called Sézary syndrome.) “Your insides fall out when you hear Stage IV of anything,” Raffer said. But, three years later, Raffer is healthy again.

Cancer, Emergency Medicine, Research, Science, Stanford News

Small molecule may protect against radiation exposure, say Stanford scientists

Small molecule may protect against radiation exposure, say Stanford scientists

P1060359No one wants to imagine a nuclear accident. But, as Fukushima and Chernobyl showed, they do happen. Unfortunately there’s no truly effective way to protect people who have been exposed to large amounts of radiation (more than 10 gray, for those of you wondering; for you overachievers out there, 1 gray is the absorption of 1 joule of radiation energy per kilogram of matter).

Many of these people will die from what’s known as radiation-induced gastrointestinal syndrome when the rapidly dividing cells in their intestinal lining begin to die. As a result, the intestine loses its ability to regulate fluid loss and prevent the entry of pathogens into the body, causing severe diarrhea, electrolyte imbalance and sepsis.

Stanford radiation oncologist Amato Giaccia, PhD, and his colleagues wondered whether a cellular pathway that controls how cells respond to stress could be involved in the intestine’s response to radiation. Their study was featured today on the cover of Science Translational Medicine. As I explain in our release:

The researchers were studying a molecular pathway involved in the response of cells to conditions of low oxygen called hypoxia. Hypoxic cells produce proteins known as hypoxia-inducible factors, which help the cells survive the stressful conditions. (The HIF proteins – HIF1 and HIF2 – are normally degraded quickly when oxygen levels are normal.)

Hypoxia often occurs in fast-growing solid tumors as cells find themselves far from oxygen-delivering blood vessels, but it can also occur during times of inflammation, or in tissues like the intestine that experience natural gradations in oxygen levels. HIF proteins help the intestine absorb needed nutrients while blocking the entry of pathogens and maintaining healthy fluid exchange.

Giaacia and lead study author Cullen Taniguchi, MD, PhD, a postdoctoral scholar, wondered if increasing the levels of HIF proteins in intestinal epithelial cells could help the them survive damaging amounts of radiation. To test their theory, they used a small molecule called DMOG to block the naturally occurring degradation of HIF proteins in laboratory mice exposed to radiation. They found that administering DMOG to the mice significantly increased their survival – even when the molecule was given 24 hours after initial exposure.

The study suggests it may one day be possible to prevent or reduce the incidence of  radiation-induced gastrointestinal syndrome in humans.  It also provides an intriguing hint that it may be possible to mitigate some of the gastrointestinal side effects experienced by patients undergoing radiation therapy for cancer.

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Breast cancer awareness: Beneath the pink packaging

We’ve partnered with Inspire, a company that builds and manages online support communities for patients and caregivers, to launch a patient-focused series here on Scope. Once a month, patients affected by serious and often chronic diseases share their unique stories. Our latest comes from a breast cancer patient from Salt Lake City.

Over the years, you may have participated in pink-themed races and donned pink shoe laces in an effort to demonstrate solidarity and support regarding breast cancer awareness.

Good intentions notwithstanding, let’s pause for a moment to consider what has truly been accomplished since National Breast Cancer Awareness Month was launched in 1985. Have fewer people gotten the disease? Have survival rates improved? The answers are disconcerting:

  • Mortality rates remain depressingly flat. In 1988 approximately 40,000 women perished annually from breast cancer; in 2013 39,620 women and 410 men will have died from the disease.
  • Today, approximately 162,000 women and men are living with metastatic breast cancer in the U.S. Some of them developed metastatic disease five, 10, 15, or even 20 or more years after their initial diagnosis. Many are relatively young – in their 20s and 30 – with growing families.
  • A diagnosis of early stage breast cancer provides no reassurance because the disease will eventually spread or “metastasize” to other organs in an astounding 30 percent of these patients.
  • Median survival after a metastatic diagnosis is only three years – with no statistically significant improvement over the past 20 years.

Imagine for a moment that you’ve been diagnosed with early stage breast cancer. You have confidence that if you follow your doctor’s recommendations, you’ll live a normal life – after all, you have been made “aware” of breast cancer! But that doesn’t always happen. Take my case: I was diagnosed with early stage breast cancer at age 39 after 4 years of misdiagnosis. I experienced a double mastectomy, six cycles of the most toxic chemotherapy available at the time, followed by five years of Tamoxifen, a hormonal therapy. I became increasingly convinced that my experience with breast cancer was safely behind me each time I underwent annual cancer checkups with normal results.

Fourteen years after my initial diagnosis, I developed a dry, persistent cough that three doctors misdiagnosed as asthma, GERD, or post-nasal drip. After four years of chronic coughing I became hoarse. Finally a doctor recognized that my vocal cord was paralyzed. He ordered a scan that revealed a tumor pressing on the laryngeal nerve, which in turn caused paralysis.

A biopsy revealed metastatic breast cancer that was hormonally receptive. By then I had developed multiple lung tumors, a liter of malignant pleural effusion and pericardial effusion. A catheter was inserted in my chest to drain the fluid until it disappeared several weeks later. Weak, ill, and terrified, I didn’t know whether I would live for another year and was determined to be as active as possible to enhance my odds of survival.

Although my oncologist recommended chemotherapy, I sought a second opinion from an oncologist who suggested hormonal treatment that has thankfully allowed me to enjoy a better quality of life. I also consult with a naturopathic oncologist regarding supplements and complementary therapies, and I’ve adjusted my diet to exclude sugar and processed foods.

My medical team is rounded out by a wonderful acupuncturist whose skills have enabled me to avoid anti-depressants. For emotional support, I exchange encouragement and information with people online who are coping with metastatic disease, and my husband has retired early so that we can enjoy time together while I am still well enough to do so.

After eight years of misdiagnosis, I’m left with little faith in the diagnostic capabilities of the medical establishment and have no illusions about living a normal life. Yet I’m one of the lucky ones: relatively old (age 60), not on chemotherapy, able to participate in daily activities, and currently pain-free. Conversely, most patients I know suffer terrible side effects from both their cancer and its treatment, such as fatigue, nausea, blistering skin, neuropathy, and excruciating bone pain.

In retrospect, I wouldn’t change any decisions regarding my disease and its treatment. But I have to realize that “early stage” breast cancer, with which I was initially diagnosed, is significantly more lethal than the media conveys – given that nearly one of three early-stage patients will eventually succumb to their disease.

It’s obvious that the battle against breast cancer, with incessant emphasis on “awareness” and early detection, has been watermarked upon the canvas of failure. Increasing awareness – especially when it’s been heavily sugarcoated – will never alter the course of this disease or reduce the victim count. Only by deriving a mechanism to irrefutably prevent breast cancer and effectively treat those who already have it will we forever close the book on stories such as mine.

Anne Loeser is a retired software project manager who was diagnosed with metastatic breast cancer 18 years after developing “early stage” disease. A passionate researcher, she continuously shares information and support on multiple forums with others who are dealing with terminal breast cancer.  Anne currently resides in Salt Lake City, Utah with her husband and parrot.

Related: Pink Think/The hitch with the breast cancer marketing pitch

Cancer, Medicine and Society

A doctor recounts his wife’s battle with cancer: “My knowledge was too clear-eyed”

We’ve written before about doctors becoming patients – but what happens when it’s the physician’s partner who becomes seriously ill? Over the weekend I came across a beautifully written, raw New York piece in which Memorial Sloan Kettering physician Peter Bach, MD, describes his late wife’s fight with cancer. He writes:

When Ruth was first diagnosed with breast cancer, friends would routinely comment to us along the lines of “It’s so good Peter knows so much about this disease.” But others disagreed, imagining I suffered more from my knowledge. Whether I was better or worse off I kept filing away as a pointless academic debate, like wondering if Edna Pontellier’s death in The Awakening was a resignation or a liberation, or whether Batman would ever just get over it. But in the lobby of my hospital, I knew the answer: My knowledge was too clear-eyed. I couldn’t pretend for another day or hour or minute that there were good days ahead.

Bach later describes the moment he knew the end was near:

We were sitting at a coffee shop when the light caught her just right and I saw it. I tried for a few moments to keep talking about whatever topic we had landed on, but I discreetly texted a friend of mine from college, also a doctor, in medicalspeak to share the terrible news—“scleral icterus.”

I couldn’t hold it in anyway. “Your eyes are yellow,” I blurted out.

She was stunned, and slightly panicked. “Why?” she asked. And then something totally unexpected—“What do they do about it?” I seized on this, my escape hatch from having to talk about her liver failing. I said I didn’t know, we’d have to ask. Another lie.

The yellowing, first of the whites of the eyes, later of the skin, is like the check-engine light turning on. The yellowing itself is irrelevant; it means bad things are happening inside. It meant her brain would soon become addled with toxins that at one time her liver could have cleared easily. She was near the end.

My phone pinged. My doctor friend, holding the medical jargon: “Oh [f**k].”

The full piece is worth a read.

Previously: A Stanford physician’s take on cancer prognoses, Both a doctor and a patient: Stanford physician talks about his hemophilia and Red Sunshine: One doctor’s journey surviving stage 3 breast cancer

Cancer, Genetics, Public Health, Research, Stanford News, Technology

Odd couples: Resemblances at molecular level connect diseases to unexpected, predictive traits

Odd couples: Resemblances at molecular level connect diseases to unexpected, predictive traits

odd coupleStanford big-data king Atul Butte, MD, PhD, has made a career out of mining publicly available databases to unearth novel and frequently surprising relationships between, for example, diseases and drugs, nature and nurture, and pain and sexual status.

In his latest Big Dig, Butte (along with his colleagues) has combed through mountains of electronically available data to identify molecular idiosyncrasies linking specific diseases to easily observed traits that on first glance wouldn’t be thought to have any such connection. The results, written up in a study published in Science Translational Medicine, may allow relatively non-invasive predictions of impending disorders.

For example, who would think that magnesium levels in the blood might be an early-warning marker for gastric cancer? Or that platelet counts in a blood sample would predict a coming diagnosis of alcohol dependency? Or that a high PSA reading, typically associated with potential prostate cancer, would turn out to be predictive of lung cancer? Or that a high red-blood-cell count might presage the development of actute lymphoblastic leukemia?

Answer: No one. That’s the beauty of Big Data. You find out stuff you were never specifically looking for in the first place. It just pops out at you in the form of a high, if initially inexplicable, statistical correlation.

But by cross-referencing voluminous genetic data implicating particular gene variants in particular diseases with equally voluminous data associating the same gene variants with other, easily measured traits typically considered harmless, Butte and his associates were able to pick out a number of such connections, which they then explored further by accessing anonymized electronic medical records from Stanford Hospital and Clinics, Columbia University, and Mount Sinai School of Medicine. “We indeed found that some of these interesting genetic-based predictions actually held up,” Butte told me.

Because checking blood levels of one or another substance is far simpler and less invasive than doing a biopsy, and because altered levels of the substance may appear well before observable disease symptoms, this approach may lead to early, more inclusive and less expensive diagnostic procedures.

Butte is one of the speakers at Stanford’s upcoming Big Data in Biomedicine conference. Registration for the May 21-24 event is open on the conference website.

Previously: Nature/nurture study of type 2 diabetes risk unearths carrots as potential risk reducers, Mining medical discoveries from a mountain of ones and zeroes, Newly identified type-2 diabetes gene’s odds of being a false finding equal one in 1 followed by 19 zeroes, Women report feeling more pain than men, huge EMR analysis shows and Cheap Data! Stanford scientists’ “opposites attract” algorithm plunders public databases, scores surprising drug-disease hook-ups
Photo by cursedthing

Cancer, In the News, Stanford News, Women's Health

Using 3-D technology to screen for breast cancer

Using 3-D technology to screen for breast cancer

Yesterday, KGO-TV aired a story discussing the use of 3-D breast-screening at Stanford Hospital. As described here, the technology has the potential to identify breast cancers more accurately, “with fewer false alarms.” More from the piece:

The technology is known as tomosynthesis. It’s a form of x-ray that produces both two dimensional and three dimensional images in a single session. If doctors notice an area that’s suspicious on the normal image, they can turn to the 3D view to essentially examine it from a different angle. Jafi Lipson, M.D. is Assistant Professor of Radiology at Stanford.

“The benefit of tomosynthesis is that you have multiple images at slightly different angles of the x-ray tube that allows you to resolve a lot of artifacts that we normally see when we take two dimensional images of the breast,” Dr. Lipson explains.

Previously: Ask Stanford Med: Radiologist responds to your questions about breast cancer screening, California’s new law on dense breast notification: What it means for women and Five days instead of five weeks: A less-invasive breast cancer therapy

Stanford Medicine Resources: