Talking to My Tatas: A Breast Cancer Researcher’s Adventure With The Disease And What You Can Learn From It is scheduled to be published February 8, 2022!
On. My. 49th. Birthday.
I’m not one for signs, but this is the second serendipitous date associated with this book baby so far. The first was getting the offer for publication from Rowman & Littlefield on November 5 of last year, the same day I was in surgery for the first step in my left breast reconstruction. This is the second. I am filled with joy and delight!
What’s next in the process? Now that I’ve turned in finalized chapters and other components of the book with edits in response to super helpful comments and notes from editor Suzanne Staszak-Silva (shout out to my amazing literary agent Barbara Collins-Rosenberg for giving me edits and notes prior to sending them to Suzanne), the manuscript enters the production phase. I’ll be receiving notes from the Production Editor, completing any revisions, going through proofs, reaching out for endorsements – shout out to the folks who already said, “Yes, send it to me for an endorsement!” – and planning for the release and promotion.
I cannot WAIT to see the cover!
I also cannot wait until this book is available to the public, including the hundreds of thousands of newly diagnosed breast cancer patients, current patients, survivors, and caregivers. If I can help even one of those people – my survivor sisters and brothers – by informing them, inspiring them, helping them cope, or giving them a much needed laugh, then I will have accomplished something really special.
This book will also help me develop a guide for newly diagnosed breast cancer patients at my institution, another labor of love.
I send love and gratitude to all of the mentors and colleagues who’ve made me into the scientist I am today, my healthcare team for saving my life and helping me thrive, and my family for being my strength and limitless supply of love.
Facebook is a great place to meet some weird-ass motherfuckers. We all know that. But I’m still surprised and more than a little dismayed by the scammers. I normally just report ads that include woo woo, sometimes leaving a snarky comment, or just hide or block scammers. It’s rare that they actively seek me out, but it does happen.
Check this out! In response to my post on a blog post about legitimate, peer-reviewed science and breast cancer, Mr. Ansari was compelled by the power of the spell caster, “Dr” Akhigbe, to testify about the amazing things the spell caster can do.
It’s an impressive list worthy of the most outrageous scammy chiropractor. He apparently has the cure for herpes (HSV – I assume the genital variety), HIV, gonorrhea, low sperm count, menopause disease (it’s not a disease, even if it feels like it sometimes; he’s big on STDs and fertility), epilepsy, asepsis (I think he means sepsis – “asepsis” refers to aseptic techniques that minimize risks of bacterial, fungal or viral contamination during surgery and medical procedures), and cancer (which kind, dude?).
Where has this paragon of the medical community been all my life? Why haven’t we heard of him?
I have a few theories, but I decided to go down the rabbit hole and read more about the good “doc” and his miraculous healing abilities. First off, he has at least three profiles. Sketchy. The spell caster profile is apparently now dedicated to marriage, fertility, and “total freedom and happiness.” Hmm, I wonder how much that costs?
The posts are a feast of stock photos with tons of woo, attractive people who seem to be happy, and hashtags a plenty (candlemagic #magicspells #candlespells #astrology #occult #spellcandles #witchyvibes #bruja #pagan #witches #astrologer #psychicreading #witchcraftspells #spellcraft #conjurer #metaphysical #lovespecialist #spellcasters #brujasofinstagram #spiritualoils #spellworker #moneyspells #spiritualawakening #healing #lovespellsmaster #follow #spellcandlesofinstagram #spiritual #altarsofinstagram).
Yup. He’s a busy, busy man. There’s a lot going on there…
I kind of hope there’s a mockumentary based on this dude. Not that it would be as good as What We Do In The Shadows, but I’d LOVE Colin Robinson to explain the history of herbal medicine to The Spell Caster until he’s utterly drained.
I’ll focus on the other profile, which deals with herbal remedies for “great diseases,” because “it’s a gift from God.”
Here’s one of his posts related to cancer:
I’ve already covered turmeric, antioxidants (this includes the berry thing), and I’m covering mushrooms in my book, so let’s dig into what garlic and ginger can do for you (and more importantly, cannot do for you) as a cancer patient.
Note: My medical oncologist is a fan of veggies as well as legitimate research on diet and breast cancer molecular signaling/drug responses. Check out his blog for legit information and some great recipes!
Garlic. It makes food delicious, your breath stinky, and wards off vampires, but what can it do for cancer? When I searched the web, the first promising result I found was from Memorial Sloan Kettering Cancer Center. Reputable enough for me! When I clicked, a big fat pop up window with a disclaimer and a “Continue” button I had to click to proceed tried to jump out of the screen:
“This Web site — Information About Herbs, Botanicals and Other Products — is for general health information only. This Web site is not to be used as a substitute for medical advice, diagnosis or treatment of any health condition or problem. Users of this Web site should not rely on information provided on this Web site for their own health problems. Any questions regarding your own health should be addressed to your own physician or other healthcare provider.”
They have a whole disclaimer to protect them from yahoos looking for woo woo!
What did it have to say about garlic? In terms of cancer, here’s the 411:
Getting into the nuts and bolts, the clinical summary (with references) states:
1. Possible correlation with garlic supplement and gastric (stomach) cancer mortality (death) but not incidence (getting cancer), but other studies found no evidence of either. Remember, correlation does NOT equal causality.
2. Mixed results on garlic and colorectal cancer, with some observation of reduced number and size of adenomas (precancerous lesions) in patients with a history of adenomas.
3. Mixed or unclear results on risk of other cancers, but possible association with reduced risk of blood cancer. Remember, correlation does NOT equal causality.
Bottom line: garlic makes food tasty! Enjoy it in your favorite recipes, but don’t rely on it to keep you safe from cancer or to treat your cancer.
As far as ginger, I found a great article that already covers it:
“Walk Gingerly Before Declaring Ginger a Cancer Cure It is not at all unusual to find plant extracts that will kill cancer cells in vitro. There are hundreds of phytochemicals that will do this. Neither is it unusual to find an effect in mice that have implanted tumours. But this is a long way away from demonstrating a viable cancer treatment in humans.”
Bottom line: this pretty much sums up the majority of studies on plant extracts and cancer. Enjoy ginger for the flavor, but don’t count on it to cure your cancer.
With the recent emergency use approval of two independent vaccines for SARS2-CoV-2, the virus responsible for the horror that is Covid-19, many folks have questions: What the heck are these vaccines? Are they safe and effective? Should I get one?
Note: I’m not going to dignify any wild conspiracy theories about vaccines and microchips. Bill Gates doesn’t care about you or me or anyone else he doesn’t know and he has better things to do that track you with a microchip in a vaccine. Seriously. People believe some weird shit… If anyone wanted to track you, they’d do it digitally by your freakin’ cell phone.
That being said, the first three questions are completely legit. My goal in this post is to break down the science behind the Pfizer and Moderna vaccines, what we know so far about their safety and effectiveness, and dispel some common misconceptions about them.
First, here’s a crash course on how your immune system fights infections. This is important, since vaccines harness the power of your immune system to mount a rapid and robust defense if and when you encounter the actual pathogen (i.e. virus or bacteria that cause disease) in your daily life. The arm of the immune system that does this is called the adaptive immune system. The other arm is the innate immune system and includes natural barriers like skin, the tiny hairs and mucous in your nose, and stomach acid.
How does the adaptive immune system work? First, it involves cells that roam around your body looking for something suspicious. Cells like macrophages and dendritic cells, which patrol various organs and tissues, find pathogens like bacteria or unhealthy cells infected by viruses like SARS-CoV-2, and eat them (fancy word is phagocytosis). Infected or damaged cells send out protein signals called cytokines as a distress call to attract macrophages and dendritic cells. While “digesting” the bacteria/infected cell, they salvage proteins or pieces of proteins—antigens—that identify the bacteria or virus as “other,” and they present these to immune cells, usually in lymph nodes, that mount an immune response. Macrophages and dendritic cells are known as professional antigen presenting cells (APCs)
When activated by APCs, immune cells called B-cells produce antibodies against the antigen, which can do a lot of things to fight an infection. Some antibodies neutralize the pathogen by binding it and stopping it from entering a cell. Other tag infected cells for other immune cells to come and kill them. Others coat pathogens or infected cells in a process called opsonization (meaning to “make tasty”), which signals other cells like macrophages to come and eat the coated pathogens/cells. Specialized B-cells called memory B-cells archive the information about the antigen so your immune system can recognize the pathogen when it hits you again and mount a faster immune response.
Other immune cells called T-cells become activated by APCs and mount a different kind of immune response. Cytotoxic T-cells seek out and kill infected or damaged cells, and helper T-cells help activate B-cells so they make antibodies, activate cytotoxic T-cells, and activate macrophages to go eat nasty invaders and infected cells. Memory T-cells also archive information about past infections to mount a rapid, strong response the next time your body sees it.
That’s a simplified by hopefully digestible explanation of immunity and the major players (there are other immune cells, but APCs, B-cells, and T-cells are the biggies). Memory is key to protection, and memory is built by exposure to pathogens.
But what if there was a way to expose your body to pathogens without making you sick? That’s where vaccines come in!
The way vaccines work is to tap into this process and activate the adaptive immune response using an artificial antigen supplied by the vaccine, getting your immune response geared up and, importantly, building those archival memory B- and T-cells that will recognize the real infection when your body encounters it so it can rapidly fight it. Types of vaccines include: Live-attenuated vaccines; Inactivated vaccines; Subunit, recombinant, polysaccharide, and conjugate vaccines; Toxoid vaccines.
Live-attenuated means using a weakened form of the virus to initiate an immune response—examples include measles, mumps, and rubella (MMR) and chickenpox vaccines. Inactivated means using a dead version of the virus that cannot infect cells but contains antigens that can be used to activate adaptive immunity—examples include flu, hepatitis A, and rabies vaccines. Subunit, recombinant, polysaccharide, and conjugate vaccines use pieces of the virus that act as antigens, like proteins and sugars—examples include HPV, hepatitis B, and shingles vaccines. Toxoid vaccines use toxins produced by the pathogen to mount an immune response against the toxic protein—examples include tetanus and diphtheria vaccines.
What the heck are these (Covid-19) vaccines?
The current FDA approved (for emergency use) Covid vaccines from Pfizer and Moderna belong to a newer class called mRNA vaccines. See my previous post on DNA to mRNA to protein (Central Dogma of Molecular Biology) for a refresher on mRNA. This is really just a modification of the subunit, recombinant, polysaccharide conjugate vaccine approach in that it delivers messenger RNA coding for the SARS-CoV-2 spike protein, which the virus uses to enter a cell, instead of delivering the spike protein itself. See my previous post on SARS-CoV-2 for information about the spike protein. The cells in your body that take up the mRNA make spike proteins themselves, which in turn activates your immune system and provides protection.
Are they safe and effective?
Since these are new vaccines approved for emergency use, and since due to the accelerated nature of their development and approval, some people are understandably wary of their safety and ability to protect against Covid.
While they may be new, a lot of the groundwork for these vaccines started in in 2002 with the emergence of the first SARS virus (SARS-CoV) and continued with study of the related MERS-CoV virus. SARS-CoV uses the same spike protein to enter target cells through angiotensin-converting enzyme 2 (ACE2). Scientists learned a great deal about coronaviruses by studying SARS-CoV and MERS-CoV, including how to develop vaccines.
Let’s look at safety first. Clinical trials involving tens of thousands of healthy volunteers have been performed. Safety concerns include allergic reactions to the vaccine or components of the vaccine. Providers who deliver the vaccine are equipped to deal with anaphylaxis on site, which is why you’ll be asked to hang around for 15 minutes after your shot just in case. You might feel feverish, fatigued, and generally yucky the day after one or both shots (the first activates the immune system and the second gives it a signal boost), which is NOT a sign that you have Covid. It actually means your immune system is working, building memory and its arsenal of weapons to fight Covid if you encounter the real virus.
The FDA is continuing to monitor those who received the vaccines in clinical trials, as well as those who received the vaccines after emergency approval. So far, they appear to be safe.
As far as effectiveness, data from trials looking at the number of Covid-19 cases in trial participants relative to the total number of participants revealed that the Pfizer vaccine is 52% effective after the first shot (39 cases of covid-19 in the vaccine group and 82 cases in the placebo group) and 95% effective after the second shot (8 covid-19 cases in the vaccine group and 162 cases in the placebo group; 43,448 trial participants) – New England Journal of Medicine (NEJM). Similar efficacy was reported for the Moderna Vaccine in NEJM.
There’s still a lot we don’t know – most importantly, we don’t know how long immunity produced by these vaccines will last. Some experts hypothesize they might provide a year or two of immunity, after which you’ll need more shots, but we won’t know until we see in real time as we track vaccinated people.
Should you get the vaccine?
The more people who are vaccinated against this virus, the better. Vaccines will slow the spread of the virus by preventing infections in vaccinated people. Along with mask wearing and social distancing, the vaccines are a vital tool in stopping this pandemic. As a cancer survivor, I’m in a high risk category, meaning Covid-19 could kill or debilitate me. The same is true for people with diabetes and other underlying medical conditions.
That’s why I got my vaccine! Had the second shot a few days ago, which gives me peace of mind as I prepare to return to work after reconstruction surgery. I’m with Dr. Fauci on this one, and I encourage everyone to talk to their healthcare providers about getting vaccinated.
First off, HUGE news! My amazing literary agent, Barbara Collins Rosenberg, landed a publishing deal for me with Rowman & Littlefield!!! I’m honored, thrilled, and still squee-ing! So, stay tuned for Talking to My Tatas: A Breast Cancer Researcher’s Adventure With The Disease And What You Can Learn From It.
Here’s the Working Blurb – it will likely change based on guidance from my amazing editor, Suzanne Staszak-Silva, but it will give you a taste of what I intend to share (my story) and spread (scientifically sound information) with this book:
Can I talk to you about my personal relationship with my breasts?
I’ve spent twenty years working as a biomedical breast cancer researcher. Then, I was diagnosed with breast cancer. I thought I knew breast cancer before it whacked me upside my left boob and left me bleeding on the curb of uncertainty. Turns out, I had a lot to learn. The purpose of this book is to share my personal adventure with breast cancer, from the laboratory bench to my own bedside, and to provide accessible information about breast cancer biology for non-scientists. I say adventure, because I’d rather think of it as an action movie with some really cool side quests instead of another tragedy-to-triumph saga. I’m not big on sagas. I am big on kickass intellectual badassery, pathological nerdiness, and talking about my sweet, sweet rack.
Why do we need another cancer memoir? In a sea of inspirational stories, celebrity survivor stories, and physician memoirs that bring a clinical perspective, nothing I’ve found in the current market tackles breast cancer through the lens of a breast cancer researcher who became a survivor. We live in an age of fake news and pseudoscience, made worse by the pervasive anti-intellectual and anti-science political culture gripping the United States and much of the world. The Internet and social media are plagued by scammers selling “alternative medicine” and woo woo “cures” for cancer. Through Talking to My Tatas: A Breast Cancer Researcher’s Adventure With Breast Cancer And What You Can Learn From It, I offer accurate, evidence-based science that is accessible to laypersons, including the more than three hundred thousand individuals diagnosed with breast cancer every year*, their caregivers, and their loved ones.
Knowledge is power, and lack of it can lead to overtreatment, unnecessary pain and suffering, and can even be deadly. By demystifying the process from mammograms, biopsies, pathology and diagnostics, surgical options, tumor genomic testing, and new treatment options, I aim to offer hope in a story intended to blend the humor and delivery style of Jenny Lawson’sLet’s Pretend This Never Happened (A Mostly True Memoir) with the integrity and scientifically sound beauty of Siddhartha Mukherjee’s The Emperor of All Maladies: A Biography of Cancer.
*American Cancer Society Facts & Figures 2020
I’ve got some work to do! In addition to writing and fleshing out chapters for my editor to review (and work her magic on), I’ve been busy working on figures and visuals for the book, cover art forms, marketing and promo plans, and getting a new headshot! The one I currently have on this page and all over the Internet is absolutely gorgeous, fun, and from 2012. A LOT has happened in 8 years, and I have aged. I’d like to think I’ve aged gracefully, but at any rate, it was time to update the image.
Lillian Boeskool is MAGIC! She made me look so good and captured the essence of my personality in a series of amazing headshots (If you’re in the greater Nashville area and need headshots or other photography, HIRE HER). I have two favorite images and I cannot decide which one to use for this page and the book. I invite y’all to enable my decision-making disorder vote for your favorite!
This one on the left is super fun and catches me trying not to laugh at something funny Lillian said and/or did. It captures my mischief, my sense of humor, and really makes my face look nice.
And, unlike the previous headshot for which I straightened my hair, this one highlights my popping natural curls!
I’m almost 48 years old. Anything that makes my face look nice is gold.
Told you she was MAGIC!
There’s just something about this next one on the right that speaks to me.
I think it captures my sass and tells my readers that I’m going to take them on a really funny adventure that will make them a smidge uncomfortable but will ultimately leave them laughing and glad they went along for the ride.
That’s me in a nutshell.
I can’t decide between the two!
And…just to throw a monkey wrench into this whole program…
This one is my husband’s favorite.
It’s nice, too.
I’m glad he thinks I look good in all of these photographs and still thinks I’m beautiful in spite of time marching across my face and body and in spite of cancer leaving me with a janky left breast-in-progress*.
He’s pretty awesome!
I think I’ll keep him.
*Janky left breast-in-progress on display in the first two photos as the line of discoloration just above my shirt collar. Lillian asked if I wanted to Photoshop it out, but I said no. It’s where I am right now. It’s why I’m blogging, writing this book, and becoming a breast cancer patient/survivor advocate as well as a breast cancer researcher. It’s a badge of fucking honor and it stays!
I recently had the great pleasure of chatting with a dear friend and fellow breast cancer survivor, Ronei Harden-Moroney. She invited me on her livestream to talk about breast cancer—science, personal experiences, and sharing what it’s like to be in this exclusive club that neither of us signed up for but brought us closer all the same.
As you can see, Ronei is an amazing lady and one tough cookie. I hope hearing her story inspires you and gives you hope. You can find her on Facebook, Twitter, Instagram, LinkedIn, and Goodreads. If you’re looking for an editor or writing coach, seriously check her out!
Originally Published in VICC Momentum September 23, 2020 | Dana Brantley-Sieders, PhD
Note: This is an essay I wrote last summer. Though my journey continues thanks to residual disease and a mastectomy after I submitted the essay, the spirit and information in the essay hold true. I have hope. And I’m still working hard to fight cancer inside the laboratory and out in the wider world.
I had been studying breast cancer for more than 20 years when I was diagnosed with invasive ductal carcinoma. My professional life was filled with hours of watching tumor cells grow and spread on plastic dishes, marveling as they branched and blebbed in three-dimensional matrices, monitoring the size of lumps from spontaneous or transplanted breast tumor tissue in experimental mouse models, and if I was lucky, watching their growth slow or even seeing them shrink when a new experimental therapeutic worked in pre-clinical testing.
Over the years, family and friends had come to me for information, reassurance and comfort in the face of their diagnoses. I’d lost a close cousin to the ravages of aggressive breast cancer. She was only 37 years old.
When my mother was diagnosed with breast cancer, I emptied her surgical drains after her double mastectomy, caring for her with a toddler clinging to my leg and a baby balanced on my hip. I brought meals to a close friend who was diagnosed with stage 3 breast cancer, visiting with her as she endured chemotherapy, surgery, reconstruction, and finding her new normal while our pre-teen daughters hovered in the background, their infectious laughter a balm to the devastation wrought by the big “C.”
After all of this, I thought I knew breast cancer. Then it kicked me in my left breast and flung me, bleeding, on the curb of uncertainty. Turns out, I had a lot to learn.
When Brent Rexer, MD, my medical oncologist, walked in to my first appointment at the Vanderbilt Breast Center, he greeted me with kindness and a wry smile. “It’s good to see you again, though I wish it was under better circumstances.” I’d known Brent for years. He and his wife were classmates of mine in graduate school, and we’d crossed paths at research seminars in the Vanderbilt-Ingram Cancer Center. I’d crossed paths with many of the clinicians and providers who would become a part of my care team. I was lucky. I knew I was in great hands.
When I got cancer, I came home.
What did I learn from the laboratory bench to my own bedside? For starters, I learned that nothing, not even a career spent tackling this disease, can prepare you for your own diagnosis. I was as shocked, devastated, and numb as any woman who hears those three terrible words — you have cancer.
I learned that radiologists save lives. The radiologist who spotted the suspicious spot on a routine mammogram and later during an ultrasound examination has over 30 years of experience in the field. Because I’m a geek, I always ask to see what’s going on in any exam. I’m “that patient,” the one who’ll ask if I can look at the computer screen after a boob squeeze, à la mammography, and in the middle of having the goo-covered wand gliding over my exposed boob during an ultrasound. When I had the chance to look at my tumor and a previously detected benign lesion side by side, I realized that this radiologist’s years of training and sharp eyes (that could tell the difference between two grainy spots on an ultrasound that looked the same to me) caught one tumor before it could become immediately life threatening. We later learned that I had two tumors of the same subtype in the same breast, which is pretty rare. But we would not have caught the smaller one, which was actually growing faster, had my radiologist not spotted the larger mass.
I learned that I had the option of saving most of my breast tissue. Thanks to years of study following outcomes of patients who chose lumpectomy and those who chose mastectomy as surgical options, we know that choosing breast conserving surgery does not increase a woman’s risk for distant recurrence. There is an increased risk for local recurrence, but that can be mitigated with radiation therapy. I was fortunate enough to be a good candidate for partial mastectomy followed by oncoplastic reconstruction, which is essentially a breast reduction and lift. I’m not going to lie – it’s like being 18 again. I’m perky! Better still, it preserved sensation in my breast skin and nipples, and the recovery time was much shorter than with a mastectomy. Note: there are no wrong choices, only informed choices. The decision to keep or remove one or both breasts after a cancer diagnosis is a deeply personal one. Each individual patient must consider the options, the benefits and risks, and decide what is right for her. This was the best decision for me, and I’m glad I was a good candidate for this surgical option.
I learned that surgeons are brilliant, and by working together, they can give you back much of what you lost. My surgical team, including Ingrid Mezoely, MD, and Galen Perdikis, MD, worked together on a plan that allowed Dr. Mezoely to remove my tumors and Dr. Perdikis to perform oncoplastic reconstruction just after. A year and a half later, I am pleased with the result, like the way I look and feel, and while I’ll never be the same as B.C. (before cancer), my new normal is better than I ever imagined.
I learned that radiation therapists are some of the nicest, funniest people on the planet. My go-to coping mechanism is humor. When I came in for a dry run prior to my first radiation therapy, the technician placed several markers on my left breast in order to properly align the beam for more precise targeting of the area where the tumors were removed while minimizing potential damage to my heart and lungs. The shiny markers formed a cute little circular pattern, so I joked that we could make it into a pastie. All I need would be some glitter and a tassel. We both cracked up, and I was able to relax, hold my breath for the designated time, and get prepared for my treatment course. During those visits, I talked with the therapists and Bapsi Chakravarthy, MD, about topics big and small — kids, work, life, research, politics, favorite books and television shows, and all manner of topics that made the discomfort during the last weeks of treatment much more bearable.
I learned the depths of compassion and generosity of my colleagues, both in the laboratory setting and in the clinic. Disclosing a cancer diagnosis to your employer and co-workers can be frightening. Will you be at risk for losing your job (a reality for too many Americans)? Will your colleagues see you and treat you differently? Will moving forward be awkward, with colleagues feeling uncomfortable and at a loss for words? I was lucky and found support and comfort, with offers to help keep the research in my laboratory going while I was out on medical leave, with encouragement, and with the honor of serving as a reminder of what all of us in cancer research work for — helping patients diagnosed with cancer survive and thrive.
I learned that, having been on both the research side and patient side of the breast cancer experience, I have a unique perspective and the opportunity to help people outside of the laboratory. Scientists are very good at communicating with one another within the research community, but I believe we need to expand our efforts to communicate with the public. After all, most of us are funded by the National Institutes of Health, which is in turn supported by tax dollars. I feel an obligation to be able to explain my work and why it’s important to anyone who asks, be it my 11-year-old son or a person sitting next to me at the airport. I have a new mission: to be an advocate for science and bring science to the public, particularly when it comes to breast cancer. Sadly, we live in an age of fake news and pseudoscience, made worse by the pervasive anti-intellectual and anti-science political culture gripping the United States and much of the world. The internet and social media are plagued by scammers selling “alternative medicine” and woo woo “cures” for cancer. Knowledge is power, and lack thereof can be deadly. I can lend my voice to fighting myths and scams for the public good through speaking, blogging and writing.
I learned that there will be good days and bad days, and that it’s OK to seek help. My prognosis is great, but my type of breast cancer can recur years or decades after surgery and treatments are complete. That thought often keeps me up and night and serves as a source of worry. Shortly after my diagnosis, I worked to the point of exhaustion in the lab, at home, and on my side gig, staying up late in the name of productivity and maximizing creativity, but I wasn’t fooling anyone. I was terrified. After a year and a half of ups and downs, I acknowledged that I was not fine, and that I needed help in the form of therapy. I’m glad I did. Tackling my fears and anxieties head on has helped me be my best self, accept my new normal as a cancer survivor and focus on living the life I have with joy and purpose. And when I go back into the well of despair, as many survivors do, I now have the tools to climb back out and get back on track, which is very empowering.
Finally, I learned that I’m still learning. I have the best job as a researcher in that I get to be a lifelong learner. So many strides have been made since I entered the field, when Herceptin was first developed for HER2-positive breast cancer. Now, we have so many new tools in diagnostics and prognostics (3D mammography and OncoType DX testing), treatments (aromatase inhibitors, CDK inhibitors, and immune therapy), and amazing new treatments on the horizon. We still have so much work to do, but we are making a difference, and I am privileged to be a part of that process.
Want to help? Donate to my fundraiser and I’ll feature your survival story (or a loved one’s story) on my blog. You can make the donation in honor of someone you love who’s battled breast cancer. My fundraiser is dedicated to my mom, a 10 year survivor, and my cousin, who I lost at the age of 37 to HER2+ breast cancer.
Want something more tangible? Well, my side hustle is writing fiction, including paranormal romance and urban fantasy, which you can read all about at D.B. Sieders. I’m donating all of my royalties from October and November to Making Strides. So you can buy some books, enjoy them, and know that your money is supporting a great cause.
This is an oldie that keeps cropping up in the sphere of (completely unvetted) wellness tips – apple cider vinegar. I’m a bit puzzled by the claims that this is a “natural remedy.” Apples are natural. Cider is processed, as is vinegar, through a fermentation process involving bacteria and yeast that occurs on an industrial scale. It’s not magic. It’s chemistry.
Anyway, a Google search revealed top hits chock a block FULL of Woo Woo claims that are fantastical in nature and, you guessed it, not scientifically vetted. The “apple cider vinegar process” is only at the top because I searched for it first, I suspect. But the rest – “apple cider vinegar gummies” (gross!), “apple cider vinegar benefits” (makes foods taste yummo, but that’s it), “apple cider vinegar pills” (WTF?), “apple cider vinegar weight loss” (maybe if all you eat are salads with apple cider vinaigrette dressing – but that’s a sad way to live), and “apple cider vinegar diet” (that doesn’t even make sense) – it’s all a bunch of doo doo!
But, since I’m a debunker of woo woo scams, I’m doing the research. A PubMed (database of peer-reviewed published biomedical research) search using “apple cider vinegar” yielded 94 results. Aside from a few articles on the antimicrobial and anti-fungal properties of ACV (not surprising, considering that ACV contains 5-6% acetic acid) and studies in rodent models (cardiovascular health, obesity, and something about boosting immunity in carp and – those were weird) that may or may not translate to humans, most of the articles covered the dangers of using ACV as a “natural remedy.”
For example, tooth erosion and esophageal injury was documented in at least two studies [Case Reports Ned Tijdschr Tandheelkd. 2012 Dec;119(12):589-91. doi: 10.5177/ntvt.2012.12.12192 “Unhealthy weight loss. Erosion by apple cider vinegar”; J Am Diet Assoc. 2005 Jul;105(7):1141-4. doi: 10.1016/j.jada.2005.04.003. “Esophageal injury by apple cider vinegar tablets and subsequent evaluation of products.”]. Seriously, do NOT use this to treat heartburn or GERD. It’s a fucking ACID and adding ACID to a condition caused by escape of stomach ACID is completely ridiculous. Don’t drink it. Cook with it, but don’t drink it.
Not only does ACV have no benefit for atopic dermatitis [(skin irritation) Pediatr Dermatol 2019 Sep;36(5):634-639. doi: 10.1111/pde.13888. Epub 2019 Jul 22. Apple cider vinegar soaks [0.5%] as a treatment for atopic dermatitis do not improve skin barrier integrity], topical skin treatments with ACV can cause chemical burns [J Am Acad Dermatol. 2012 Oct;67(4):e143-4. doi: 10.1016/j.jaad.2011.11.934. “Chemical burn from topical apple cider vinegar.”]! Don’t put it on your skin. Please.
One study reported a lack of antiglycemic (lowering of blood sugar) by vinegar, including ACV, in humans [Nutr Res. 2009 Dec;29(12):846-9. doi: 10.1016/j.nutres.2009.10.021. “Vinegar lacks antiglycemic action on enteral carbohydrate absorption in human subjects.”]. So no, it won’t help people with diabetes.
Fun rando fact – apparently ACV attracts several species of fruit flies, so if you want to collect some wild ones as pest control or for DIY experiments at home, try it! I’m not citing these. Look it up yourself. There are a surprising number of studies documenting this.
Bottom line – there are no validated health benefits in humans for this “natural remedy,” but there are plenty of bad things that can happen if you drink a lot of cider vinegar, put it on your skin, or take pills (and presumably gummies).
And ACV does NOT cure or treat cancer. Only two references came up in a PubMed search for “apple cider vinegar cancer,” and neither reported any benefits for treatment of warts or moles, let alone skin cancer.
BUT…ACV can make tasty salad dressings and delicious sauces. One of my favorites for fall is apple glazed baked chicken. Here’s the recipe:
1 whole broiler chicken, apple jelly, apple cider vinegar, apple pie spice, apples (tart or sweet)
Preheat oven to 325 degrees. Season the chicken with olive oil, salt, and pepper. Bake chicken for 1 1/2-2 hours. While chicken is baking, slice apples and prepare glaze. To prepare glaze, heat 1/2 jar of apple jelly with an equal volume of apple cider vinegar and 1-2 teaspoons of apple pie spice. Boil until volume is reduced by 1/2. Remove chicken from oven, drain chicken stock (can be used to prepare some DELICIOUS rice), cover with glaze, and place apple slices around chicken in the baking dish. Cook another 1/2 hour or until chicken is done. Serve with rice or potatoes, green beans, and enjoy!
It occurred to me that while I’ve told you that I’m a cancer researcher, you might not know what that actually means. There are many kinds of researchers who conduct many diverse types of cancer research, as detailed here. All are important and complimentary, and they often overlap. I am an academic (work at a University) laboratory researcher in the broad field of Cell Biology, with a focus on Cancer Biology and Cancer Treatment research, specifically working as a “wet lab” researcher. This means I conduct and supervise hands-on experimental research with cells in a dish, mouse models, and tissue/cell extracts (where we grind up or pulverize tissues and cells, separate them into their components like DNA, RNA, or protein, and analyze them using molecular biology or biochemistry). Other researchers use computational models and datasets to conduct their “dry lab” research.
Both types of research are important, and one informs and shapes the other. For example, I’ll use information found in large databases generated by dry labs that containing data from actual human cancers (e.g. cBioPortal for Cancer Genomics, Kaplan-Meier plotter, and The Human Cancer Metastasis Database) to find clues about how the gene product molecules I study might be driving cancer cell growth, survival, and invasion. The data I generate then feeds back into these databases, linking known functions in laboratory models along with data about where these gene product molecules are expressed and at what level in human cancers. In fact, all of the cancer research fields listed in the link feed into and fuel each other. Science these days is multi-disciplinary, meaning scientists from diverse fields bring their expertises to the table in order to do better, more advanced, more impactful science. Case in point – I’m working with Dr. Craig Duvall, Biomedical Engineer right now, applying his cutting-edge nanoparticle and carrier technologies to targeting the expression of cancer-driving genes in the cell culture and mouse models in my laboratory.
So, what is it exactly that I do…do?
These days, I split my time between the bench (doing actual experiments, which is why I became a scientist in the first place) and the office (doing endless paperwork as quickly and as efficiently as possible so I can get back to the bench). I also supervise a phenomenal medical student and co-mentor insanely smart graduate students, support and collaborate with a team of amazing junior and senior faculty, write grant proposals (more on that below), write up scientific findings into manuscripts for peer review and publication, prepare and deliver scientific talks, maintain compliance (biosafety, environmental safety, radiation safety, responsible care and use of laboratory animals, etc.), make sure the laboratory staff have what they need to perform their research, make sure equipment gets serviced and is operational, attend faculty meetings, scientific seminars, professional development meetings, student thesis committee meetings.
Lots of meetings…
As far as what I research, I use cell culture and mouse models of breast cancer, including metastatic breast cancer, to test new experimental therapeutics.
The goal is to discover more specific, effective, less toxic (looking at you, chemo) treatments for breast cancer. I’ll blog more about specific projects later, but what this normally involves is seeing if the new drug makes cancer cells in a petri dish stop growing and/or die, stops cancer cells in a dish from moving and invading, and if a new drug stops tumors in mice from growing or kills them, and, better yet, if the new drugs can actually shrink the tumors. For more information, see the copy of my NIH Biosketch, the mini-resume that we add to every grant application to prove our published expertise, pasted below.
How did I become a cancer researchers? Lots of school and training! I earned a B.A. in Biology from Maryville College in 1995. After graduating, I completed graduate studies at Vanderbilt University, earning a Ph.D. in Cell Biology in 2000. After graduate studies, I completed postdoctoral training in the laboratory of Jin Chen at Vanderbilt University Medical Center from 2000-2003, supported by an American Heart Association Postdoctoral Fellowship Award (I was studying tumor blood vessels, so it was legit!) and a Department of Defense Breast Cancer Research Program Postdoctoral Fellowship award, before being promoted to Research Instructor. I was promoted to Research Assistant Professor in 2006, and during that time I earned a K01 career transition award from the National Institutes of Health/National Cancer Institute. (NIH/NCI – the major funding agency for biomedical cancer research in the united states). This led to my first NIH/NCI independent investigator R01 award in 2011. I was promoted to Assistant Professor of Medicine, Tenure Track, in 2015, and am still at Vanderbilt University Medical Center. I am currently supported by 2 NIH/NCI R01 grants as well as funds from my institution that allow me to generate preliminary data necessary to apply for more grants.
Have you spotted a theme? The theme is “grants” or “awards.” One of the most important jobs I have for my research laboratory is to successfully apply for grants – meaning I write up a proposal about the cool science I want to do, explaining how and why it will benefit patients with breast cancer and move the field forward, and I submit it to the funding agency and compete with a bunch of other super smart, top notch scientists for limited research dollars. These days, money is tough to come by. When I first entered the field as an independent scientist, the top 15% of NCI applications were funded (compared with a funding rate of 25% earlier). These days, it’s at 10%. My colleagues and I literally just missed out on getting a really innovative research proposal funded by 1%! I’m worried how Covid-19 will affect funding over the next 5-10 years, too, as are most of my colleagues. Why is that important? Well, if we want the U.S. to remain on the cutting edge of research and innovation, and if we want to keep discovering new and better ways to detect and treat cancer, we need to invest in science, especially academic science. If you are a cancer survivor, know a survivor, or just want to make the world a better place with less cancer, write your representatives Congress to let them know you want support and full funding of the National Institutes of Health and the National Cancer Institute.
OMB No. 0925-0001 and 0925-0002 (Rev. 10/15 Approved Through 10/31/2018)
NAME: Dana M. Brantley-Sieders
eRA COMMONS USER NAME (credential, e.g., agency login): BRANTLDM
POSITION TITLE: Assistant Professor, Medicine/Rheumatology, Vanderbilt University School of Medicine
EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, include postdoctoral training and residency training if applicable. Add/delete rows as necessary.)
INSTITUTION AND LOCATION
DEGREE (if applicable)
Completion Date MM/YYYY
FIELD OF STUDY
Maryville College, Maryville, Tennessee
Vanderbilt University School of Medicine
Vanderbilt University Medical Center
A. Personal Statement
I have the expertise, leadership, training, and motivation to successfully carry out the proposed investigation of how EphA2 receptor tyrosine kinase contributes to breast cancer bone metastasis, particularly in terms of tumor-osteoclast interactions that mediate osteolysis in clinically relevant in vivo models that mimic human breast-to-bone metastasis. I have a broad background in cancer research, with specific training and expertise in mouse models of breast cancer and host-tumor interactions (genetically engineered mouse models and orthotopic allograft/xenograft models, including PDX), as well as three-dimensional cell culture and co-culture models, and data mining human tissue microarray and patient datasets to validate clinical relevance of findings in my laboratory model systems. I also have experience testing novel experimental therapeutics in clinically relevant models of breast cancer, including metastatic disease. My research includes analysis of breast cancer cell growth (multiple molecular subtypes), survival, invasion, and host-tumor interactions. Dr. Sterling, Dr. Pellecchia, and I have established a fruitful collaboration that will continue as a part of this exciting investigation
Werfel, T.A., Wang, S., Jackson, M.A., Kavanaugh, T.E., Joly, M.M., Lee, L.H., Hicks, D.J., Sanchez, V., Ericsson, P.G., Kilchrist, K.V., Dimobi, S.C., Sarett, S.M., Brantley-Sieders,D.M., Cook, R.S., and Duvall, CL. (2018) Selective mTORC2 Inhibitor Therapeutically Blocks Breast Cancer Cell Growth and Survival. Cancer Res 78:1845-1858. PMID: 29358172. PMCID: PMC5882532.
Sarett, S.M., Werfel, T.A., Lee, L., Jackson, M.A., Kilchrist, K.V., Brantley-Sieders, D., and Duvall, C.L. (2017) Lipophilic siRNA targets albumin in situ and promotes bioavailability, tumor penetration, and carrier-free gene silencing. PNAS 114: E6490-E6497. doi: 10.1073/pnas.1621240114. Epub 2017 Jul 24. PMID: 28739942. PMCID: PMC5558996.
Song, W., Hwang, Y., Youngblood, V.M., Cook, R.S., Balko, J.M., Chen, J., and Brantley-Sieders, D.M. (2017) Targeting EphA2 impairs cell cycle progression and growth of basal-like/triple-negative breast cancers. Oncogene 36: 5620-30. PMID: 28581527. PMCID: PMC5629103.
Shiuan, E., Inala, A., Wang, S., Song, W., Youngblood, V., Chen, J., and Brantley-Sieders, D.M. (2020). Host deficiency in ephrin-A1 inhibits breast cancer metastasis. [version 2; peer review: 3 approved]. F1000Research 2020, 9:217 (https://doi.org/10.12688/f1000research.22689.2). PMID: 32399207. PMCID: PMC7194498.
B. Positions and Honors
Positions and Employment
Postdoctoral Fellowship, Vanderbilt University School of Medicine
Research Instructor, Vanderbilt University School of Medicine
2006-2015 Research Assistant Professor of Medicine, Vanderbilt University School of Medicine
2015-present Assistant Professor of Medicine, Vanderbilt University School of Medicine
Other Experience and Professional Memberships
1998 Molecular Biology and Pathology of Neoplasia, Edward A. Smuckler Memorial Workshop,Keystone, Colorado
1998-present Member, American Association for Cancer Research
2002 Harvard Medical School Department of Continuing Medical Education and Massachusetts General Hospital Department of Radiation Oncology Seventeenth Annual Offering of Critical Issues in Tumor Microcirculation, Angiogenesis, and Metastasis; Biological Significance and Clinical Relevance Workshop, Cambridge, Massachusetts
2005 National Cancer Institute (NCI)-sponsored Organotypic Models Training Program; received training in orthotopic tumor cell transplantation in mice within several organs, including mammary gland fat pad, bone, lung, spleen, pancreas, bladder, and cecum in the laboratory of Dr. Isaiah J. Fidler, MD Anderson Cancer Center, Houston, Texas
2007-present Ad hoc reviewer for Nature, Cancer Research, PLoS One, Oncogene, Clinical Cancer Research, Neoplasia, European Journal of Cell Biology
2009-2016 Peer reviewer Department of Defense Breast Cancer Research Program
2012 Peer reviewer NCI TME study section
1997-1998 Department of Defense Breast Cancer Pre-doctoral Fellowship
1998-1999 Dissertation Enhancement Award, Vanderbilt University Graduate School
1998-1999 Coordinator for Developmental Biology Student Organization, Vanderbilt University
2000-2001 Public Health Service Vascular Biology Postdoctoral Fellowship
2001-2003 American Heart Association Postdoctoral Fellowship
2001-2002 American Heart Association Basic Cardiovascular Science Council
2003 NIH NRSA Postdoctoral Fellowship 1 F32 CA101419-01 (award offered, declined due to overlap with 2003 DOD award)
2003-2006 Department of Defense Breast Cancer Research Program Postdoctoral Fellowship DAMD17-03-1-0379
2006-2011 NCI Mentored Career Development Award K01CA117915
C. Contributions to Science
My early publications from graduate studies directly addressed how signaling pathways that regulate normal mammary epithelial morphogenesis (e.g. NF-kappaB transcription factors) can contribute to hyperplasia, a hallmark of neoplastic transformation. These publications provided the first evidence that NF-kappaB transcription factors are expressed and active in normal mammary epithelium during post-pubertal development, and that IkappaBalpha deletion in mammary epithelium, which promotes constitutive activation of NF-kappaB transcriptional activity, promotes pervasive intraductal hyperplasia in vivo. These studies laid the foundation for investigating the role of these transcription factors in breast cancer, and also provided training for me in animal models and mammary fat pad clearing and transplantation techniques that have formed a cornerstone of my independent research program and contributed to numerous collaborations, including those with Dr. Chen. I served as primary author for each of these studies and independently designed experiments, interpreted data, and prepared the manuscripts for publication. Funding from my Department of Defense Breast Cancer Pre-doctoral Fellowship award supported this work. I also contributed directly to collaborations that led to publication of work related to the role of NF-kappaB transcription factors to development and disease as a part of my graduate studies.
Brantley, D.M., Yull, F.E., Muraoka, R.S., Hicks, D.J., Cook, C.M., and Kerr, L.D. (2000) Dynamic expression and activity of NF-kappaB during post-natal mammary gland morphogenesis. Mech Dev 97:149-55. PMID: 11025216.
Brantley, D.M., Chen, C.-L., Muraoka, R.S., Bushdid, P. B., Bradberry, J. L., Kittrell, F., Medina, D., Matrisian, L. M., Kerr, L.D., and Yull, F. E. (2001) Nuclear factor-kappaB (NF-kappaB) regulates proliferation and branching in mouse mammary epithelium. Mol Biol Cell 12: 1445-55. PMID: 11359934. PMCID: PMC34596.
Bushdid PB, Brantley DM, Yull FE, Blaeuer GL, Hoffman LH, Niswander L, Kerr LD. (1998) Inhibition of NF-kappaB activity results in disruption of the apical ectodermal ridge and aberrant limb morphogenesis. Nature 392: 615-8. PMID: 9560159.
I continued to pursue the connection between signaling pathways that regulate development and contribute to tumorigenesis and progression during my post-doctoral training, providing the first evidence that EphA2 receptor tyrosine kinase regulates angiogenesis and tumor neovascularization. These publications showed that EphA2 regulates endothelial cell assembly and motility through a PI3K/Rac1-GTPase-dependent mechanism and regulates tumor angiogenesis in cooperation with the VEGF signaling pathway in vivo, providing novel insight on the molecular regulation of tumor angiogenesis and host-tumor interactions. I served as primary author for each of these studies and independently designed experiments, interpreted data, and prepared manuscripts for publication. Funding from my American Heart Association and Department of Defense Breast Cancer Postdoctoral Fellowship awards supported this work.
Brantley, D. M., Cheng, N., Thompson, E. J., Lin, Q., Brekken, R. A., Thorpe, P. E., Muraoka, R. S., Pozzi, A., Jackson, D., Lin, C., and Chen, J. (2002). Soluble Eph A receptors inhibit tumor angiogenesis and progression in vivo. Oncogene 21: 7011-26. PMID: 12370823.
Brantley-Sieders, D. M., Caughron, J., Hicks, D., Pozzi, A., Ruiz, J. C., and Chen, J. (2004). EphA2 receptor tyrosine kinase regulates endothelial cell migration and vascular assembly through phosphoinositide 3-kinase-mediated Rac1 GTPase activation. J Cell Sci 117: 2037-49. PMID: 15054110.
Brantley-Sieders, D.M., Fang, W.B., Hicks, D.J., Zhuang, G., Shyr, Y., and Chen, J. (2005) Impaired tumor microenvironment in EphA2-deficient mice inhibits tumor angiogenesis and metastatic progression. FASEB J 19: 1884-6. PMID: 16166198.
Brantley-Sieders, D.M., Fang, W.B., Hwang, Y., Hicks, D., and Chen, J. (2006) Ephrin-A1 facilitates mammary tumor metastasis through an angiogenesis-dependent mechanism by EphA2 receptor and Vascular Endothelial Growth Factor (VEGF) in mice. Cancer Res 66: 10315-24. PMID: 17079451.
As PI or co-investigator on several university- and NIH-funded grants, I laid the groundwork for an independent research program by showing that (1) EphA2 receptor tyrosine kinase is necessary for normal mammary epithelial morphogenesis, (2) EphA2 receptor tyrosine kinase promotes mammary tumorigenesis and metastasis in vivo in HER2-dependent models of breast cancer through physical and functional interaction with HER2 and activation of Ras/Erk and RhoA signaling, and, (3) demonstrating clinical relevance of these observations by interrogating patient mRNA datasets and human tissue microarrays to show that high levels of EphA2 correlate negatively with overall and recurrence-free survival in human breast cancer across multiple subtypes.
Brantley-Sieders, D.M., Zhuang, G., Hicks, D., Fang, W.B., Hwang, Y., Cates, J.M.M., Coffman, K., Jackson, D., Bruckheimer, E., Muraoka-Cook, R.S., and Chen, J. (2008) EphA2 receptor tyrosine kinase amplifies ErbB2 signaling, promoting tumorigenesis and metastatic progression of mammary adenocarcinoma. J Clin Invest 118: 64-78. PMID: 18079969. PMCID PMC2129239.
Brantley-Sieders, D.M., Jiang, A., Sarma, K., Badu-Nkansah, A., Walter, D.L., Shyr, Y., and Chen, J. (2011) Eph/ephrin profiling in human breast cancer reveals significant associations between expression level and clinical outcome. PLoS One 6: e24426. PMID: 21935409. PMCID: PMC3174170.
Zhuang G, Brantley-Sieders DM, Vaught D, Yu J, Xie L, Wells S, Jackson D, Muraoka-Cook R, Arteaga C, Chen J. (2010) Elevation of receptor tyrosine kinase EphA1 mediates resistance to trastuzumab therapy. Cancer Res 70: 299-308. PMID: 20028874. PMCID: PMC3859619.
My independent research career continues to focus on molecular mechanisms that regulate breast tumorigenesis, host-tumor interactions, and metastatic progression in clinically relevant cell culture and in vivo models. Work initiated in my mentor’s laboratory and supported by an NCI K01 Career Development Award pioneered a role for angiocrine factors regulated by EphA2 in tumor cell growth and invasion in culture and in vivo, providing the first evidence that inhibition of the tumor suppressive angiocrine factor, Slit2, by EphA2 receptor tyrosine kinase promotes tumor cell proliferation and invasion. These studies became the basis of my first independent NIH/NCI R01 grant (CA148934) and publications dissecting the molecular mechanisms through which EphA2 receptor and ephrin-A1 ligand cooperate with VEGF and Slit2 to modulate normal vascular remodeling and tumor angiogenesis in vivo. I served as primary author for the first study and senior author/PI for subsequent studies. I have also recently initiated a collaborative investigation of the role of Rictor/mTORC2 in mammary epithelial morphogenesis and breast cancer with Dr. Rebecca Cook.
Youngblood, V.Y., Wang, S., Song, W., Walter, D., Hwang, Y., Chen, J., and Brantley-Sieders, D.M. (2015)Elevated Slit2 activity impairs VEGF-induced angiogenesis and tumor neovascularization in EphA2-deficient endothelium. Mol Cancer Res. 13:524-37. PMID: 25504371. PMCID: PMC4416411.
Morrison-Joly, M., Hicks, D.J., Jones, B., Sanchez, V., Estrada, M.V., Young, C., Williams, M., Rexer, B.N., Sarbassov, D.D., Muller, W.J., Brantley-Sieders, D., and Cook, R.S. (2016) Rictor/mTORC2 drives progression and therapeutic resistance of HER2-amplified breast cancers. Cancer Res 76:4752-64. PMID: 27197158.
In addition to the contributions described above, with a team of collaborators, my experience in manipulation of the mouse mammary gland, including xenograft/allograft models, has directly promoted numerous studies elucidating the molecular mechanisms that regulate breast cancer growth/survival, metastatic progression, and host-tumor interactions. Moreover, these studies have benefitted the community at large (e.g. 2012 PLoS One community profiling study provided data for resource allocation requests by Susan G. Komen for the Cure Middle Tennessee Affiliate) and have forged collaborations that will be key in developing new research directions. I served as a collaborator on these studies, contributing to experimental design, interpretation of data, and manuscript preparation/application for funding (some projects).
Takahashi, K., Sumarriva, K., Kim, R., Jiang, R., Brantley-Sieders, D.M., Chen, J., Mernaugh, R.L., and Takahashi, T. (2016) Determination of the CD148-interacting region in thrombospondin-1. PLoS One 11: 5):e0154916. doi: 10.1371/journal.pone.0154916. eCollection 2016. PMID: 27149518. PMCID: PMC4858292.
Young, C.D., Zimmerman, L.J., Hoshino, D., Formisano, L., Hanker, A.B., Gatza, M.L., Morrison, M.M., Moore, P.D., Whitwell, C.A., Dave, B., Stricker, T., Bhola, N.E., Silva, G.O., Patel, P., Brantley-Sieders, D.M., Levin, M., Horiates, M., Palma, N.A., Wang, K., Stephens, P.J., Perou, C.M., Weaver, A.M., O’Shaughnessy, J.A., Chang, J.C., Park, B., Liebler, D.C., Cook, R.S., and Arteaga, C.L. (2015) Activating PIK3CA mutations induce an EGFR/ERK paracrine signaling axis in basal-like breast cancer. Mol Cell Proteomics 14: 1959-76. PMID: 25953087. PMCID: PMC4587316.
Stanford, J.C., Young, C., Hicks, D., Owens, P., Williams, A., Vaught, D.B., Morrison, M.M., Lim, J., Williams, M., Brantley-Sieders, D.M., Balko, J.M., Tonetti, D., Earp, H.S. 3rd, and Cook, R.S. (2014) Efferocytosis produces a prometastatic landscape during postpartum mammary gland involution. J Clin Invest 124: 4737-52. PMID: 25250573. PMCID: PMCID: PMC4347249.
Brantley-Sieders DM, Fan KH, Deming-Halverson SL, Shyr Y, Cook RS. (2012) Local breast cancer spatial patterning: a tool for community health resource allocation to address local disparities in breast cancer mortality. PLoS One 7:e45238. PMID: 23028869. PMCID: PMC3460936.
Complete List of Published Work in MyBibliography:
*Gap in publications 2018-2019 due to personal breast cancer diagnosis and medical leave.
NextGen RNAi delivery to breast tumors for selective mTORC2 blockade.
The goal of this study is to optimize advanced nanocarrier technologies for application to targeting the conventionally undruggable cancer driver mTORC2 in breast cancer, including the impact of systemic rictor-targeting RNAi delivery, alone or in combination with chemo and molecularly targeted therapies, on tumor growth/survival, progression, metastasis, and the tumor microenvironment.
Role: Multi-PI with Craig Duvall and Rebecca Cook – no overlap
The Role of EphA2 Receptor Signaling in Host-Tumor Interactions
The goal of this study is to determine if native, membrane tethered ephrin-A1 ligand activates endothelial expressed EphA2 RTK, linking specific domains of the receptor to initiation of endothelial cell migration and neovascularization.
The Role of EphA2 Receptor Signaling in Host-Tumor Interactions
NIH/NCI (Brantley-Sieders) 04/01/2011-03/31/2017
EphA2 receptor in endothelial cell-mediated tumor progression
The goal of this study is to determine how angiocrine factors secreted by tumor endothelilum enhance tumor cell growth and motility, as well as angiogenesis.
NIH/NCI (Chen and Brantley-Sieders) 07/14/2014-05/31/2019
Ephrin-A1 in lipogenesis and breast cancer metastatic progression
The goal of this study is to determine how ligand-independent signaling of EphA receptors in the absence of eprhin-A1 promotes HER2-dependent breast tumor progression, metastasis, and lipid metabolism.
When you’re diagnosed with breast cancer, no matter what stage or subtype, odds are you’ll be looking at surgery as part of your treatment plan. Got a tumor in your boob? Gotta have it cut out. Thankfully, patients have options when it comes to surgery, and, this is important…
THERE ARE NO RIGHT OR WRONG CHOICES – ONLY INFORMED CHOICES.
Whew, now that I got that off my chest (see what I did there?), let’s talk about two of those surgical options: lumpectomy and mastectomy (single mastectomy in my case, though many women opt for a double mastectomy and that’s okay). A lumpectomy involves removal of the tumor and surrounding tissue while preserving the rest of the natural breast tissue. A mastectomy is complete removal of breast tissue, leaving only skin and the underlying chest muscle behind. I’ve had both, so I speak from personal experience as well as through the lens of science. Here’s the scoop:
In 2018, I opted for a large lumpectomy followed by oncoplastic reconstruction. I’ll blog more about reconstruction options later, but oncoplasty refers to a breast reduction and lift. My tumors were small, I was early stage, and was a great candidate for this less invasive, breast conserving surgery. Even though I was later diagnosed with residual disease, I regret nothing. I simply got unlucky, and mastectomy was always an option if I had recurrence just as it was an option when I was diagnosed with residual disease.
In 2020, when we detected a pesky little 6 mm tumor that didn’t show up the first time, I opted for a mastectomy for the left breast. I chose this so I could maintain sensation on my right side. This was a personal choice – again, no right or wrong choices, only informed choices. I have the same risk of developing cancer in the right breast as I always had (no additional risk by having it in my left breast), and for me, being able to feel touch on the right side was important. Plus, as this 2017 article notes, “Contralateral prophylactic mastectomy (taking off both breasts including the one without cancer) is becoming increasingly common in the United States, and patients considering this option must be counseled about its lack of a survival benefit, its higher complication rate, and the fact that it is risk-reducing but not risk-eliminating.”
When combined with radiation, patients who opted for lumpectomy had outcomes that were comparable (even slightly better on average) than patients who opted for mastectomy. Bottom line – for early stage disease, outcomes are comparable for breast conserving surgery versus breast removal.
*Disclaimer – ALWAYS ask your doctor about outcomes and survival odds for your specific breast cancer type, stage, and grade.
For the lumpectomy, my surgeon removed my tumors and surrounding tissue. Before that, my tumors were marked with Savi Scout devices, radar locators inserted into my left breast with GIANT FUCKING NEEDLES THE SIZE OF SCREWDRIVERS WHILE MY LEFT BOOB WAS IN MAMMOGRAM COMPRESSION. Yes, this is horrifying, but it’s waaaaay better than wire localization, having ACTUAL WIRES STICKING OUT OF YOUR BOOBS to help the surgeon find the target area. After my breast cancer surgeon cut out the tumor, my plastic surgeon took over to perform a reduction (cutting out tissue on both sides) and lift (cutting around my nipples and jacking them up along with the attached breast tissue and stitching the whole thing up in what I like to call an “anchors away” pattern.
For my mastectomy, which was a skin and nipple-sparing procedure, my surgeon cut out all of my breast tissue except for a small portion underneath the skin that contains blood vessels necessary to sustain the remaining skin. The point is to de-epithelialize (fancy term for getting rid of the glandular epithelium that is the source of breast cancer) the tissue to make sure no cancer/pre-cancerous cells are left in the chest area. In many cases, including mine, a tissue expander was implanted between the remaining skin and my chest muscle. After recovery and removal of surgical drains (see below), you go to your plastic surgeon’s office to have a nurse locate the built in port with a magnetic port finder and then stick a GIANT FUCKING NEEDLE into the port to fill it up with saline solution, stretching your skin in preparation for reconstruction. After the final fill, you have to wait THREE MONTHS with a HELLA UNCOMFORTABLE foreign body in your chest before reconstruction. That’s where I’m at right now – waiting for my surgery date.
Pros and cons? If you opt for mastectomy, you can most likely skip post surgical radiation therapy. Radiation therapy sucks! It’s painful, causes fatigue, and it takes several months to fully recover. If you opt for a lumpectomy, your surgical recovery time is much faster! I was up and about within 2-3 weeks after lumpectomy/oncoplastic reconstruction. For my mastectomy on the left side, I was down for the count for 6 weeks and not really back to myself until after 8 weeks and completing physical therapy (didn’t need PT with lumpectomy – another advantage). For lumpectomy, I was able to maintain sensation in both breasts/nipples. I could even still feel the one that got nuked (i.e. radiation therapy). For my mastectomy, sensation on the left side is all gone and most likely will never return. Lumpectomy followed by oncoplastic reconstruction gave me a great shape and aesthetic result. My tits were GORGEOUS (as a part of the reconstruction process, I had a reduction and lift on the right breast in order to achieve symmetry)! I went from saggy D cups to very perky, pretty C cups. It was like being 18 again! But, even though the odds were low, I was one of the unlucky patients who had residual disease following lumpectomy and radiation.
Another consideration – mastectomy required surgical drains. With the removal of tissue and damage resulting from cutting into the body, fluid accumulates in the wounded area and, if undrained, can result in a seroma. To mitigate this complication, the surgeon leaves plastic tubes in the area attached to external suction devices that look like grenades and that need to be emptied several times a day. What comes out ranges from pale liquid to blood red liquid to what I can only describe as “chunky salsa” as pieces of tissue drain out and can sometimes clog the drain and/or the bulb. Yes, it’s that gross. These drains can stay in for up to two weeks, making it impossible to shower, bathe comfortably, exercise, and otherwise operate like a normal, functional human being.
Okay, you CAN function normally, but you’ll fucking pay for it when your drains start filling up faster with bloody, chunky salsa because you overdid it, dumbass. Yeah, I was a total dumbass because “the rules don’t apply to me.”
The rules totally apply to me. Chunky. Salsa.
And, as noted. spending a minimum of three months with one or two expanders in your body following a mastectomy is a level of sucktastic that I can only describe as follows: I’m kinda like a femebot but without the cool guns. I mean, if you’re going to be a cyborg, you should at least get some cool powers, right? That’s a BIG con when it comes to mastectomy. My oncoplastic reconstruction for lumpectomy happened immediately after my tumor removal surgery, which was super efficient and came with a relatively easy recovery.
Bottom line (louder, for the folks in the back): THERE ARE NO RIGHT OR WRONG CHOICES – ONLY INFORMED CHOICES. Knowledge is power. Get as much information from your healthcare team as possible. Ask questions. Do your research (using reputable sources that cite peer-reviewed data). Ask more questions. You are your own best advocate!