A cancer diagnosis affects all aspects of a person’s life, and that includes employment. Coupled with the astronomical cost of cancer healthcare, especially for the un- and underinsured, the short and long term impact of cancer on financial stability and employment can be disastrous. If you are female, a person of color, disabled, and/or LGBTQIA+, these negative impacts are very often compounded by sexism, racism, ableism, and homophobia.
The stigma is real*.
Sexism, racism, discrimination, and other biases make working, maintaining productivity, and feeling valued for your work much more challenging in the face of cancer. I’ll cover some of those challenges in this post, as well as protections in place within the United States to alleviate them (with the caveat that we need more), and additional policies and protections that we could implement to protect and support cancer patients and survivors in the workplace. I’ll focus on breast cancer, but many of these challenges and solutions apply to people diagnosed with other types of cancer.
What are some of the challenges cancer patients and survivors face when it comes to work and careers? According to a recent study published in the Journal of Clinical Oncologychallenges like job loss, decreased earnings, and increased spending (the last two described as “financial toxicity”) are some of the greatest. It seems like a no-brainer: if you lose your job or part of your income plus healthcare coverage while the medical bills for treatments pile up, you’re not really surviving all that well financially, let alone thriving. But we like and trust peer-reviewed data here, so let’s look at data.
Financial distress caused by job loss/lost wages not only makes you feel worse, it has also been linked to “increased symptom burden and emotional distress and to decreased quality of life and treatment adherence.” In other words, if you’re strapped for cash or you’re suffering from the mental health effects of a cancer diagnosis without resources, you’re not as likely to be treatment or medication compliant. That leads to poor outcomes. Worse, cancer patients are more than twice as likely to file for bankruptcy after diagnosis, and bankruptcy is associated with almost double the risk of death among survivors.
That’s the biggie, and adds insult to injury. You have to pay for your treatments in order to live, but you may have to go bankrupt to do it, which increases your risk of DYING!
2. The scope is significant. Around 45% of people diagnosed with cancer in the United States are working age (20-64). This affects a LOT of people, y’all!
These are the same essential workers we’ve failed as a nation to support during the global pandemic.
4. Aside from concrete challenges, the mental and emotional health costs of a cancer diagnosis can reduce social engagement and a patient’s sense of self worth. I work as a cancer researcher and a cancer center, have a TON of privilege, and even I’m not immune to these challenges*. If I’m not, imagine how awful it is for patients and survivors with fewer resources and protections.
5. I cover disparities related to cancer care, outcomes, and financial toxicity in my book, but suffice to say, if you are female, not white, not able bodied, and not straight, you are likely to disproportionately experience all of these challenges on a much more significant level thanks to racism, sexism, homophobia, and ableism.
Existing and Future Solutions
In addition to FMLA and ADA protections (for those who qualify), many non-profit organizations offer financial assistance to cancer patients. Funds are available from Susan G. Komen for the Cure, the American Cancer Society, Young Survival Coalition, and other organizations, many of which I cover in my book, that can be used to cover the costs of treatments, bill pay, home health care and childcare, and a variety of other expenses.
But to truly and comprehensively tackle this issue, we need systemic changes. Some of the more so-called “progressive” solutions, like universal healthcare coverage, tend to be met with skepticism or outright hostility from free-market (*cough, cough – rich, white conservatives – cough, cough*) advocates who complain about lack of “personal responsibility,” think the current system works just fine, and/or think vouchers for purchase of private insurance and other non-government solutions work better (even though universal healthcare works very well in most other industrialized nations).
Aside from universal healthcare, there are other initiatives that have worked in other nations that might appeal to conservatives while making a significant impact on job retention and financial stability for cancer patients and survivors. For example, as noted in the Journal of Clinical Oncology Society study cited above, “A 2012 systematic review evaluated the effectiveness of government policies in place from 1990 to 2008 in Canada, Denmark, Norway, Sweden, and the United Kingdom to change employer behavior with regard to return to work. The most successful policies included financial incentives for employers to hire people with disabilities; flexibility and adaptations in the work environment, particularly with flexible schedules and giving employees more control over work demands; and programs that involved employers in return-to-work planning.” These incentives benefit everyone, including employers, patients/survivors, and society as a whole.
Patient-oriented interventions that tackle physical, psycho-educational, and/or vocational portions of cancer patients’ employment retention were associated with higher return-to-work rates compared to patients who received standard care. And patients who received this type of multidisciplinary intervention “experienced a significant increase in perceived importance of work, work ability, and self-efficacy with regard to returning to work, and return to work was 59%, 86%, and 83% at 6, 12, and 18 months, respectively.”
It’s going to take a lot of work in the form of political will, advocacy, legislation, and incentives to solve this problem. What can you do to help? Contact your elected officials and voice your support for programs that support cancer patient financial stability and access to reliable and affordable healthcare, job retention, and return to work with appropriate accommodations. It’s the right thing to do, and it’s good for the economy, society, and humanity.
If you’ve experienced workplace discrimination based on your status as a cancer patient/survivor, click here for information about your rights and what you can do to protect them.
You’d think being a cancer researcher who works at an academic institution dedicated to cancer care, research, and saving and improving the lives of those diagnosed with cancer, I’d be immune to the bullshit discussed above.
In many ways, I am. Thanks to a supportive Department Chair and Division Chief (both female), I was granted an extension on my tenure clock, additional discretionary funds, and professional/personal support from my (largely female) colleagues. To these individuals, I see you. I appreciate you. I love you.
Then there are the (largely male) colleagues who have made my experience working while undergoing cancer treatment and returning to work after the Covid-19 shutdown and a (very short) medical leave a lot shittier. My passion for breast cancer researcher didn’t diminish when I was diagnosed. I became MORE passionate! I worked through radiation treatments, horrible systemic therapies while trying to find one I could live with for 10 years, and after surgeries when I remained swollen, sore, fatigued, and mentally struggling with all of the emotional fallout associated with cancer.
And yet…a peer reviewer for a grant I submitted felt the need to make the following comment in his (I’m 99.999999% certain it’s a dude) review summary: “Dr. Brantley-Sieders is an Assistant Professor of Medicine…who completed her Postdoctoral fellowship in 2003. A concern is her lack of productivity, with only a single first or last author publication since 2017, and only 4 in total since 2012. That said, as noted in her letter of support by [DEPARTMENT CHAIR], she is a breast cancer survivor and there may be circumstances that underlie her less than optimal extent of productivity.”
First of all, it’s not true. I had and have more first/senior author publications since 2017 and 2012. In fact, I have published over 55 papers in high tier journals, which demonstrates my highly collaborative approach to science. Secondly, WHAT THE ACTUAL FUCK??? This reviewer thought it was okay to weaponize my own breast cancer diagnosis on a grant I submitted to a BREAST CANCER RESEARCH ORGANIZATION in the presence of other BREAST CANCER SURVIVORS serving as consumer reviewers. But, since my application wasn’t de-identified, and with my hyphenated last name (for which I’ve received inappropriate feedback about), this reviewer felt entitled to pose this outrageous and untrue criticism on an application by a female scientist.
Rather than hiding in a corner to lick my wounds, I reported this to the organization starting with leadership. Was it a risk? Of course! Backlash and retaliation are always a risk, especially for women who dare to speak out. But, if I stayed silent, I would have become part of the problem. I refuse to do that. I’ll be part of the solution.
I’m in the middle of another situation with a colleague I once trusted (my mistake) that centers around perceived shortcomings related to how I am balancing my work and ongoing treatments. What started as a communication issue is rapidly escalating into something more serious. At best, it’s a problematic situation. At worst, it may represent a serious violation of policy. I hope to resolve it in a way that is fair and satisfactory to both parties, but the damage is done in terms of trust and my perceived value to the project. Again, I could just sit quietly and accept it, but I’m not going to be part of the problem. I’m a fighter. I’m a damned good researcher who has made and will continue to make valuable contributions to science, and I’m worth it.
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 had breast cancer. I didn’t have to have chemo. I’m lucky and benefited from decades of biomedical research that made OncoType DX testing possible (I WILL get around to blogging about this test eventually, I swear), and I happened to have a low score.
I still had cancer. I’ve had three surgeries (and I’m not done), radiation, and I’ve got a ten year sentence with estrogen blockers and medically induced menopause. I’m still lucky. I know and understand that. Very well.
I still had cancer. When someone in or out of the survivor club (it’s always worse when it’s another survivor) tells me I had “baby cancer” or “good cancer,” I get a special kind of homicidal that will probably get me locked up someday when I finally lose my .
Never, ever, EVVVVVVVVVER say that to someone who has had cancer. It’s not a contest. It’s a suck fest and no one, not even fellow survivors, should not presume to understand the level of suffering endured by cancer patients and survivors.
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!
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!
It’s been a while! I’ve taken time to recover from my mastectomy (will blog about that later) and, like many folks in self-isolation, I’ve been doing things like gardening, cooking/baking, home improvement, and family activities to fill the time. I waver between being grateful, bored, peaceful, restless, and generally anxious about the immediate and long-term future.
And, like many other people battling cancer in the midst of the pandemic, I’ve been dealing with uncertainty about my ongoing treatments on top of the “normal” concerns. I’ll get to my specific case in a bit, but first we’ll go over highlights from a recently published article.
How has cancer care changed in the era of Covid? A recent article from the New England Journal of Medicine provides insight into some of the challenges for breast cancer care. The article is part case study and part discussion of alternative approaches to cancer care designed to mitigate risks of cancer patient exposure to SARS-CoV-2 in healthcare settings. These include delays in surgical tumor removal in some cases where rapid growth/progression of the tumor isn’t a significant risk. One interesting approach is the use of neoadjuvant (a fancy term for treatment before surgery) endocrine therapy (a fancy term for use of estrogen hormone blocking agents like tamoxifen and aromatase inhibitors). As discussed in the article, the advantages of this approach for hormone receptor positive breast cancer include: 1) shrinking the tumor before surgery and improving chances of getting clear margins (no extra tumor left behind after surgery); 2) making breast conserving surgery a safer and more aesthetically pleasing option; 3) giving more time for genomic testing (e.g. OncoType DX – will blog about this later, too) results to come back; 4) determining sensitivity of the patient’s tumor to estrogen suppression, which can also help with the decision whether or not to add chemotherapy.
The downside, of course, is that delayed surgery and neoadjuvant endocrine therapy require more monitoring (examination, imaging, biopsy, etc.), which takes place in healthcare settings and increases the risk of exposure to the virus. With chemotherapy, which targets rapidly dividing cancer cells (along with hair follicles, cells lining the gut, and immune cells), the risks for exposure to coronavirus is especially problematic as patients are rendered immunocompromised (unable to fight off infections with the body’s natural defenses) or immune fragile (less able to fight off infections). Approaches to mitigate these risks are discussed in the article for hormone receptor positive breast cancer as well as HER2+ and triple negative subtypes. It also discusses ways healthcare providers can and should effectively communicate with patients about treatment decisions and risk management.
Communication – this is an ongoing issue with my care. There are many factors, not the least of which is Covid-19, but we’ve had some…confusion about the schedule for reconstruction following my mastectomy (Note: the surgical team managing my case are PHENOMENAL at what they do, but in both cases, communication with me has not been on par with their skills). When we first scheduled the mastectomy, we also discussed which option might be best for reconstruction and settled on a TUG flap autologous reconstruction. This will involve using a flap of skin, fat, muscle (transverse upper gracilis), and blood vessels from the upper thigh is used to reconstruct the breast. It is a rather involved surgery, which includes microsurgery to reattaches the blood vessels of the TUG flap to the blood vessels in the chest. The nature of the grafting procedure means close monitoring to make certain the graft has sufficient blood flow to survive and thrive, and therefore requires a one night stay in the ICU.
An ICU stay in the era of Covid-19 is a risky and scary prospect!
Because of the risks, my plastic surgeon called and suggested we postpone reconstruction (could have theoretically been done immediately after mastectomy) to minimize the risks of exposure to the coronavirus. That made perfect sense and I agreed. During this conversation, he mentioned reconstruction 6-8 weeks following mastectomy (scheduled for May 11 – meaning reconstruction around June 22 – July 6).
This did not happen. I *think* what happened was a change in timeline due to the need for an expander implant after surgery – this serves as a temporary, fillable implant that can stretch the skin in preparation for reconstruction. I had a skin/nipple sparing mastectomy (glad the nip made it – it was dicey for a week or so), and the expander sat underneath the skin. With an expander, weekly injections into the port with saline gradually increases tension on the skin and stretches it. When I first started expansion, there was talk from the doctor about reconstruction in August.
This did not happen. I *think* it’s because the doctor forgot to let me know that there’s a three month waiting period between the last expansion and reconstruction. Right now, as far as we know, I’m looking at reconstruction around the end of September/beginning of October.
I hope this happens. Again, healthcare providers and patients must be flexible during the pandemic. I trust that my team will make the safest decision about reconstruction.