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.
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.
Wow, I haven’t posted since January??!! Shame on me! But I’ve been busy writing, and I now have a completed draft of Talking to My Tatas: A Breast Cancer Researcher’s Adventure With The Disease and What You Can Learn From It.
It feels pretty freakin’ AWESOME! I learned so much through the research, especially about the clinical aspects and how my own experience fits with breast cancer care in the United States. I also learned more about emerging therapies, disparities, and mental health related to breast cancer.
When I started this process, I had been writing fiction for about 10 years and understood more or less how to construct a story in my genre, how to query agents and small presses, how to self-publish when a particular book or story doesn’t fit with traditional publishing, and how to write blurbs (it’s HARD), synopses (it’s TORTURE), and other things that go along with the fiction universe.
When it came to nonfiction, aside from my scientific manuscripts, I had no clue where or how to start. Fortunately, I had the amazing Alice Sullivan in my corner to coach me through the process. A long time ago in a pre-COVID galaxy far, far away, I became friends with Alice, and she sent me a guide to writing nonfiction proposals. That proved to be one of the BEST tools I had in hand when I started the process for Talking Tatas.
Unlike fiction, which requires a full, complete, polished manuscript (for the most part) prior to querying agents/publishers, nonfiction requires a proposal rather than a completed manuscript. Memoirs are sometimes the exception. What is a proposal? It’s basically a plan for your nonfiction project. It includes a working blurb, detailed outline of each chapter, what makes your book stand out from other comparable titles in the market, unique selling points, a marketing plan, your credentials (or reasons for writing the book, like personal experience), and sample chapters.
A tight, well-written, carefully crafted proposal is the key to getting an agent and a publisher if you’re going the traditional publishing route. Even if you’re not, it’s a great way to map out and organize your thoughts and to be thinking about defining your target market and how you’ll reach readers in that market. If you’re planning a nonfiction project, check out these sites for proposal essentials/how to, templates, and examples of successful proposals: Nonfiction Authors Association, Reedsy Blog, Scribe Media.
Once you write the proposal and craft a killer query letter, you start the long and arduous task of sending these items to literary agents (whom you’ve selected based on research and matching interests) and hope to get some interest. It’s not speed dating, but you’re definitely looking for a connection. Be prepared for LOTS of rejections with the understanding that it’s not personal. I repeat. IT’S NOT PERSONAL. If you take rejections personally, you’re going to have a tough time in the publishing biz. That being said, if you’re lucky enough to get feedback with a rejection, put it to good use by revising your proposal. For example, I received a lot of rejections based on the fact that my proposal was cross-genre (story of my writing life/same issue with my fiction). In Tatas, I’m blending elements of memoir with the personal story and prescriptive, which is the informational component.
Ultimately, I restructured my proposal to focus more on prescriptive and less on memoir (about 80/20), and that worked!
Once you get an agent, you’ll most likely tweak your proposal again for submission to editors, perhaps having a few drafts tailored for different editors. The submission process can also be a long, arduous process, and remember, rejections are NOT PERSONAL.
Trust me – you want an agent and editor who are super enthusiastic about your work. Someone who’s lukewarm won’t be as likely to champion you, and in this very competitive business, you need champions.
While you’re querying/submitting, you should be working to build or expand your platform. This blog is part of my platform. It gives readers information to supplement what I include in the book, to showcase my style and strengths, and to hopefully connect with readers who are likely to be interested in my book. It’s also great to network with other folks who have platforms with interests that match yours. I LOVE The Bloggess and have been lucky enough to connect with her by advertising on her blog and cultivating a relationship based on fangirling and promoting her stuff. It wasn’t so much strategic as it was OMG-I-LOVE-HER-AND-EVERYONE-NEEDS-TO-KNOW-ABOUT-HER! I also adore SciBabe, A Science Enthusiast, and Sana Goldberg, so I’ve been connecting with them.
Thanks to my day job, I’ve cultivated relationships with a lot of influential people and organizations in the cancer research field and I’m forging relationships in the patient/survivor advocacy community – of which I am now a part. All of this will help me spread the word about my book, get endorsements, and hopefully make the book a success.
It’s been one hell of an adventure! Stay tuned for more. In the meantime, I’m working on a new Screw the Woo Woo post on a “spell caster” who was recommended to me on Facebook. That one’s going to be wacky and fun. Mwahahahahahaha!
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.
I’ve met and admired many survivor sisters over the years. After my diagnosis, they held me in their arms and lifted me up so I didn’t have to face breast cancer alone. Before I was diagnosed, I got to know a really cool woman named Tanisha Jones. We were represented by the same literary agency at the time, writing romance and urban fantasy* and trying to break into the fiction publishing world in a big way.
*Side note: If you’re a fan of Anne Rice and J.R. Ward, TREAT YOURSELF to Tanisha’s The Fallen Series. This exciting series is full of vampires, Fae, Weres, demons, and other supernatural beings hiding in plain sight in New Orleans. Throw in a hot homicide detective with some supernatural abilities of his own and you’ve got one helluva story!
Like me, Tanisha works in academics (one of her many jobs). She also has a daughter, just a little bit older than mine. She has hopes, dreams, highs, lows, a wicked sense of humor and a drive and work ethic to rival any I’ve seen in my almost 48 years on the planet.
Like me, she has breast cancer. Unlike me, she’s living with metastatic breast cancer (MBC). While there is no cure, she hasn’t allowed MBC to define her life or steal her dreams. She’s still writing – she published Unbound, Book 3 in The Fallen series, this month. She’s still raising her daughter. Due to health issues related to MBC, she isn’t working at the moment but she’s worked since her diagnosis in 2016.
Because America is still balking at the idea that healthcare is a human right rather than a privilege reserved only for the white and wealthy (and healthy), like many Americans, Tanisha is struggling financially due to the cost of her cancer care. I could write an entire rage post on the topics of American healthcare’s failures that include the real possibility of financial ruin, disparities in access and care, and the lack of healthcare equality and equity that is still VERY much a problem in 2020 in this country, and I will.
But right now, what matters is helping my friend who’s struggling with breast cancer.
Tanisha’s family also has a GoFundMe initiative (you know, the largest healthcare “plan” in the United States) to help her. Click here to donate what you can. It helps. It matters.
I have taken the extra book royalties I earned in November plus a small windfall that came to me at just the right time to support Tanisha. I can think of no better person in whom to invest.
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.
With so much uncertainty in the world, it’s nice to be fairly certain about one thing: tomorrow, I will get a new left breast. It’s a mixed bag of emotions for me, but the strongest are relief and hope.
When I wake up tomorrow afternoon from anesthesia, Covid will still be ravaging the planet. We may or may not know who will be the next president of the United States. I have no idea whether or not my latest research grant will be funded, nor do I know what will happen to my quest for tenure in 2021. But, if all goes well, cancer’s reshaping of my body will end.
A wise friend once told me that the only certainty in life is uncertainty. I’ve found that to be true in my almost forty eight years of living. For someone who suffers from anxiety, it is a difficult truth to face. I’m the type of person who thrives on stability, on knowing what to expect, and on consistency. There has been precious little of those comforts for me since April 19, 2018, and especially since February 2020. Discovering that I still had residual disease in the form of a 6 mm tumor remaining in my left breast pulled the rug out from under me and stole my illusion of safety.
That’s one lesson I learned from cancer—there is no such thing as safety or certainty.
So how do I cope? How can we as survivors cope? Building Resilience.
For me, one strategy has been to let go of the illusion of control. Or, to really refine the concept, I’ve been working hard to catalog the things I can control, like staying as healthy as possible with diet, exercise, regular health screenings, medication, and yoga/meditation. These measures may or may not prevent a recurrence, but they will help me live a better, healthier life. There’s no downside.
Other things I can control include the effort I put into taking care of my family. I can love them, feed them, create special moments and memories that nothing can take away, not even cancer. I can take pleasure in the small, daily moments that I used to take for granted. For example, I spent about thirty minutes this morning watching birds at my feeders. We have so many birds, from tit mice (snort) to a red-bellied woodpeckers, and chickadees to sparrows! I’ve always found solace in nature. Other small moments like a cup of tea enjoyed sitting on my deck with a chill in the air and the sun caressing my face bring me joy. I’ve had the BEST time cooking with my kids. Potstickers with my daughter and meat and rice bowls with my son have sustained us physically and emotionally. Again, there’s no downside to savoring the small moments of joy in everyday life.
I cannot control whether funding agencies select my research grants for support, but I can control the quality and integrity of my research. Funding is even more uncertain today than when I entered the field, but it is still an exciting and hopeful time to be a scientist! There are many exciting avenues of breast cancer research open for me to pursue, and if I have to leave the field (or, more likely, switch from tenure track to research track) in a few years, I’ll leave behind a body of work that I can take pride in, and I can and will continue to work in other avenues, like education and outreach. I can control how I adapt to career challenges.
The best I or any of us can do is to live every single day to the fullest. We can choose kindness, positivity, and follow our paths to making the world a better place, starting with ourselves and our community. Every day is a gift, and tomorrow’s gifts are yet unknown but so inviting. I look forward to being physically whole. I look forward to getting back to regularly scheduled life with a newly restored body, building strength and resilience.
I look forward to hope, which is something I can rely on.
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.
So I’m 5 months out from my mastectomy, waiting for reconstruction of my left breast, and I feel fugly. Not just ugly, but the kind of grotesque that can only come from looking in the mirror and STILL being shocked to see one nipple hanging significantly higher than the other. When I’m clothed it’s slightly better. I can shove my fake boob into my bra and sort of look balanced.
I say “sort of” because the damned insert moves around and is slightly bigger than my intact right boob, so I have to stuff the other freakin’ side with inserts from sports bras, which also move around, and I swear I can tell that I’m lopsided when I look at recent photos.
My family assures me that no one else notices, and maybe they’re right, but I notice, and it makes me self-conscious. It sucks. I also feel old. I’m coming up on my 48th birthday, which technically means I’m still middle-aged. But between the breast cancer diagnosis three years ago, two surgeries, radiation, and three years in medically-induced menopause plus estrogen suppression, I swear I’ve aged ten years.
Am I grateful to be alive? You bet! Do I feel lucky that my prognosis is great? Of course! Is every day a gift? Abso-fucking-lutely! But there are days when cancer and all that comes with it crashes down on me and I get sad, tired, and pissed off about what the big C has done to me.
I’m not alone. If you’re out there feeling the same way, you aren’t alone. We are strong. We are survivors. But we are also human and we will have bad days. And that’s okay. We can’t avoid them, and we have to endure them, but we don’t have to get sucked into the pit of despair. Here are some coping strategies I’ve found helpful. Maybe they’ll help you.
Put on some cute clothes
Fall is here, and that means it’s time to pull out those fuzzy sweaters, leggings, boots, and cute scarves. I’m self conscious about my neck and my cleavage, so scarves have REALLY helped. I’m not going out as much thanks to Covid, but I’ve made it a point, at least once a week, to put on real clothes (instead of the athleisure wear I’ve been rocking since work-from-home became a thing). I choose colors that make me feel bright and shiny, and select from outfits that I’ve been complimented on before. It helps! Those are the days when I can focus more on what I like about my body and face rather than what I don’t like. Have fun, wear what makes YOU feel beautiful, and don’t worry about the folks who say women of a certain age/weight/body type shouldn’t wear certain clothing. The only thing a woman should NEVER wear is the weight of other people’s expectations.
Have Fun with Makeup
I’ve always been pretty basic when it comes to makeup. Foundation, blush, concealer on the blemishes, and boom – done! Fortunately, I have a teen who is super creative, into cosplay, and LOVES makeup. Thanks to her, I’ve upped my makeup game and it has helped me feel pretty. A lovely sales associate at Sephora taught me how to contour, another fantastic salesperson at Ulta recommended primer and an eyeshadow pallet that I LOVE – dramatic eyes really work in the era of masks – and my teen routinely helps me out with the eye makeup game. The old barn does look better with some fresh paint!
Simple Self Care
Anything from drugstore face masks to bathbombs to nice-smelling lotion can be cheap ways to pamper yourself when you’re feeling like a wart on the ass end of a troll. Have a soak, wash your hair (especially if it’s been daaaaaaaaays), brush your teeth, put on some perfume, and treat yourself like the absolute fucking QUEEN you are. You are worth it.
Take a Freakin’ Selfie and Send it To Your Friends
I stole this one from “Everything is Awful and I’m Not Okay,” which I totally recommend you print out and post to your bedroom door. Take a selfie, send it to your friends and/or put it on social media – Facebook, Instagram, Snapchat, hell, make a TikTok video. Speaking of TikTok, get on there and find yourself some support from Your Fairy Godmother @starr_mcqeen_, Your Non Binary Uncle @thaddeusshafer, and the aggressively supportive @angryreactions. They don’t think you are pretty, precious, loved, and worthy, and awesome, they KNOW it and they’ll tell you. Your friends and social contacts will tell you you’re pretty, and you’ll believe them and feel better.
Send ME a selfie and I’ll tell you how pretty you are!
Got any other tips? Let me know. I can use all the help I can get, and I’ll share the love!
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.