One of the things I love about my work in advocacy is discovering amazing people who are doing the work and making a difference! Valeda Keys is one such remarkable person. She’s a Global Ambassador for Breast Cancer Awareness, using her platform and the Non-Profit organization she founded, Valeda’s Hope, to assist women in their journey from diagnosis to remission. She has one hell of a compelling story that includes a family history of breast cancer, a personal battle with breast cancer that included seven surgeries, and finding strength and empowerment in helping others.
When I learned about her work on LinkedIn, I was blown away.
Valeda, who is an Author, Speaker, LPN, Non-Profit Founder, Breast Health Navigator, and all around incredible human being, helped her mother through a breast cancer diagnosis, treatment, and later recurrence. A dream told her that she would one day endure her own battle with breast cancer, which unfortunately came true in 2010. Luckily, because of her family history, Valeda started receiving mammography screening at the age of 27 and kept up with her screenings, which allowed her healthcare team to detect her first breast cancer at an early stage. After a lumpectomy, she received the results of her genetic testing, which revealed that she carries a variant of theBRCA-2(BReast CAncer gene 2) gene associated with an increased risk of breast and ovarian cancer.
Quick Science Break
Everyone has two BRCA1 and two BRCA2 genes, but sometimes a variant of one of these genes that doesn’t work gets passed down from one of your parents. If something happens to the other copy of the BRCA gene in a cell (for example, a cell from your breast or ovary), it can increase your risk for cancer. Why? BRCA genes encode information to make proteins that help fix damage to DNA. DNA molecules encode and store all the information a cell needs to make proteins, which allows a cell to live and perform its function. When DNA is damaged, it messes with the code, and if the damage isn’t repaired, cells make defective proteins that don’t function well or in the case of cancer-causing oncogenes, function too well. Defects in some genes make cells grow uncontrollably, and sometimes those cells turn into cancer cells. Variants of BRCA genes that don’t function to fix DNA damage makes it more likely for oncogenes to get activated and make cells grow uncontrollably, leading to cancer. In the graphic above, you can see a DNA repair deficient breast cell in which the BRCA genes encode DNA repair proteins that don’t work. Because the defective BRCA gene produces a defective protein, the cell can’t repair DNA damage and gets a lot more mutations in a lot of different genes. Some of these mutations create defective proteins that let the cell grow uncontrollably, even without estrogen (E2) or other cues from the body that tell cells when to grow. See my Cancer 101 blog post and my other blog poston how cells become cancerous for a refresher on the cell biology of breast cancer, DNA damage and how it leads to cancer, and oncogenes.
End Science Break
Now, back to Valeda’s story. Since she carries a variant of BRCA-2 that doesn’t work, she was still at risk for getting another breast cancer or ovarian cancer after her first breast cancer diagnosis. She decided to keep her breasts and get screened more often, a valid choice. (Note: there are no right or wrong choices when it comes to keeping your breasts or having a double mastectomy. There are only informed choices you make with your healthcare team that are right for you.). She also endured radiation therapy that led to some serious complications, and was treated with tamoxifen, a drug that blocks estrogen function. In spite of this, she was diagnosed with a new breast cancer in 2011 and opted for a double mastectomy and autologous reconstruction (i.e. reconstruction using her own tissue from her abdomen to build new breasts), which unfortunately came with some complications, and later had a hysterectomy.
Through it all, she remained focused and determined not to let breast cancer get in the way of living a full life and achieving her goals. Her faith helped her through, and it gave her a mission to educate, empower, and help other women through their own breast cancer journeys. Among the many amazing things she does through Valeda’s Hope, Valeda sponsors a ton of mobile mammography events and encourages women to keep up with life-saving screenings. She shares her knowledge and experience through speaking engagements and educational events like Valeda’s Hope Pink & Pearls Luncheons. Valeda also hosts events that provide emotional and physical support as well as information about genetic testing for breast cancer risk genes, and so much more.
I’ve said it before, and I’ll say it again: the breast cancer survivor community is so supportive! Survivors support other survivors, patients, and caregivers. As a survivor, Valeda is using her voice and actions to help other women survive and thrive, and that deserves a spotlight, kudos, and celebration!
For a brief, beautiful, shining moment, it was the #1 New Release in Breast Cancer and Oncology on Amazon, and I have the screenshots to commemorate it!
Want a sneak peek? Of course you do! Here’s an excerpt from Chapter 16 that deals with an exciting new development in cancer research and treatment – harnessing the patient’s own immune system to seek out and destroy cancer cells through immune checkpoint inhibitors.
I’ll also take comfort in the fact that we’re getting new weapons in the arsenal for fighting breast cancer. Antitumor immunity is the hottest thing to hit the field of cancer research since the 2001 approval of Gleevec (a game-changer drug used to treat chronic myelogenous leukemia that targets the oncoprotein product of the Philadelphia chromosome that drives the disease) and the 2006 approval of Gardasil (first vaccine targeting the human papilloma virus strains that cause most cervical cancers). Recently Frontiers in Immunology published the history of antitumor immunity efforts leading to the development of immune-checkpoint inhibitors available in the clinic today, the use of engineered T-cells taken from patients and altered to fight their cancer, and oncolytic viruses.2 I’ll go over the basics, including how antitumor immunity works and the challenges we still face in getting tumors to respond.
Before we get into how antitumor immunity works, we need to understand how the immune system works to fight infection. It’s a complex beast, but here are some basics. Your immune system functions to mount a rapid and robust defense when your body encounters a pathogen (e.g., a virus or bacteria that causes disease) in your daily life. The arm of the immune system that does this is called the adaptive immune system (figure 16.1). The other arm is the innate immune system, which includes natural barriers like skin, the tiny hairs and mucous in your nose, and stomach acid. The adaptive immune system is what antitumor immunity treatments harness. It is also altered by tumors to suppress tumor immune responses and exploited to work for the tumor. (More on that in a bit.)
The adaptive immune system works like this: Specialized cells identify a potential threat (e.g., an infection), and they carry information about that threat in the form of bits of protein called antigens to other immune cells. If the threat is credible, those immune cells get activated and fight the threat. First the specialized cells that identify a potential threat patrol your body, looking for something suspicious. Cells like macrophages and dendritic cells, which roam around various organs and tissues, find pathogens (a bacteria, virus, or other microbe that causes disease) or unhealthy cells infected by pathogens, and eat them (the fancy term is phagocytosis). Infected or damaged cells send out protein signals called cytokines as a distress call to attract these patrolling macrophages and dendritic cells. While “digesting” the bacteria or infected cell, macrophages and dendritic cells 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, which in turn 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 antibodies tag infected cells as a signal for other immune cells to come and kill them. Others coat pathogens or infected cells in a process called opsonization (meaning “the process of making tasty”), which signals other cells like macrophages to come and eat the coated pathogens or cells. Specialized B-cells called memory B-cells store 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, which are particularly relevant to antitumor immunity, 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 store information about past infections to mount a rapid, strong response the next time your body sees it.
That’s a simplified but 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.
Put a pin in that concept for when we get to anticancer vaccines, and also remember what T-cells do for when we get to engineered CAR T-cells and oncolytic viruses.
Working out how to harness your body’s own immune system to fight cancer isn’t a new idea. It’s been under investigation since the nineteenth century. In fact, in chapter 5 we covered the way trastuzumab (trade name Herceptin), a humanized anti-HER2 antibody, targets HER2-expressing breast cancer cells for death. Herceptin and other monoclonal antibodies mimic the natural activity of antibody- producing B-cells to deliver therapies and tag cancer antigen–expressing cells for immune-mediated destruction. But it was the discovery of checkpoint inhibitors—proteins that put T-cells in a state of exhaustion and inactivity in pathways that are exploited by many cancers— that led to the first molecularly targeted therapies designed to boost antitumor immunity. Doctors James Allison and Tasuku Honjo pioneered this Nobel Prize–winning work.3
What are immune-checkpoint inhibitors, and how do they work? T- cells, particularly cytotoxic T-cells that actively kill their targets, bind to antigens on tumor cells through their T-cell receptors. But tumor cells, being the adaptable beasts that they are, can produce proteins like PD-L1 (programmed death ligand 1), which bind to PD-1 (programmed cell death protein 1), proteins on T-cells. This interaction tells the T- cell to stand down by tricking it into thinking that the tumor cell is “self” and should be protected. Signaling networks like this normally promote self-tolerance so that your immune system doesn’t attack your own healthy cells (figure 16.2). In tumors, it works by telling tumor- infiltrating T-cells, if present, to go into a state of inactivity. Drugs that target PD-L1—like atezolizumab (trade name Tecentriq), durvalumab (trade name Imfinzi), and avelumab (trade name Bavencio)—and drugs that target PD-1—like nivolumab (trade name Opdivo) and pembrozolimuab (trade name Keytruda)—are FDA-approved mono- clonal-antibody therapies that block interactions between PD-1/PD-L1 to unleash an antitumor immune response.4
Other immune-checkpoint molecules exploited by cancers include cytotoxic T lymphocyte antigen 4 (CTLA-4), the target of the first FDA-approved immune-checkpoint inhibitor ipilimumab (trade name Yervoy). Approved in 2011 for advanced melanoma, this drug had remarkable results. In fact, over 20 percent of the patients enrolled in the initial ipilimumab clinical trials (before the 2011 approval) are still alive and show no evidence of disease (NED).
There’s some incredible potential in targeting checkpoint inhibitors.
CTLA-4 is part of a cellular-signaling pathway that normally fine- tunes immune responses. CTLA-4 and a similar receptor, CD28, are expressed on two different T-cell types: (1) CD4+ helper T-cells, which help activate other immune cells to mediate adaptive immune responses, and (2) CD8+ cytotoxic T-cells, those cells that kill infected cells, damaged cells, and, if properly activated, tumor cells. Antigen- presenting cells make a protein called B7, which can bind to either CD28 or CTLA-4 on T-cells, and the effects on T-cell function are very different depending on what B7 binds. If it binds to CD28, B7 activates T-cell responses as a part of a complex of proteins that includes the T-cell receptor. Binding of B7 to CTLA-4 shuts down T- cell functions. CTLA-4 probably serves as protection from self-antigen recognition by inducing immune suppression, since laboratory mouse models engineered to not express CTLA-4 die from autoimmunity. This is the aspect of CTLA-4 function that gets highjacked by tumor cells. Drugs like ipilimumab block the suppressive activity of CTLA-4, which can allow T-cells to attack tumor cells.5
Here’s the kicker: The tumor actually has to have infiltrating T-cells for this to work, and not all tumors do. Tumors with T-cells that can be activated to fight the tumor are called “hot,” whereas tumors without T-cells are “cold.” One of the most aggressively researched topics in tumor immunology right now is how to make a cold tumor hot and thus responsive to antitumor immune therapies.
This is especially important for breast cancer, since most subtypes produce cold tumors. Right now, immune-checkpoint therapies are only approved for advanced triple-negative breast cancers that make the PD-L1 protein. Not all triple-negative breast cancers make PD-L1. Ongoing research is looking to expand the use of immune therapy in inflammatory breast cancer and the HER2+ subtype.6 Hopefully, with more research, we’ll figure out how to make more tumors responsive to immune therapy by making them hot (full of T-cells) and by discover- ing other immune checkpoints that can be targeted.
3. Heidi Ledford, Holly Else, and Matthew Warren, “Cancer Immunologists Scoop Medicine Nobel Prize,” Nature, October 1, 2018, https://www.nature. com/articles/d41586-018-06751-0.
4. See American Cancer Society medical and editorial content team, “Immunotherapy for Breast Cancer,” Treating Breast Cancer, American Cancer Society, Cancer.org, last revised December 3, 2020, https://www.cancer.org/ cancer/breast-cancer/treatment/immunotherapy.html.
6. Devon Carter, “Does Immunotherapy Treat Breast Cancer?” MD Anderson Center (website), University of Texas, March 26, 2021, https://www .mdanderson.org/cancerwise/does-immunotherapy-treat-breast-cancer.h00 -159385101.html.
Sometimes, if you’re lucky, something comes into your life just when you need it the most. That was my introduction to The Bloggess (aka Jenny Lawson aka Amazing/Funny/Fabulous human being). I LOVED her first book, Let’s Pretend This Never Happened (A Mostly True Memoir), gifted to me by my BFF. If you haven’t read it, treat yourself. Her other books are just as poignant, engaging, and hilarious. They’re like Pokemon – gotta catch them all! Or maybe potato chips – betcha can’t read just one. Something like that.
Better yet, grab the Audiobook! Jenny narrates it, and the humor and heartache and hope just flows from her voice directly to your brain cells, releasing serotonin and making you feel better no matter what you’re going through. Which brings me back to my first point – the something-that-comes-into-your-life-just-when-you-need-it-the-most point:
The day I endured two breast biopsies was a bad day. It would have been worse without Jenny, who allowed me to escape into her world and kept me company while I was waiting to go on the slab. And guess what?
SHE FOLLOWED ME BACK ON TWITTER!!!!
This was the highlight of my year, people! It also kept me going and inspired me while writing Talking to My Tatas. Jenny’s story touched and inspired millions, and she’s saved lives, y’all! I wanted to do the same. Whenever I got frustrated, stuck, or wanted to just give up on the writing, querying, and rejections, I remembered Jenny.
Fast-forward to the present, and guess what? Jenny Lawson endorsed my book!
“I don’t know much about cancer, but I know good writing and humor, and Dana Brantley-Sieders has those in spades.” — Jenny Lawson, #1 New York Times-bestselling author of “Let’s Pretend This Never Happened”
I’m delighted, grateful, and I’m totally going to stalk visit her at The Nowhere Bookshop someday soon. Thanks, Babe!
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.
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!
First off, HUGE news! My amazing literary agent, Barbara Collins Rosenberg, landed a publishing deal for me with Rowman & Littlefield!!! I’m honored, thrilled, and still squee-ing! So, stay tuned for Talking to My Tatas: A Breast Cancer Researcher’s Adventure With The Disease And What You Can Learn From It.
Here’s the Working Blurb – it will likely change based on guidance from my amazing editor, Suzanne Staszak-Silva, but it will give you a taste of what I intend to share (my story) and spread (scientifically sound information) with this book:
Can I talk to you about my personal relationship with my breasts?
I’ve spent twenty years working as a biomedical breast cancer researcher. Then, I was diagnosed with breast cancer. I thought I knew breast cancer before it whacked me upside my left boob and left me bleeding on the curb of uncertainty. Turns out, I had a lot to learn. The purpose of this book is to share my personal adventure with breast cancer, from the laboratory bench to my own bedside, and to provide accessible information about breast cancer biology for non-scientists. I say adventure, because I’d rather think of it as an action movie with some really cool side quests instead of another tragedy-to-triumph saga. I’m not big on sagas. I am big on kickass intellectual badassery, pathological nerdiness, and talking about my sweet, sweet rack.
Why do we need another cancer memoir? In a sea of inspirational stories, celebrity survivor stories, and physician memoirs that bring a clinical perspective, nothing I’ve found in the current market tackles breast cancer through the lens of a breast cancer researcher who became a survivor. We live in an age of fake news and pseudoscience, made worse by the pervasive anti-intellectual and anti-science political culture gripping the United States and much of the world. The Internet and social media are plagued by scammers selling “alternative medicine” and woo woo “cures” for cancer. Through Talking to My Tatas: A Breast Cancer Researcher’s Adventure With Breast Cancer And What You Can Learn From It, I offer accurate, evidence-based science that is accessible to laypersons, including the more than three hundred thousand individuals diagnosed with breast cancer every year*, their caregivers, and their loved ones.
Knowledge is power, and lack of it can lead to overtreatment, unnecessary pain and suffering, and can even be deadly. By demystifying the process from mammograms, biopsies, pathology and diagnostics, surgical options, tumor genomic testing, and new treatment options, I aim to offer hope in a story intended to blend the humor and delivery style of Jenny Lawson’sLet’s Pretend This Never Happened (A Mostly True Memoir) with the integrity and scientifically sound beauty of Siddhartha Mukherjee’s The Emperor of All Maladies: A Biography of Cancer.
*American Cancer Society Facts & Figures 2020
I’ve got some work to do! In addition to writing and fleshing out chapters for my editor to review (and work her magic on), I’ve been busy working on figures and visuals for the book, cover art forms, marketing and promo plans, and getting a new headshot! The one I currently have on this page and all over the Internet is absolutely gorgeous, fun, and from 2012. A LOT has happened in 8 years, and I have aged. I’d like to think I’ve aged gracefully, but at any rate, it was time to update the image.
Lillian Boeskool is MAGIC! She made me look so good and captured the essence of my personality in a series of amazing headshots (If you’re in the greater Nashville area and need headshots or other photography, HIRE HER). I have two favorite images and I cannot decide which one to use for this page and the book. I invite y’all to enable my decision-making disorder vote for your favorite!
This one on the left is super fun and catches me trying not to laugh at something funny Lillian said and/or did. It captures my mischief, my sense of humor, and really makes my face look nice.
And, unlike the previous headshot for which I straightened my hair, this one highlights my popping natural curls!
I’m almost 48 years old. Anything that makes my face look nice is gold.
Told you she was MAGIC!
There’s just something about this next one on the right that speaks to me.
I think it captures my sass and tells my readers that I’m going to take them on a really funny adventure that will make them a smidge uncomfortable but will ultimately leave them laughing and glad they went along for the ride.
That’s me in a nutshell.
I can’t decide between the two!
And…just to throw a monkey wrench into this whole program…
This one is my husband’s favorite.
It’s nice, too.
I’m glad he thinks I look good in all of these photographs and still thinks I’m beautiful in spite of time marching across my face and body and in spite of cancer leaving me with a janky left breast-in-progress*.
He’s pretty awesome!
I think I’ll keep him.
*Janky left breast-in-progress on display in the first two photos as the line of discoloration just above my shirt collar. Lillian asked if I wanted to Photoshop it out, but I said no. It’s where I am right now. It’s why I’m blogging, writing this book, and becoming a breast cancer patient/survivor advocate as well as a breast cancer researcher. It’s a badge of fucking honor and it stays!
I recently had the great pleasure of chatting with a dear friend and fellow breast cancer survivor, Ronei Harden-Moroney. She invited me on her livestream to talk about breast cancer—science, personal experiences, and sharing what it’s like to be in this exclusive club that neither of us signed up for but brought us closer all the same.
As you can see, Ronei is an amazing lady and one tough cookie. I hope hearing her story inspires you and gives you hope. You can find her on Facebook, Twitter, Instagram, LinkedIn, and Goodreads. If you’re looking for an editor or writing coach, seriously check her out!
Originally Published in VICC Momentum September 23, 2020 | Dana Brantley-Sieders, PhD
Note: This is an essay I wrote last summer. Though my journey continues thanks to residual disease and a mastectomy after I submitted the essay, the spirit and information in the essay hold true. I have hope. And I’m still working hard to fight cancer inside the laboratory and out in the wider world.
I had been studying breast cancer for more than 20 years when I was diagnosed with invasive ductal carcinoma. My professional life was filled with hours of watching tumor cells grow and spread on plastic dishes, marveling as they branched and blebbed in three-dimensional matrices, monitoring the size of lumps from spontaneous or transplanted breast tumor tissue in experimental mouse models, and if I was lucky, watching their growth slow or even seeing them shrink when a new experimental therapeutic worked in pre-clinical testing.
Over the years, family and friends had come to me for information, reassurance and comfort in the face of their diagnoses. I’d lost a close cousin to the ravages of aggressive breast cancer. She was only 37 years old.
When my mother was diagnosed with breast cancer, I emptied her surgical drains after her double mastectomy, caring for her with a toddler clinging to my leg and a baby balanced on my hip. I brought meals to a close friend who was diagnosed with stage 3 breast cancer, visiting with her as she endured chemotherapy, surgery, reconstruction, and finding her new normal while our pre-teen daughters hovered in the background, their infectious laughter a balm to the devastation wrought by the big “C.”
After all of this, I thought I knew breast cancer. Then it kicked me in my left breast and flung me, bleeding, on the curb of uncertainty. Turns out, I had a lot to learn.
When Brent Rexer, MD, my medical oncologist, walked in to my first appointment at the Vanderbilt Breast Center, he greeted me with kindness and a wry smile. “It’s good to see you again, though I wish it was under better circumstances.” I’d known Brent for years. He and his wife were classmates of mine in graduate school, and we’d crossed paths at research seminars in the Vanderbilt-Ingram Cancer Center. I’d crossed paths with many of the clinicians and providers who would become a part of my care team. I was lucky. I knew I was in great hands.
When I got cancer, I came home.
What did I learn from the laboratory bench to my own bedside? For starters, I learned that nothing, not even a career spent tackling this disease, can prepare you for your own diagnosis. I was as shocked, devastated, and numb as any woman who hears those three terrible words — you have cancer.
I learned that radiologists save lives. The radiologist who spotted the suspicious spot on a routine mammogram and later during an ultrasound examination has over 30 years of experience in the field. Because I’m a geek, I always ask to see what’s going on in any exam. I’m “that patient,” the one who’ll ask if I can look at the computer screen after a boob squeeze, à la mammography, and in the middle of having the goo-covered wand gliding over my exposed boob during an ultrasound. When I had the chance to look at my tumor and a previously detected benign lesion side by side, I realized that this radiologist’s years of training and sharp eyes (that could tell the difference between two grainy spots on an ultrasound that looked the same to me) caught one tumor before it could become immediately life threatening. We later learned that I had two tumors of the same subtype in the same breast, which is pretty rare. But we would not have caught the smaller one, which was actually growing faster, had my radiologist not spotted the larger mass.
I learned that I had the option of saving most of my breast tissue. Thanks to years of study following outcomes of patients who chose lumpectomy and those who chose mastectomy as surgical options, we know that choosing breast conserving surgery does not increase a woman’s risk for distant recurrence. There is an increased risk for local recurrence, but that can be mitigated with radiation therapy. I was fortunate enough to be a good candidate for partial mastectomy followed by oncoplastic reconstruction, which is essentially a breast reduction and lift. I’m not going to lie – it’s like being 18 again. I’m perky! Better still, it preserved sensation in my breast skin and nipples, and the recovery time was much shorter than with a mastectomy. Note: there are no wrong choices, only informed choices. The decision to keep or remove one or both breasts after a cancer diagnosis is a deeply personal one. Each individual patient must consider the options, the benefits and risks, and decide what is right for her. This was the best decision for me, and I’m glad I was a good candidate for this surgical option.
I learned that surgeons are brilliant, and by working together, they can give you back much of what you lost. My surgical team, including Ingrid Mezoely, MD, and Galen Perdikis, MD, worked together on a plan that allowed Dr. Mezoely to remove my tumors and Dr. Perdikis to perform oncoplastic reconstruction just after. A year and a half later, I am pleased with the result, like the way I look and feel, and while I’ll never be the same as B.C. (before cancer), my new normal is better than I ever imagined.
I learned that radiation therapists are some of the nicest, funniest people on the planet. My go-to coping mechanism is humor. When I came in for a dry run prior to my first radiation therapy, the technician placed several markers on my left breast in order to properly align the beam for more precise targeting of the area where the tumors were removed while minimizing potential damage to my heart and lungs. The shiny markers formed a cute little circular pattern, so I joked that we could make it into a pastie. All I need would be some glitter and a tassel. We both cracked up, and I was able to relax, hold my breath for the designated time, and get prepared for my treatment course. During those visits, I talked with the therapists and Bapsi Chakravarthy, MD, about topics big and small — kids, work, life, research, politics, favorite books and television shows, and all manner of topics that made the discomfort during the last weeks of treatment much more bearable.
I learned the depths of compassion and generosity of my colleagues, both in the laboratory setting and in the clinic. Disclosing a cancer diagnosis to your employer and co-workers can be frightening. Will you be at risk for losing your job (a reality for too many Americans)? Will your colleagues see you and treat you differently? Will moving forward be awkward, with colleagues feeling uncomfortable and at a loss for words? I was lucky and found support and comfort, with offers to help keep the research in my laboratory going while I was out on medical leave, with encouragement, and with the honor of serving as a reminder of what all of us in cancer research work for — helping patients diagnosed with cancer survive and thrive.
I learned that, having been on both the research side and patient side of the breast cancer experience, I have a unique perspective and the opportunity to help people outside of the laboratory. Scientists are very good at communicating with one another within the research community, but I believe we need to expand our efforts to communicate with the public. After all, most of us are funded by the National Institutes of Health, which is in turn supported by tax dollars. I feel an obligation to be able to explain my work and why it’s important to anyone who asks, be it my 11-year-old son or a person sitting next to me at the airport. I have a new mission: to be an advocate for science and bring science to the public, particularly when it comes to breast cancer. Sadly, we live in an age of fake news and pseudoscience, made worse by the pervasive anti-intellectual and anti-science political culture gripping the United States and much of the world. The internet and social media are plagued by scammers selling “alternative medicine” and woo woo “cures” for cancer. Knowledge is power, and lack thereof can be deadly. I can lend my voice to fighting myths and scams for the public good through speaking, blogging and writing.
I learned that there will be good days and bad days, and that it’s OK to seek help. My prognosis is great, but my type of breast cancer can recur years or decades after surgery and treatments are complete. That thought often keeps me up and night and serves as a source of worry. Shortly after my diagnosis, I worked to the point of exhaustion in the lab, at home, and on my side gig, staying up late in the name of productivity and maximizing creativity, but I wasn’t fooling anyone. I was terrified. After a year and a half of ups and downs, I acknowledged that I was not fine, and that I needed help in the form of therapy. I’m glad I did. Tackling my fears and anxieties head on has helped me be my best self, accept my new normal as a cancer survivor and focus on living the life I have with joy and purpose. And when I go back into the well of despair, as many survivors do, I now have the tools to climb back out and get back on track, which is very empowering.
Finally, I learned that I’m still learning. I have the best job as a researcher in that I get to be a lifelong learner. So many strides have been made since I entered the field, when Herceptin was first developed for HER2-positive breast cancer. Now, we have so many new tools in diagnostics and prognostics (3D mammography and OncoType DX testing), treatments (aromatase inhibitors, CDK inhibitors, and immune therapy), and amazing new treatments on the horizon. We still have so much work to do, but we are making a difference, and I am privileged to be a part of that process.
I’m thrilled and delighted to announce that I’ve signed with Barbara Collins Rosenberg of The Rosenberg Group to represent a nonfiction project based on my experience as a breast cancer researchers who was diagnosed with breast cancer! My goal is to expand on what I do here, providing accessible science with a healthy dose of humor and hope. Here’s a preview from my proposal:
Can I talk to you about my personal relationship with
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.
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 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’s Let’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.