Carol Fabian recalls the emotional hardship that came with treating women for breast cancer in the 1970s and eighties.
“This was prior to adjuvant trastuzumab, and despite aggressive cytotoxic adjuvant treatment, too many of these young women relapsed and died,” said Carol Fabian, director of the Breast Cancer Prevention and Survivorship Research Center, holder of the Medical Oncology Mark and Bette Morris Family Professorship in Cancer Prevention, Mark and Bette Morris Foundation, and University Distinguished Professor at the University of Kansas Medical Center.
“These women often had young children and/or were at the height of their careers,” Fabian said to The Cancer Letter. “This was a tragedy over, and over, and over again. It was becoming emotionally very difficult to handle.”
Fabian’s husband recognized the toll this took on her, and suggested another field of medicine.
“I did not want to give up oncology, but for balance wanted to switch to a research focus, with a little more light at the end of the tunnel. That research focus was cancer prevention,” Fabian said.
While Fabian still treated breast cancer patients, she pivoted to prevention work and developed a minimally invasive technique to collect healthy breast tissue in women called fine needle aspiration.
“Most women with a family history of breast cancer, of course, had never had a biopsy. So, we had to have a comfortable, minimally invasive way of getting the tissue,” Fabian said. “That’s when I decided that maybe we could just modify the fine needle aspiration technique I used in the locally advanced research study to sample benign tissue from high- risk women.”
Many doubted that this technique would work.
“Most pathologists at the time thought random periareolar fine needle aspiration (RPFNA) to sample breast tissue for risk assessment was the most ridiculous idea they ever heard of,” she said. “Any histopathologist ‘knew’ that if you put a needle blindly into the breast without directing it towards a mass, that the only thing you would harvest is fat.”
Luckily, Fabian wasn’t a pathologist, “and was unaware of these basic pathology tenets.”
“Dr. [Fritz] Linn did not want to dampen my enthusiasm, although he thought I was perhaps misguided,” she said. “In fact, to his astonishment, we did get ductal and lobular tissue from the majority of high-risk women probably because we were performing the procedure mainly on women in their 40s and early 50s not 60s and 70s.”
Ten years later, Fabian and her team had aspirated 480 high-risk women and followed them for an average of five years.
“In fact, cytologic atypia in high-risk women was a strong short- term predictor of DCIS and invasive breast cancer and stratified risk based on the Gail model,” she said.
Is prevention something she could have anticipated when she first started out in medicine, when so many women were dying of breast cancer?
“I would not have dreamed it,” she said. “Just like I could not have imagined the necessity of a laptop computer, the internet and email, business by zoom meetings, or a cell phone as a necessary body appendage. I felt fortunate as a beginning faculty in the late 70s to have Wite-Out for typo correction and a fax machine. Technological advances have really increased the pace of discovery.”
Fabian spoke with Alexandria Carolan, a reporter with The Cancer Letter and associate editor with the Cancer History Project.
Carol Fabian: Actually, believe it or not, it was fine.
I was born year one of the baby boom. There were lots and lots of people applying to medical school, including probably more women than ever had before. Having said that, there were only six women, I believe, in a class of 125.
Whether it was working on cadavers in anatomy or going through clinical rotations, we tended to be arranged by sections of the alphabet, and there was only one woman in my section. When she dropped out of our class at the end of our first year to get married—it was just me and the guys from A to H, and then we went through the rest of medical school together.
I was extremely well treated by my classmates. You just learned to live with what the guys liked to talk about. Actually, most people in medicine like to talk about their experiences in medicine, and to this day I probably have as many close friends that are men as women.
In the late ‘60s and early seventies, state supported medical schools, and associated hospitals were seriously underfunded, with facilities nothing like you would see today. Four-bed wards, or even more bed wards, were very commonplace. Medical students were often expected to take up the slack for the lack of funds to hire sufficient aides and technicians, as well as assist the nurses.
We performed most of the blood draws, started IVs, placed nasogastric tubes, and were responsible for various unsavory extractions of things. Dictation was a luxury reserved for hospital discharge summaries, radiology, operative, and pathology reports reserved for residents and staff. History and physicals and progress notes were handwritten, and students were the favorite vehicle for this type of documentation.
Probably, the thing I will never forget as a third-year student was having to go into one of the four-bed wards and do a history or physical on a young man. There were three other men in the room, and these beds were only separated by a very meager curtain. While attempting to perform the history and physical, we were entertained with various shouts of encouragement from his other roommates. I don’t know who was more embarrassed, myself or the patient.
There were also a lot of people inbetween you and the patient when you were a medical student, including the fellow, a senior resident, a junior resident, and often a fourth-year medical student. By the time that you got to see a newly admitted patient as a third-year student, the last person the patient wanted to talk to was you. He’d already repeated his history and been examined by three to five other people. By the time I got through with my third year, I really felt like I was an expert in drawing blood, starting IVs, and digging out impactions, but I really didn’t know too much about being the first guy on the scene and trying to diagnose and treat a patient.
At the end of my third year, because I was single, I was sent on a preceptorship five hours outside of Kansas City, to a place you’ve probably never heard of called Dodge City, KS, a small town once inhabited by outlaws and other unsavory characters.
I spent a month at a small hospital which was a wonderful experience in which I was often the first on the scene with the patient. I really felt that I needed more frontline experience like that.
I graduated about six months early, canceled my plans to do my internship and residency at an academic institution and went to a very good private hospital, Wesley, in Wichita, KS. In fact, it was becoming part of KU’s teaching facility, but it wasn’t quite yet. The teaching staff were extremely well trained and came from a variety of good institutions including the Mayo Clinic and MD Anderson.
Women, believe it or not, were anxious to be part of a research project that they thought could potentially help their sisters, their daughters, and other women who had a family history of breast cancer.
They were young, they were enthusiastic, and they loved the house staff. The nurses loved us as well. The facilities there were like a five-star hotel, the food was great (and free to the house-staff). I thought I was in heaven. I loved every aspect of internal medicine but I felt a real bond with both the hematologist and oncologist who were there at the time. Almost right away, I knew I really wanted to go into oncology.
In the early seventies if you had a solid tumor of any kind that could not be removed in its entirety, chance of cure was slim. Screening mammography was not what it is today, nor was it embraced by as many women. Cancers were larger when detected, and even if they could be removed from the breast, there was a 50% chance of metastasis. If that happened, death was the eventual result.
Adjuvant chemotherapy for breast cancer was just starting, and was generally reserved for women with positive nodes. The primary adjuvant regimen was simple by today’s standards (cyclophosphamide, methotrexate and 5-FU +/- vincristine and prednisone), and was often administered under the direction of breast surgeons, not hematologists/medical oncologists.
In fact, oncologists often did not see breast cancer patients until she developed metastatic disease. During my residency, I was really touched by the oncologist’s approach to often very difficult patient situations. In the seventies, we did not have good antiemetics, we didn’t have central lines, we didn’t have growth factors to protect against leukopenia. We did not have bisphosphonates or RANK ligand inhibitors, such that individuals with bone metastasis often died after enduring a prolonged period of disability and excruciating pain.
In 1975, I headed back to Kansas City, to an oncology fellowship at KU. My entire extended family was from the Kansas City area. There was never any doubt in my mind that I would go back to Kansas City. My parents probably would’ve killed me if I went anywhere else.
The head of the oncology division (which was separate from hematology) was a very colorful character by the name of Barth Hoogstraten. In 1975 Dr. Hoogstraten was also the chair of the Southwest Oncology Group. He had immigrated from the Netherlands after his initial medical training. He had refused to sign a loyalty pledge to the Nazis during World War II, while he was in Medical School, and had to go into hiding.
I highly recommend a book he wrote, called “Eyes of the Blind.” It talks about his experience in occupied Holland, the women who sheltered him from the Nazis, and the process of staying alive, including working in a coal mine. It kind of reads like the Diary of Anne Frank.
CF: Barth worked at Mt Sinai in New York from 1959 to 1970, with a focus on hematology and multiple myeloma. He had only been at KU for about five years when I arrived for my fellowship in 1975.
Barth grew up in the school of hard knocks. Being a physician, working with patients, and the opportunity to do research should be its own reward.
His expectation was that physicians working for him would want to work very hard; forgoing personal time for the good of a cancer patient and the potential financial rewards of private practice for cancer research.
He was a tall wiry man, with a seemingly inexhaustible supply of energy, and was also a bit of a penny pincher.
CF: Yes, and he was also chair of the Southwest Oncology Group, which since 1972 had its operations office in Kansas City. Emil “Tom” Frei at MD Anderson had resigned as SWOG chair to head up the Cancer Program at Dana Farber.
It was always assumed that his protege Dr. Emil J Freireich would succeed him as chair of the Southwest Oncology Group.
Dr. Freireich was also a very colorful figure, who was committed to improving the prognosis of leukemia patients, but had no difficulty in publicly “calling out” other physicians who might not agree with him. “Fried by Freireich” was considered somewhat of a right of passage by SWOG investigators.
CF: I saw that—a great article, and right on. As I understand it from various sources, Dr. Hoogstraten was a relative unknown in 1972, when he was approached by several group principals while washing his hands in the men’s room at a SWOG meeting, and was asked to run for group chair.
They really were not as interested in Barth as avoiding what was feared to be major group polarization under Dr. Freireich. Dr. Hoogstraten was elected, but little did many of his supporters realize at the time that Barth could be a rather vocal and opinionated individual himself. Perhaps that was characteristic of many oncology leaders of the time. I can still recall overhearing several very loud and heated phone conversations between Barth and Vince DeVita when Dr. DeVita headed the NCI.
Regardless, Barth was a great research mentor to me. Early on, this likely had more to do with proximity than anything else, as my “desk” the first year of my fellowship consisted of a card table in his university office. Space and funds were limited, why buy a desk for a fellow when there was a perfectly good card table which could be pressed into service?
During my first few fellowship months, I helped him write an article on anemia and cancer, and at that point he decided that perhaps I had a future in cancer research, but I would have a lot to learn. My early research lessons” included:
- Extended stays in the clinical research unit drawing the blood myself, so I would understand what patients who participated in pharmacokinetic studies had to go through.
- Spending a week in learning how to do an estrogen receptor assay with William McGuire’s group in San Antonio (mainly in the cold room), so I would have a better appreciation of how hard the laboratory investigators worked.
- Physically going to the library to look up old manuscript references, so I would not pass on others’ mistakes, and
- Learning how to do a life table analysis with a calculator, to reduce study design dependence on statisticians—whom he admired, but am not sure ever totally trusted.
Ron Stephens, who was essentially in charge of the oncology division at that time, was my clinical mentor. A really great experience on both fronts. I started fellowship thinking I wanted to go into private practice, but after a few months was certain my place was at the university, doing research as well as patient care.
CF: We were taught that the patient was always first. We had to think about cure, but also we had to think about comfort and quality of life. From the mid-seventies to the mid-eighties there was an explosion of new drugs. We were sure we could cure patients if we could detect their tumor earlier and treat the micro-metastatic disease with adjuvant chemotherapy, and in the case of breast cancer, anti-hormone therapy.
In 1975, when I was a first-year fellow, tamoxifen was still considered an investigational drug and was primarily used to treat postmenopausal women with metastatic disease. I was very interested in the possibility of giving it to premenopausal women and whether utilizing loading doses would facilitate a clinical response.
Barth encouraged me to team up with a pharmaceutical chemist on the Lawrence campus, Larry Sternson, who developed an assay for both tamoxifen and a new metabolite 4-OH tamoxifen, one of the most active forms of the drug.
We had some impactful early publications in tamoxifen pharmacology. We were even invited to present in the UK and Italy, which cemented my already burgeoning interest in breast cancer. In addition to manuscripts, Dr. Hoogstraten now gave me SWOG protocols to review.
The card table was becoming crowded. By my second fellowship year, I had a semi-official position in the Southwest Oncology Group, reviewing and helping to fix protocols before they went to the NCI. The card table was a thing of the past, I had an office of my own, a Dictaphone, and a phone with a hold button. I felt I had arrived.
My time at SWOG as the special assistant to the group chair was an incredible learning experience. I began to work directly with the disease committee and study chairs as well as individuals at the NCI reviewing the work. I was also involved in the negotiations, which I assure you were much less formal than today. By the end of my fellowship, I had SWOG protocols of my own, in Hodgkin’s disease and breast cancer, and had achieved “Fried by Freireich” status.
In the early eighties, Barth had left KU for another institution, after getting into a public squabble with an administrator over how to move KU to NCI-designated cancer center status. SWOG had come under the leadership of Chuck Coltman, and the operations office had moved to San Antonio.
As a result of my SWOG experience, I had developed several research mentors outside of KU.
One of my early and best mentors was Dr. Larry Baker, now at the University of Michigan, but then at Wayne State in Detroit. Larry suggested that I apply for an R01 to extend my early clinical pilot study, which involved identifying the best time to administer chemotherapy following a high physiologic dose of estradiol to increase the growth fraction of ER+ locally advanced cancers.
The general concept had been initiated by Marc Lippman. I was not sure, exactly, sure what a successful R01 looked like as no one currently in the oncology division had ever had one, but ever optimistic, I submitted what I had written. Lo and behold, it wasn’t funded. I was devastated. I didn’t realize that it was unusual to get funded on the first attempt.
Dr. Bruce Kimler, a radiation biologist, had just been recruited to KU. He read the grant and the review and said I cannot fathom why you are in such despair. Fix this, this, this, and turn it back in. I did and he was right. This translational study in advanced cancer was particularly important for two reasons other than to test the primary hypothesis:
- It started a 35 year+ research collaboration in which, amongst other things ,Bruce has continued to tell me what to fix, and
- When my focus turned to early phase prevention trials, I already knew how to perform breast tissue sampling myself and did not have to rely on someone else.
CF: For many years, I was one of the very few female medical oncologists in town and was involved in research. In the eighties, it seemed like every young female with breast cancer, particularly later stages of breast cancer, was referred to me.
This was prior to adjuvant trastuzumab, and despite aggressive cytotoxic adjuvant treatment, too many of these young women relapsed and died. These women often had young children and/or were at the height of their careers. This was a tragedy over, and over, and over again. It was becoming emotionally very difficult to handle.
My husband said, “I can’t stand seeing you like this. Maybe you should try some other field of medicine.” I did not want to give up oncology, but for balance wanted to switch to a research focus, with a little more light at the end of the tunnel. That research focus was cancer prevention.
We were just beginning to appreciate that adjuvant tamoxifen reduced contralateral breast cancer in women who had estrogen and progesterone receptor positive tumors. I knew that pharmacotherapy to reduce the risk of developing cancer in the first place was just around the corner, but for good uptake of drugs like tamoxifen, we would need a way to identify who was at very high short-term risk of developing breast cancer.
I thought, if we could detect a precancerous field effect by randomly sampling breast tissue in women with a family history of cancer, we could identify those most likely to benefit from what would come to be known as “chemoprevention.”
Most women with a family history of breast cancer, of course, had never had a biopsy. So, we had to have a comfortable, minimally invasive way of getting the tissue. That’s when I decided that maybe we could just modify the fine needle aspiration technique I used in the locally advanced research study to sample benign tissue from high- risk women.
I reasoned that the upper outer and inner quadrants contained most of the lobular and ductal tissue in most women, so that is where I would sample with the help of a little local anesthesia. My laboratory technician at the time tipped me off that putting some bicarb in the local dramatically reduced the stinging and made the procedure more comfortable for the patient (he had learned this from a friend of his who did hair transplants).
In 1989, I got $25,000 from a women’s organization, and a lot of grassroots institutional support from Dr. William Jewell, who then was the head of breast surgery as well as from clinical pathology, and Dr. Fritz Linn, head of clinical pathology and a cytopathologist in his own right.
Most pathologists at the time thought random periareolar fine needle aspiration (RPFNA) to sample breast tissue for risk assessment was the most ridiculous idea they ever heard of. Any histopathologist “knew” that if you put a needle blindly into the breast without directing it towards a mass, that the only thing you would harvest is fat.
Luckily, I was a medical oncologist and was unaware of these basic pathology tenets. Dr. Linn did not want to dampen my enthusiasm, although he thought I was perhaps misguided. In fact, to his astonishment, we did get ductal and lobular tissue from the majority of high-risk women, probably because we were performing the procedure mainly on women in their 40s and early 50s, not 60s and 70s.
He set me up with a young woman he felt was his most talented cytopathology fellow, Carol Zalles. She interpreted all the morphology slides from then on.
Ten years later, we had aspirated 480 high risk women and had followed them for an average of four years. In fact, cytologic atypia in high-risk women was a strong short- term predictor of DCIS and invasive breast cancer and stratified risk based on the Gail model.
That was the big study that was published in 2000 in the JNCI.
CF: Yes, it was. We did not have genetic testing then. The Gail Model was published initially in 1989 the year the clinic was started.
Women, believe it or not, were anxious to be part of a research project that they thought could potentially help their sisters, their daughters, and other women who had a family history of breast cancer.
CF: I am not aware of other long-term prospective studies begun at this time with fine needle aspiration cytomorphology.
There were others beginning to assess other risk biomarkers by this time, including Norman Boyd with his mammographic density studies and Mary-Claire King and Henry T. Lynch looking at genetics, but BRCA1 was not even discovered until 1995.
The importance of precancerous tissue was appreciated, and investigators from Mayo Clinic and Vanderbilt had begun to establish benign tissue repositories made up of diagnostic biopsies taken from women who presented with a lump or abnormal mammogram.
Relative risk as a result of atypical hyperplasia observed in benign biopsy series was remarkably similar to relative risk from atypia from the fine needle aspirations from high-risk patients.
CF: Obviously, I was not the only person in the United States who was very interested in prevention. There were a number of individuals who wanted to try to develop agents for primary prevention other than tamoxifen, but there was not a good workable model for early-phase trials.
We could not just line up 5,000-10,000 women every time we wanted to test a new strategy. How can we predict if a new agent is likely to work? Modulation of molecular biomarkers in tissue and blood as well as changes in imaging was the likely answer.
I’ve always wondered why, if we can put people in space stations, we can’t we invent some type of birth control to be administered to an adolescent, which would provide the molecular, hormonal, and immunologic protection from breast cancer of early childbirth, while fixing their acne.
The NCI became very, very interested in our work in terms of acquiring tissue for early-phase breast cancer prevention trials. It was a heady time for chemoprevention, not only for phase III cancer incidence trials, but smaller biomarker-based studies of multiple disease sites in an effort initially led at the NCI by Gary Kelloff.
Unfortunately, we were trying to do too many things at one time. Prevention researchers were trying to assess potential efficacy of new agents before we clearly understood which risk biomarkers would be most indicative of response to that agent at the dose employed.
The reproducibility and rigor of the sampling methods and assays utilized could also be a problem, along with suboptimal attractiveness to patients of some study designs. The result was often a protracted accrual for randomized trials, which failed to live up to the promise of animal models or single-arm pilot studies. Consequently, after this initial, incredible rush, I think enthusiasm waned somewhat for clinical prevention research, not just for breast, but for other organ sites as well.
Despite all that, there are those of us who strongly believe in prevention and are still performing early-phase trials. In breast, Dr. Andrea Decensi’s recent landmark phase III study of low-dose tamoxifen, which was preceded by a decade or more of careful early phase trials with biomarker endpoints, has brought renewed enthusiasm to prevention trial research.
CF: Oh, absolutely. I think if it hadn’t been for advocates like Fran, we would never be where we are today. The women in Susan Komen for the Cure, and the Breast Cancer Research Foundation are particularly focused on finding answers for breast cancer prevention as well as treatment.
These organizations, along with the Department of Defense, had lay advocates on the grant review panels very early on. A good thing for prevention as cancer prevention is a major area of interest for both survivors and previvors. Lay advocates also made it clear they had more enthusiasm for natural products and lifestyle modification for primary breast cancer prevention than in prescription drug interventions.
I was awarded a large Komen for the Cure Promise Grant supporting a multi-center trial of 12 months of a lignan (such as those found in flaxseed) versus a placebo in premenopausal women. This study probably would never have been funded at the time via a regular NIH study section.
Because of the type of contraceptive used or endometrial ablation, a sizable proportion of these women did not have regular cycles, and we had to guess at when they were likely to be in the follicular phase for tissue sampling. Both lignan and placebo showed a reduction in the proliferation marker KI67 in benign breast tissue from baseline to 12 months.
When we restricted the analysis to only those who could be shown to be in the same phase of the menstrual cycle at baseline and 12 months by progesterone levels, the lignan group still showed a significant within-arm reduction in Ki-67 but reduction was no longer significant for the placebo group. Perhaps a different biomarker or different eligibility restrictions would have produced a significant reduction in proliferaton.
It’s possible that for some types of cancer, such as HER2-positive DCIS, that an effective vaccine might be in our near future. I think overall, breast cancer is such a multifaceted disease that there is not going to be any one-size-fits-all ,or any simple explanation, or any simple vaccination that is going to work.
Prevention should be early—something we start working on in childhood and adolescence. I’ve always wondered why, if we can put people in space stations, we can’t we invent some type of birth control to be administered to an adolescent, which would provide the molecular, hormonal, and immunologic protection from breast cancer of early childbirth, while fixing their acne.
Prevention should also be tailored to a woman’s risk, and life phase, and other health needs. For example, two thirds or more of women as they go through early menopause, will have very troublesome hot flashes and other menopausal symptoms. It’s ludicrous to think that women who are already miserable with these symptoms are going to volunteer to take tamoxifen or other anti-estrogens that could worsen these symptoms.
We have just started an R01 multi-center trial looking at bazedoxifene and conjugated estrogen in peri and postmenopausal women with hot-flashes. Other site PIs include Judy Garber from Dana-Farber, Seema Khan from Northwestern, Laura Esserman from UCSF, and Lisa Yee and Vicki Seewaldt from City of Hope.
We know this combination relieves hot flashes and reduces risk of osteoporosis.
The question is whether it will also reduce breast cancer risk. Based on changes in breast density, benign breast tissue proliferation and decreases in estrogen response gene expression—we think it will.
CF: That word never even entered my mind.
Remember, back at that point in time, we were just starting with the idea of adjuvant therapy. We’re just going to eradicate micro-metastasis and cure everybody unlucky enough to develop breast cancer—prevention was not on the radar. It was really a shock when we found out that, yes, early detection and adjuvant therapy reduced recurrence and improved survival, but we didn’t cure everybody.
So, no, in the seventies and early eighties, I would not have dreamed it. Just like I could not have imagined the necessity of a laptop computer, the internet and email, business by Zoom meetings, or a cell phone as a necessary body appendage. I felt fortunate as a beginning faculty in the late 70s to have Wite-Out for typo correction and a fax machine. Technological advances have really increased the pace of discovery.
CF: In terms of my own personal research, we’re also looking at interventions that are likely not associated with hot flashes and other quality-of-life altering side effects in premenopausal women, as well as ways to reduce obesity and insulin-resistance fueled breast cancer development.
We have a new study approved in concept form by the NCI via the University of Michigan Early Phase Prevention Trial Group of acolbifene, a newer selective estrogen receptor modulator, versus low-dose tamoxifen in premenopausal women. Acolbifene may have some advantages over tamoxifen in terms of avoiding certain types of endocrine resistance and certain undesirable metabolic effects such as an increase in triglycerides. Neither agent at the doses we are using is likely to significantly increase hot flashes.
Our study will look at change in endocrine resistance and estrogen response gene expression as well as breast density and metabolic endpoints.
Thirty five percent to 40% of adult women in the U.S. are obese, and the majority of these women will have insulin resistance, which increases risk of breast cancer. Obesity also is associated with chronic adipose inflammation, which increases risk. Several different anti-inflammatory interventions are being studied by numerous investigators in addition to diet and exercise.
We have demonstrated that prescription strength marine omega-3 fatty acids enhance the biomarker modulatory effects of diet and exercise induced weight loss and this needs to be followed up in future trials.
We also need more innovative and less expensive ways of tying biomarker modulation to cancer incidence reduction, particularly for non-prescription drug interventions that may not go to phase III trials.
One method is to employ human and animal model co-trials in which a biosimilar dose of the agent and biomarkers are used for both trials, but part of the animal cohort is allowed to progress to cancer. In that manner, we can correlate biomarker modulation with change in cancer incidence. My group has been working on this model with Dr. Steve Hursting at UNC for several years, and Steve was a co-PI in the lignan trial.
Earlier, I mentioned vaccines. There’s a lot of excitement in that area. I’m not an immunologist, but again, for targeted populations, I think that’s definitely an area of emphasis at the NCI right now.
CF: People sometimes ask me, why have you stayed at KU your whole career? Where exactly is Kansas City anyway?
For those individuals that are really interested in prevention, I just like to say two things: First, your cohort is everything if you’re a clinical researcher. Stay with your cohort. Second, stay where people are collaborative and are supportive of your work. My father gave me some very good advice when I was 18 and thinking about switching one date for another. “Daughter—dance with them that brought you.”
KU has been very good to me and under the direction of Dr. Roy Jensen (a breast pathologist who trained at Vanderbilt) the University of Kansas did achieve NCI cancer center designation in 2012.
Even in the years where there was a dearth of resources, the cancer center was always supportive, and I have thoroughly enjoyed working with program officers and division heads in cancer prevention at the NCI, who are extremely dedicated. Among those are Dr. Karen Johnson, who worked tirelessly in this area until succumbing to ovarian cancer in 2010.
A future challenge will be in getting more young investigators, especially oncologists, involved in prevention research. The NCIs Early Phase Prevention Consortia and similar RFAs are likely to be a step in the right direction in that regard.