Shortly after Craig Jordan finished his PhD in the 1970s, he was invited by Michael Harper to work at the Worcester Foundation, the “home of the oral contraceptive.”
Jordan arrived only to find that Harper had left for Geneva, leaving the recent graduate on his own. “I don’t know anything!” Jordan, professor of breast medical oncology as well as molecular and cellular oncology at MD Anderson Cancer Center, said at the time.
Harper was the co-patent holder of ICI’s experimental drug 46,474, which had failed as an oral contraceptive.
So, Jordan decided to work with what he had.
“‘Why don’t we turn ICI 46,474 into a breast cancer drug?’ There’s been one publication on that and it shows it’s as good as estrogen,” Jordan, who is also a member of the U.S. National Academy of Sciences and the National Academy of Medicine and an honorary fellow of the Royal Society of Medicine, said.
ICI 46,474 would later come to become known as tamoxifen, and Jordan’s work would change the face of breast cancer prevention and treatment for the next 30 years.
Recently, Jordan published a scientific memoir, “Tamoxifen Tales: Suggestions for Scientific Survival” (The Cancer Letter, May 27, 2022).
Jordan’s early animal studies with tamoxifen showed promise, and his career gained speed as he presented these results around the country. Jordan’s animal studies also showed that cancer in rats was hormone-dependent.
“You could take the ovaries out, the tumors would regress, you could take the ovaries out, put the carcinogen in, then they wouldn’t get tumors, because you needed estrogen to do that,” he said.
“So, I did studies on prevention for the first time, and did the first presentations at international meetings on that. What if we could prevent breast cancer? They hadn’t invented prevention at that time. So, you’re talking to a brick wall,” Jordan said. “Prevent breast cancer? Oh God, here comes Craig Jordan talking about tamoxifen again. Pretend you haven’t seen him.”
As his success grew, Jordan began establishing his “tamoxifen teams,” groups of young scientists who were trained by Jordan to perform experiments with tamoxifen—groups that later moved on and changed the understanding of biology in multiple institutions.
Jordan continues to advocate for young scientists. “The real philosophy is that young people have potential that is never realized because they’re in hostile environments with bad bosses. If you’ve got a bad boss, get out of there. He’s never going to change.”
Jordan’s career was varied. He had the opportunity to meet Diana the Princess of Wales when she attended a symposium at Northwestern University, while Jordan was the head of the breast cancer program at the Robert H. Lurie Cancer Center (The Cancer Letter, Feb. 5, 2021). After this meeting, Jordan kept up a correspondence with the princess, and after her passing was named the inaugural Diana Princess of Wales Professor of Cancer Research.
“I proudly held that title before other titles that I got in other universities.”
Jordan’s list of honors is extensive, and it includes the 2008 David A. Karnofsky Award lecture.
Thirty-eight years earlier, Jordan attended Sir Alexander Haddow’s inaugural 1970 Karnofsky lecture, in which Haddow noted that the tumors in some postmenopausal women who were treated with high-dose estrogen “melted away.”
“Haddow, in his Karnofsky lecture, said, ‘It’s really sad, because nobody’s particularly interested in finding out why this happens. It’s a very important observation for a few patients, but it’s not enough to make a difference,’” Jordan said.
“So, when I won my Karnofsky Lecture years later, I basically dedicated it to Alexander Haddow, and said, ‘We figured it out. We know why that happens.’”
Jordan credits his extensive, even photographic, knowledge of the scientific literature as a major factor for his success.
“You can make discoveries when you’re not anticipating them, you’ve just got to keep awake during the experiment to be able to say, ‘Now I understand something strange is going on.’ Let’s just go back in history.”
Jordan spoke with Alexandria Carolan, associate editor of the Cancer History Project.
A podcast recording of the conversation is available here.
Craig Jordan: Yes. I basically originally was going to do a PhD at the University of Leeds in crystallizing an estrogen and an antiestrogen with the estrogen receptor, which I was going to purify and do the x-ray crystallography, and that was going to be my PhD. Boring. Nobody cared. Antiestrogens weren’t used for anything at that particular time, but they had been discovered in the laboratory as being morning-after pills in rats and mice.
Fortunately, when they put the clinical trials in women, these were found to induce ovulation instead of stop ovulation. So, they weren’t contraceptives, but they are actually used to this day to induce ovulation, to make women who are having difficulty in childbearing to have a child and get fertilized.
Not big news, totally irrelevant to the idea of the oral contraceptive, which completely revolutionized everything and no company really wanted that.
So, out of my PhD came the realization that you couldn’t do what I wanted to do, irrespective of if we had good physical chemistry, x-ray crystallography. You couldn’t crystallize the estrogen receptor.
So, that was the end of that. So, I had to do a fairly boring PhD. But the reality was, when I came to have my PhD examined, nobody in the country wanted to examine my PhD. Everybody says “Who cares?” So, nobody said that.
So, here’s how chance takes a hand. I’d worked on a summer project at a company, ICI Pharmaceuticals, near where I lived in Cheshire, and I had a summer job there. I had met all of the people who were in the reproduction program, including Dr. Arthur Walpole.
At the time I was doing my PhD, now about four or five years later, the head of my department was the head of the cardiovascular program at ICI and he became a professor of the Department of Pharmacology. So, he asked Arthur Walpole if he would examine my PhD, because nobody in the country wanted to do that.
The university went berserk. You can’t have somebody from industry coming into these hallowed halls of academia examining our students. But there’s nobody else in the country.
Okay. So, I got it examined and then went off to America to do my BTA—Been to America. That was for two years.
I couldn’t find any way to go and do it until Arthur Walpole’s colleague, Michael Harper, said, “You can come to the Worcester Foundation,” which is the home of the oral contraceptive. He was now working on contraception from different points of view. But he was the co-patent holder of ICI’s experiment 46,474 with Arthur Walpole.
So, I get over to America and he says, “I decided to leave. I’m going to Geneva. You are on your own.” But I don’t know anything! “And now you’re on your own.”
So, I phoned up Arthur Walpole and said, “Why don’t we turn ICI 46,474 into a breast cancer drug?” There’s been one publication on that and it shows it’s a good as estrogen, because high-dose estrogen was used for post menopausal women before antigens came along. And just as an aside, my group discovered why that is. Nobody knew why estrogen would kill cancer cells, but we discovered all of that about 15 years ago.
CJ: This would be 1972.
CJ: So, it was a code name: ICI 46,474. And wasn’t on the market in America and wasn’t on the market in Britain. So, we had before Christ; BT—before tamoxifen. So, I saw the beginning if you like, but it wasn’t in the company. I just had ideas.
The company was not interested in breast cancer, so that’s the important thing. They were a reproduction company—very, very interested in that, and a whole variety of cardiovascular drugs, so this was not their feel-good zone.
CJ: Well, I was a cheap date.They were trying to get a company, ICI Americas, going. They didn’t have anybody to teach ICI Americas, you know, what to do and all of the rest of it. So, basically what they wanted to do is to give money for me to work on tamoxifen, to do the early studies on breast cancer. They didn’t do any of the early studies. They just gave me the money to do the studies.
And I was excited. I was going round to clinical trials organizations like the NSABP and the Eastern Cooperative Oncology Group speaking all about this.
I mean, I was famous in my own lifetime! I hadn’t got any publications. I had just done a few experiments, sort of self taught by pictures. And I learned all of the people in the business, all the people in clinical trials, and it became an advantageous thing to happen. The University of Wisconsin—I was at Leeds at the time, after I’d gone back—they offered me a position to come back to Wisconsin and set up a breast cancer program at the University of Wisconsin at the end of the 1970s.
CJ: For what I did with my animal studies, I showed that there were various animal models of how you could create mammary cancer in rats, okay? Standard models. And these were hormone dependent. You could take the ovaries out, the tumors would regress. You could take the ovaries out, put the carcinogen in, then they wouldn’t get tumors because you needed estrogen to do that.
So, I did studies on prevention for the first time, and did the first presentations at international meetings on that. So, you know what if we could prevent breast cancer? They hadn’t invented prevention at that time. So, you’re talking to a brick wall.
Because what do you know? Prevent breast cancer? Oh god, here comes Craig Jordan talking about tamoxifen again. Pretend you haven’t seen him.
So, the treatment of breast cancer I did next, and found that only mammary tumors that had estrogen receptors in them had a response to the tamoxifen. So, the principles I sort of developed in the early 1970s, back in Leeds before I came to America, were: number one, you needed the estrogen receptor in there; number two, it didn’t work if it was an estrogen-receptor negative tumor. And if you treat it early enough on a daily basis, you could prevent the tumors’ coming.
So, you could prevent things, you could target things. That really set what the whole of breast cancer with tamoxifen became for the next 30 years.
CJ: But in a suit! I was a snappy dresser. I had very catchy ties, not vulgar, but very English. And I could move into international conversations and, “Well, here comes Craig, he comes from England.” And so all that, what’s the word? Mystery.
So, all the things were put into place, and I then started making, for the next 40 years, “my tamoxifen teams.” I would move from place to place, given to opportunities to make a tamoxifen team from young, bright individuals.
And just as a sidebar, I’ve now written all of this down because The Cancer Letter has done a book review of my book. And Skip Trump did that. That really tells the story of these tamoxifen teams.
None of them knew anything either. It became a sheer leadership thing of, “Try this, oh, that didn’t work. Try that, that didn’t work. That did work, didn’t give us the right answer. What does it mean?”
And then it becomes a discovery. This was exciting stuff because nobody else was doing it, at all. And certainly, ICI wasn’t doing anything on it.
CJ: So, I came to the conclusion, “have brain, will travel.” And so, literally my first tamoxifen team back in Leeds, when I got back from America, between 19, Let me see.
What decade was that? So, the 60s, I was an undergrad, 70s… 80s… So, the seventies I was at the University of Leeds, okay? And then I had to wait for a visa to come to America. So, I went to Switzerland, set up a cancer thing called a Ludwig Group in Switzerland, which gave me access to flying all over the world, looking at all of these Ludwig Groups and teaching them about estrogen receptor assays.
And we were doing clinical trials on tamoxifen. One year of tamoxifen, pay attention to me. But they only did a year of tamoxifen. It didn’t do very much. Five years, it’s saving 30% of the lives of women. Totally different world. Totally different world. So, then I came to Wisconsin in the early 1980s and stayed there for about 13 years.
There, I got talent spotted to go down to Chicago at Northwestern University, and built a breast cancer program from scratch. And the clinical head of the program was Dr. Monica Morrow, who was, at that time, at the University of Chicago. So, the two of us worked as a team, me doing the breast cancer research, her doing all of the clinical interactions. And exciting times there, started winning prizes for tamoxifen.
I mean, just open the mail and these things are all coming down. “Oh, by the way, Craig, the chancellor would like to talk to you, of Northwestern University. People magazine wants you to organize the symposium because Diana, the Princess of Wales, wants to come to Chicago.”
CJ: Okay. And so, all of the tamoxifen workers come together now to get international attention. Not for me, but because Diana was coming. So, every TV station in the world was there and—sorry, I’m going to cry. It was very hard for me when she died, because I had been promised to have her support and when she died, Diana’s family agreed that I would be the Diana Princess of Wales, Professor of Cancer Research. And so, I proudly held that title before other titles that I got in other universities.
CJ: Yes. I met her. In my book, there’s a picture of me and Diana, the president of the university got Diana—and everybody wants to talk to her—and said, “Craig, you go talk to her there. We’ll have a couple of tough guys to keep everybody away. Get on with it.”
And we corresponded. In the ASCO Post, I had published my last letter from Diana, and I was Craig and she was Diana in our correspondence. So, very meaningful. And the whole royal family thing, because of all of the awards that I got from the British establishment for my tamoxifen work and for inventing a drug called SERMs, I’ve got more than you could ever imagine to be able to get recognized as the person most recognized for changing women’s health in Britain.
CJ: Oh, well they were very good because she was very curious about everything. But it’s like with the queen—the times that I’ve talked to the queen, you’re never allowed to tell what the royal family asked you questions about, because they don’t want them to get in the papers. So, I’m afraid my lips are sealed, both with the queen and with Diana.
Fantastic. Taking it back to tamoxifen a little bit—we went from the beginning work that you had there to then receiving these awards and communicating with Princess Diana and obviously it was a great success. What do you think was the turning point for you? Is there one moment or one study that sticks out in your mind as being the moment that broke the mold for tamoxifen?
Fantastic. Taking it back to tamoxifen a little bit—we went from the beginning work that you had there to then receiving these awards and communicating with Princess Diana and obviously it was a great success.
What do you think was the turning point for you? Is there one moment or one study that sticks out in your mind as being the moment that broke the mold for tamoxifen?
CJ: I think it’s a bit more complex than that. It’s complex only because one of the things that I found that I was very good at is creating the story of the research. I could get up and give a talk and I would hear senior people in societies say, “That was one of the best talks I’ve ever heard.” And I’m thinking, but I’m half the age of everybody in this group.
That was my key—I could get out and lead the audience through the story for people to be able to say, “Wow.” And that’s happened at least a dozen times in my life. And after those dozen times, I ended up with big awards. I passed the audition.
Because it wasn’t all about me. It was all of the pieces of the jigsaw puzzle, with these clinical trials and that clinical trial. It’s not my work, it’s how this teamwork of the academic community, both clinical—we put our pivotal things in—but how all of the clinical things fit, really like pieces into a jigsaw puzzle. And all of those clinical trials, either long-term tamoxifen therapy or doing chemoprevention with tamoxifen, they all came from rats and the principals still held.
CJ: So, with the establishment of tamoxifen—and it’s use in both pre- and postmenopausal women as a single agent—people, because it was being used so much, started to get concerned of what the harmful side effects may be, if we were treating women for half a decade, a decade, or whatever.
So, that became the next phase and it really was addressed by looking at animal experiments. We started off looking at bone density in mature rats to see if tamoxifen or a failed breast cancer drug, which became raloxifene, would cause a decrease in bone density. This would give us a red flag, for this might actually happen in women over a long time.
Simultaneously, we used raloxifene and we used tamoxifen to look at the inhibition of mammary cancer in our normal mammary cancer models. Was it doing something or not doing something in these long term experiments?
The big surprise was the fact that what we had and hadn’t anticipated, the prejudice we went in with, was that if estrogen is good for bone, then antiestrogen is going to be bad for bone. So, it would be a warning sign that you could get severe osteoporosis after years of treatment.
The animal experiment that we did in the 1980s basically demonstrated the exact opposite. In fact, it was so amusing that when I tried to publish these data and said, “Gosh, we’ve really found something interesting here,” we tried to put it into bone journals and they said, “You can’t publish this because it can’t be true. An antiestrogen can’t build animal bone in ovariectomized animals. It won’t work.”
We tried two different journals. And then, it got published in Breast Cancer Research and Treatment because we’d measured the tumors as well to see whether the anti-estrogen was able to block estrogen-stimulated growth.
Bottom line: what we found was there’s an estrogenic tickle inside what we now call selective estrogen receptor modulators that switch on and switch off target sites around an oophorectomized animal or a postmenopausal women’s body. Never seen before.
So, a whole new drug group got really discovered at that point, and this opened up a huge market. For example, the failed breast cancer drug that became raloxifene. Eli Lilly, about five years later, they reinvented it as preventing osteoporosis but preventing breast cancer in the same time in the same women. So, all of that was written down in the literature, and it presaged what happened within the pharmaceutical industry.
The second important thing is really discovery favoring the prepared mind. So, the whole idea that you can make discoveries when you’re not anticipating them, you’ve just got to keep awake during the experiment to be able to say, “Now I understand something strange is going on. Let’s just go back in history.”
The beginning of ASCO, the first Karnofsky Lecturer in ASCO was Alexander Haddow, and he got the award for having the first chemical therapy to be able to treat breast cancer. So, before tamoxifen, postmenopausal women that were at least five years after the menopause, they’d been estrogen starved. They were treated with high dose estrogen and some of the tumors just melted away.
So, Haddow, in his Karnofsky lecture said, “It’s really sad because nobody’s particularly interested in finding out why this happens. It’s a very important observation for a few patients, but it’s not enough to make a difference.”
So, when I won my Karnofsky Lecture years later, I basically dedicated it to Alexander Haddow, and said, “We figured it out. We know why that happens,” and he had in his paper all the requirements: they had to be five years after the menopause. If it was before the menopause, estrogen treatment for breast cancer didn’t work. So, they had to be estrogen starved for a period of time.
What we found in our experiments, in the laboratory, if you starve animals for up to five years and more, estrogen would make the tumors decrease. They start to disappear. If you started to treat after one or two years with the estrogen, they grow. So, it’s the estrogen starving and it’s how the tumor cells learn to survive in this estrogen starvation.
I liked to make the analogy that suddenly they’re all starving of the estrogen, and learned to grow without the estrogen, and then suddenly this tidal wave of estrogen comes in, but now it gives some super simulation of those cancer cells and they die. That became an important thing. But it also laid the groundwork of what was called the Women’s Health Initiative.
And the Women’s Health Initiative is a huge trial that was done by the National Cancer Institute, and what it was looking at was, does hormone placement therapy in women actually do anything? Everybody’s been giving it since the Second World War, but nobody’s actually documenting what it does, and what harm might it do, and does it do any good at all?
So, all the results came out periodically over the next 20 years, and the thing that I found fascinating was that with the hormone replacement therapy, everybody said, “Gosh, if we give hormone replacement therapy, what we do with estrogen and a synthetic progestin, medroxyprogesterone acetate, we get more tumors.”
Everybody says, “Well, we all know that’s what hormones do,” okay? Then, if you look at estrogen alone without any medroxyprogesterone acetate, it’s fewer tumors. So, everybody says, “Well, that’s interesting, but no idea.”
And I go, “Hello, I’ve got an idea that we can do in the laboratory,” and this is what we’ve found.
We’ve done a whole mode of experiments that we didn’t understand, but it took this huge, if you like, incompletely designed clinical trial on hormone replacement therapy to open the door to being able to understand. Medroxyprogesterone acetate is the standard progestin to stop the uterus in intact women from getting endometrial cancer from estrogen alone. So, that’s the important thing.
CJ: Yes, that brings us to the Women’s Health Initiative. Estrogen plus medroxyprogesterone acetate causes more tumors to grow. So, everybody says, “Well, that’s what hormones do, makes tumors grow,” and what we’ve done looking at the actual molecular biology of this whole process of estrogen killing tumor cells, what we found is that these have a big inflammatory response before the tumor cells died.
So, okay, hold that thought: inflammatory issue, don’t know what that means. And I spent a lot of time walking around the rivers around Washington trying to figure out why this happened. And then I remembered, back from medicinal chemistry when I was an undergraduate, that medroxyprogesterone acetate is not a pure synthetic progestin, not a pure compound. It has anti-inflammatory activity.
So, we documented all of this inflammatory activity with estrogen-induced apoptosis. So, we proposed that what was happening is the anti-inflammation quality of the medroxyprogesterone acetate has now stopped the apoptosis, and that would cause these tumors to grow.
So, that was the first hypothesis. Well, the second thing is, is it the medroxyprogesterone acetate that’s actually doing that because it’s a progestin? And we solved that. If it didn’t have glucocorticoid activity, it didn’t have the promoting effects of the progestin in these particular people. So, that is really the three different facets over 50 years of how we’ve taken a failed contraceptive that nobody cared about. Then, we take that failed contraceptive and then it gets turned into tamoxifen.
But it’s tamoxifen that’s no better than anything else at the treatment of advanced disease, but if we give long term therapy as an adjuvant, it keeps people alive. So, that was completely a breakthrough in modern medicine.
Millions of women are alive because of that. It will prevent breast cancer in women. So, they stopped getting second breast cancers. It’s a protective agent in multiple sites in the breast. So, that’s the benefit. Do you get the idea? That having this class of compounds that can switch on and switch off sites around a woman’s body so they can make bones stronger, you can lower your cholesterol, you can protect yourself against breast cancer.
It won’t protect you against endometrial cancer, but there are anti-estrogens now in the SERM category that will do that. Raloxifene is one of those. Tamoxifen isn’t. So, you have to keep checking that nobody taking tamoxifen is getting endometrial cancer.
Then finally, we can understand what huge clinical trials actually do to large patient populations to be able to make breast cancer go up and down. And it’s all to do with estrogen-induced apoptosis. So, these three different stages in the life of SERMS, or anti estrogens, or contraceptives—they started out as failed contraceptives—gives the 50 year story about millions of women that benefit.
CJ: Oh no, I knew about it. I was a PhD student when Alexander Haddow, in 19… It would’ve probably about ‘71, the first one, I read his Karnofsky Lecture and he said, “It’s a disappointment this and it’s a disappointment that, and it’s all very interesting stuff. And by the way, I don’t think cancer can ever be killed.”
That’s what he said. “It’s too much like human cancer. In bacteria, we can test their sensitivity by growing them on plates. We can’t do that in cancer. It’s just a lump of pathology.”
And I’m thinking, “God, this is a bit disheartening,” and reading all of that. But when I saw with my own eyes what estrogen could do in these estrogen deprived cells, I already had the Karnofsky data in my brain in that first lecture in ‘73. So, you have to prepare yourself as a young individual to learn all of the literature, whether it seems relevant or not, because it’s it’s called a discovery. You’ve just got to know what the building blocks are to get you to that point.
CJ: I’m awfully shy.
CJ: No. God, here’s Craig Jordan, talk about something else.
CJ: Well, it doesn’t come at the beginning obviously. So, I had to go to Northwestern to get talent spotted to go to the Fox Chase Cancer Center and be their director of research, and then go from there to be the director of research at Georgetown in Washington, and end up here at MD Anderson.
When I was thinking of retiring, I didn’t want to move back to Europe. My mother was elderly, I mean, lots of complications came in. So, I started putting things down at Georgetown, so that would be 10 years ago. So, I wrote one version and it then went through a metamorphosis about 10 years ago, when I came here.
I got a different perspective, I changed some things around. I got different stories I wanted to put in there and I wanted to focus on the young people, give them the opportunity to speak.
What was it like being in Craig Jordan’s tamoxifen teams? So, there’s about 10, 15 of those young people, whether they’re postdocs or MDs or whoever it is. How did this help you?
I had 10, but I’ve now got 12 scientific survival suggestions. So, a couple of other things leap up that you think you want to put in there. And a new chapter cropped up that was called “Invested in the Young,” because my mentor, earlier in my career, was Sir James Black, Nobel Prize winner. He worked at ICI, so there was that connection there. I’d been a summer student with ICI.
I mean, so everything’s a sort of little incestuous group but you don’t know it. Jimmy Black was one of my strong supporters before I left England and went to America. He invited me, at the age of 28, to be the chairman of pharmacology at his university. At 28!
CJ: And that came to revisit me, because when I got to Wisconsin, they were putting me up for an award from the British Pharmacological Society and they asked James Black to say something and I eventually saw what Jimmy Black’s letter was, which got me the award.
“I invited Craig to be the chairman of pharmacology at my university. He decided to go to America instead.” Full stop. That was it.
CJ: Well, I want to make some definitive points. The definitive point is: I was not destined to be the Craig Jordan of now. What I was, was keen and enthusiastic on chemistry. My mother allowed me to convert my bedroom into a chemistry laboratory. Not one of these children’s chemistry sets.
I’d steal things from school. I go round to the chemist, he’d sell me this, sell me that. I mean, nobody cared in those days. Now, you’d be a terrorist or something. So, a real chemistry set. My mother had a glass tabletop, and the drawers, the cabinets, walk in closets, were all put shelves in so they could have all of the different chemicals.
I’d be throwing burning things out of the window, ripping the curtains down, throwing them out of the window. It was never quiet. My mother used to say, “Well, at least we know where he is,” as in, “If he was doing this somewhere else he could die. At least we might catch it at times.”
It was this idea that I had not been the stellar student in my teams. I didn’t know how to research, I didn’t know how to seek out and train for an ambition. I didn’t know how my brain could be trained.
I learned those things and you have to fail to be able to understand the process. And I got one interview at one university in a pharmacology school at the University of Leeds, their medical school. And the man who was tutoring me had allowed me a laboratory at the school to teach chemistry to the other students, unsupervised. And I could teach university-level biochemistry there.
Those teachers had to come up with a smart eye-catching thing for the people who selected you for an interview. So, it started off, “Craig Jordan is a very unusual young man, period. A very unusual man in capital letters, exclamation point.”
I got one interview, in one university, and I knocked the ball out of the court. Didn’t know anything about physics, which I’d never done. So, they said, “If you do physics and you get the right grades for chemistry, you can come on a four year course, not a three year course. You’re going to have to make up chemistry.”
So, there were good people who chose Craig Jordan to succeed. I mean, this was quite unusual in those days. Because these people had been through the Second World War, and they knew what failure and death was all about, but we have to help young people. And they’d lived through it. So, they had to build a better brick. That’s where we are.
CJ: With great antagonism to authority. Do you want me to start?
CJ: So, my grandfather was an army officer in two world wars. And his house was a tribute, if you liked the British Empire, with the banners and the rifles and the pistols he’d got in his wars. I mean, it wasn’t a bad world then. Respectable people were allowed to house these weapons in their house. England was not considered to be a threat to anybody.
So, he said to me as I was growing up, surrounded by this panoply of empire, if you like, he said, “Have nothing to do with the army, nothing at all. But when the war comes, you had better be ready.”
Meaning you have to train yourself in peace not to be rifleman number three, going over the top of the trench to be shot right away. You have to put yourself with the right training to do things, to become indispensable, use your brain, whatever it is. Do not be killed in the first six weeks.
So, I went off to Leeds University officer training school, which stated, hanging on the door, “Want to sign up?” I signed up and everything. And then I was called back—mine’s a bit complicated—and they said, “You were born in America, of an American father, and you have American nationality. You are not eligible to be an officer in the British army. You resign immediately. Goodbye.”
So, without telling my parents, at the age of just 18, I contacted our family lawyer, and the family lawyer said, “But your stepfather adopted you as his son.” My mother’s second husband adopted me as a son.
“By British law, you cannot be denied any of the rights of being a British citizen, including joining the military.” So, he represented me. “I have a letter from the Home Office, which has all of this written down. That is the absolute proof that you did this.”
So, I got back in, went back into the OTC, went through my training all very quickly, and as you read it in the book, first training: nearly killed, nearly got killed.
Everything was really realistic. It was only by luck that I did not kill or be killed. By chance, by sheer chance. So, I’ve led that life where, now, towards the end of my life, and because of the circumstances I find myself in at moment, I feel I’ve been guided by forces I don’t understand, but we will call it God, to do the things that I’ve been asked to do, and to do them well.
So, when I’m a PhD student, I decide I’m going to get in and do what I can do. I’m a scientist. I’ve got a first class honors degree. I’m very, very good at organic chemistry. I will do everything I know about nuclear, chemical, and biological warfare to become an expert.
With my interview to get into the army, I could hear, through the door, these horrible words, “We better interview him anyway.”
Obviously, they were not my friends. I decided to attack and said, “I want to do all the nation’s nuclear, chemical, and biological warcraft.”
This is ‘69 at this point. So, I go and do this three week course, and come back. I found it really boring, with the young 18-year-old officer cadet from whence I had come, because they were really boring and I was now doing much more exciting things. I said to the people in the OTC, “Will you send me down to the intelligence call center down on Ashford and Kent? I’d like to explore the possible opportunities there.”
So, I went down there and there’s all these people in a big room from Oxford and Cambridge speaking Slavonic languages and Russian. Not me.
A colonel in his uniform comes up to me and says, “Why do you want to join the regular army in the intelligence corps?” To which I said “Absolutely not. I’ve got a first class honors degree. I’ve got a scholarship to do my PhD. I want to become the expert for Britain on nuclear, chemical, and biological warfare.”
Next week, the next two days, I’m sitting in the Ministry of Defense being interviewed by the deputy chief scientist who basically says, “If you pass security clearance to top secret,” and now everybody knows all of this is with Trump and all the rest of it, what you can see and what you can’t see, “then we will let you join this unit.”
So, that happened. Everybody’s a colonel. And on my 24th birthday, I became the youngest captain of the British army, because you couldn’t become a captain before a certain age.
I used to go off to places all over Germany, and couldn’t tell my family where I was. Everything was very secret to what I was doing. And then I got to go into the department, but you have to go to America, and you have to complete two years in America.
So, I got a passport that’s from my baby era from America, and I’ve got the British passport that is from my modern nationality. So, I called up the American Embassy and said, “My name is Dr. Craig Jordan and I want to go to America. I want to know, do I renew the passport that’s out of date from when I arrived here as a child, or the British passport that I can have being a British citizen? Oh, and by the way, I’m a captain in Intelligence School, top secret.”
“Well no, we are taking your nationality away from you if you stay as an officer in the army of a foreign power, especially with top secret clearance, because you can’t be trusted by us.” And I said, “I’ll give you that. Where do I go and give up my American nationality?”
So, I do all of that. Go over to America, do something very naughty, volunteer to become part of the Defense of New England.
So, I get my boss, the deputy chief scientist, to tell the Americans that I am a trained nuclear, chemical, and biological warfare officer, which they don’t have, so that I would be talking to Air Force One in the event of nuclear war.
Are you kidding? I mean, I’m 23.
CJ: I’m not being paid for this. So, I used to go to training. I trained everybody in the event of that, and then came back to Britain, having given up my citizenship, and wasn’t going to ever come back to America. But opportunity came. I came back to America and as luck would have it, America gave me my citizenship back.
Because after 9/11, I was called down to the federal office in Chicago and they said, “We’re all on the same side now, welcome back.” The British and Americans were now allies.
CJ: I didn’t apply.
CJ: Because there’s no book like it.
There’s no book that has written down what I did at five or six institutions, training dozens and dozens of young people, from nothing, everywhere that I went. How do you have the people skills, in my case, to be able to put these teams together and mold them into workable groups that move on and change medicine in multiple institutions? I mean, three times.
The queen said, that’s happening for international breast cancer research or for things for women’s health. Everything that I have, it’s not what I say, what we were taught in our schools. It’s the pieces of paper that say, what did you do? Not what you say you did, what third parties say you did. And what your superiors say you did. So, that’s the test. You have to be able to live up to what you say, but you don’t say it. Others say it and recognize it.
CJ: Well, the only other thing is, so how did you get into the toughest special forces regimens in the world?
CJ: A man banged on my door in a suit one day and he says, “You’ve got 30 seconds to answer this question. I need your help. I know everything about your background and everything. I know about the intelligence corps. Before I was in this regimen, I was in the intelligence corps. I need your help to defend the lives of my men behind Russian lines, should they invade West Germany in time of war. You’ve got 30 seconds.”
So, I now find myself among 1,500 of the toughest men in the world, and my job is to help keep them alive, so that we can keep Western Europe alive. My big asset was that they wanted: I’d done two years working with the Americans in New England with nuclear, chemical, and biological warfare there.
Therefore, I could relate to the American way of thinking because in reality I was. And the only thing that the SAS did for me: it made me incredibly proud to be able to serve Britain to such an unusual extent that could have helped the western world.
I’ve been thinking about the situation a lot in Ukraine and saying to myself, if this was 30 years ago, I’d already be involved as a research officer, because all of this was going to happen. You have to be there to start with.
CJ: No. The real philosophy is that young people have potential that is never realized because they’re in hostile environments with bad bosses. If you’ve got a bad boss, get out of there. He’s never going to change.
You have to know yourself and you have to know, what I put in my book, is that you have to know everything about your subject, whether it’s relevant at the moment. You’ve got to know who did what, where, why, and that’s what I did with antiestrogens. Never thinking they would ever be important, because who would care?
But then when I came to America, I met all of the famous people, and I could talk to them about every bit of the work that they had done in the whole of their careers. So, I’ve got a sort of photographic memory, if you like.
And they became my friends, even though they were 20 or 30 years my senior. They’re the ones who helped support me and talent spotted me, and I won prizes with many of them. I was the child and they were the grownup.
So, if Craig Jordan surrendered his U.S. citizenship in 1972 and lived as an alien in the land of his birth, how is it he is an elected member of the U.S. National Academy of Sciences and the National Academy of Medicine ?
That is one question that he answers in his autobiographical book “Tamoxifen Tales: Suggestions for Scientific Survival” (The Cancer Letter, May 27, 2022).
Selected excerpts are available here.