Filmmaker Joseph McCarthy

DATE August 8, 2001 ACCOUNT NUMBER N/A
TIME 12:00 Noon-1:00 PM AUDIENCE N/A
NETWORK NPR
PROGRAM Fresh Air

Interview: Dr. John Mendelsohn discusses recent developments in
cancer research
NEAL CONAN, host:

This is FRESH AIR. Terry Gross is on vacation. I'm Neal Conan.

Cancer may be the single most dreaded word in the English language. We all
know that medicine has made huge strides and that the diagnosis is not
necessarily a death sentence, but cancer is still the second-leading cause of
death in this country. And the most effective treatments--radiation, surgery
and chemotherapy--can be painful and debilitating. Now, though, a new
generation of cancer drugs is beginning to become available, smart drugs that
target cancer on a microscopic level with many fewer side effects.

Twenty years ago, Dr. John Mendelsohn helped create and develop one of the
most promising of these new cancer drugs. It's called C225, and it's in
phase III of its clinical trials. It's been shown to be effective with few
and relatively minor side effects. Dr. Mendelsohn is now president of the
M.D. Anderson Cancer Center in Houston, Texas. He's also a professor of
medicine there. And he serves on the board of ImClone Systems, the company
that's developing C225.

When Dr. Mendelsohn started his research 20 years ago, there was just a
handful of promising anti-cancer drugs in development. Today more than 400
are in the pipeline. I asked him what's changed?

Dr. JOHN MENDELSOHN (President, M.D. Anderson Cancer Center): Well, a lot has
changed, and it boils down to the fact that we understand the cause of cancer.
Cancer is caused by mutations or malfunctions in certain genes that regulate
the growth of cells. And if these are functioning improperly, the cells
either die or they grow at an incredibly advantaged way compared to the other
cells and become cancer.

CONAN: What about this process do we understand better?

Dr. MENDELSOHN: Well, we've got a catalog now. The genome project has
identified around 30,000 genes. And that's a great telephone book now with
30,000 addresses in it. So we know where each of these genes is located. But
we don't know what goes on at most of those addresses. We've got a lot of
work to do still. But we do know that about--estimated about 400 of those
genes are very important for controlling cell growth and cell proliferation.
And if one or two of those genes that control cell growth, out of that list of
400, is functioning improperly, the cell's in trouble. That might be if
you're driving your car and the foot brake doesn't work, and the steering is
very difficult. You can still use your hand brake and you can still stop and
save yourself. But if three or four of those genes that are critical are not
working, in your car, your accelerator is stuck down, your steering wheel
stops working and your brakes don't work, you're either going to crash, or
you're going to win the race, if the road's straight.

And that's really what happens in cancer. If three or four of those genes
that control proliferation are abnormally functioning, the cell either dies,
which is what we'd hope, or it goes on to become malignant. And now that
we've identified these genes, we have targets. Chemotherapy in the past was
using toxins and poisons that we were trying to tame and make useful for the
treatment of cancer.

CONAN: The treatment was almost as bad as the disease.

Dr. MENDELSOHN: Well, I wouldn't go that far, because it did cure the
disease sometimes. But the first anti-cancer agent came from mustard gas in
World War I. When the poor soldiers were dying because the mustard gas got in
their lungs, the doctors noticed that their white blood cell counts went down
before they died, and after the war, they tried to harness mustard gas, and
they created a drug called nitrogen mustard, which they could give in the vein
in a controlled way, and they used this to treat disorders of white blood
cells, and it was effective.

CONAN: Leukemia?

Dr. MENDELSOHN: Leukemia and lymphoma--especially lymphoma and Hodgkin's
disease, actually.

CONAN: Now when these cells stop working properly, is that because we've
inherited bad genes from our parents?

Dr. MENDELSOHN: Well, it's a very important question, because now that we
know that genes are the target, it doesn't mean that this is all a hereditary
problem. Genes can be abnormal for two reasons. We might inherit defects in
those genes, or we might acquire the defects in the genes from the
environment. And we believe that in the majority of cases, the abnormal genes
come from the environment, and we feel that about a third of all the
abnormalities that are created that cause cancer come from the carcinogens in
tobacco smoke, so it's a...

CONAN: A third.

Dr. MENDELSOHN: A third. We all quit smoking, one-third of all cancers
would go away. No more gene research, no more pharmaceuticals, just go away.
It's a very--it's the most important think I can say on this program. If
everyone quit smoking, one-third of all cancers would disappear.

CONAN: Now is this--you're now able to understand how this operates at the
molecular level, so as opposed to the broad stroke, the broad brush approach
of chemotherapy or radiation treatment, is this now the equivalent of a smart
weapon that zones in on precisely the right target?

Dr. MENDELSOHN: That's right. The big drug companies, the biotech companies
and all the academic institutions in the country are zeroing in and
collaborating, I think fairly effectively, to design targeted therapies that
will fix the problems that these 300 or 400 abnormal genes can create, and we
might replace the gene. The gene product is called a protein; we might disarm
that protein, or we might put in a protein that is more effective than the one
that's abnormal. There's a lot of different approaches to attack the problem
that any particular gene abnormality creates.

CONAN: In the past, cancer researchers have been incredibly reluctant to use
words like `optimism,' `breakthrough,' certainly `cure,' because of the
enormous weight that so many people put on this. There are so many people who
are so desperate for any kind of a cure, and we've all heard stories of people
going to Mexico to get Laetrile and all those other things. Yet now, people
are speaking in real optimistic phrases. Is this justified, in your view?

Dr. MENDELSOHN: It's justified, but it has to be cautious. This is not a
case of one big home run, one great discovery that will eliminate all cancers.
As I explained, there are probably 400 different targets that we're going to
have to develop anti-cancer agents that will affect. And it's usually a
combination of four or five of these targets that are abnormal that result in
cancer.

Now there's been one wonderful breakthrough that I'm sure you'll bring up, so
I'll bring it up, and that's Gleevec. It's a drug that treats chronic
myelocytic leukemia. That's a disease of the white blood cells and the bone
marrow that get out in the blood. Now in that particular form of cancer, we
believe that one gene abnormality is the cause of the cancer, rather than the
usual four or five that I mentioned; there could be six or seven. And so when
a drug was developed that could disarm the product of that particular gene
that causes chronic myelocytic leukemia, we had just striking results in
patients.

CONAN: You said an interesting thing: particular kinds of cancer. It's
important to understand that this is not one disease, but a lot of different
diseases.

Dr. MENDELSOHN: Right. I think the way we've thought about cancer in the
past is it's in the breast or it's in the lung or it's in the brain, and the
tissue where the cancer occurred was the target. Now we're thinking that
cancer can occur in any of those areas, but it might be some of the same genes
causing the cancer, whether it appeared in the brain or in the colon or in the
lung. The most common gene abnormality we've discovered so far--and `we' is
the collective scientific community...

CONAN: Sure.

Dr. MENDELSOHN: ...is p53, which was the molecule of the year in Science
magazine a few years ago, and p53 is abnormal in the majority of all cancers,
so we're treating p53 problem rather than colon cancer or lung cancer. Do you
see what I mean?

CONAN: Mm-hmm. And as you look at, for example, if I were a patient, you
would look at my disease on the molecular level rather than saying `There's a
spot on your lung. You've got lung cancer.'

Dr. MENDELSOHN: That's right. Stanley Hamilton is our new head of
pathology, and we recruited him here to set up a program where we're going to
do gene screening on all cancers from all patients, so when the path specimen
comes from Mrs. Smith's breast cancer and is sent to the pathology department,
in the past, we'd look in a microscope and we'd stain the specimen with some
dyes that were invented in Germany in the late 1800s, and we'd say, `This is
breast cancer,' or `It's not breast cancer,' and `It looks more aggressive' or
`less aggressive.' But in the future, a piece of that tumor will be sent to
the molecular pathology lab, rather than the microscope lab, and we're going
to get a list of the five or six genes that are abnormally expressed in that
particular patient's cancer.

CONAN: So if you're not devising, you know, ond single magic bullet that
will, you know, eliminate this entire range of diseases, are you convinced
that now you guys are on the right track, that this is the right approach, and
that this is just the beginning?

Dr. MENDELSOHN: I believe that very strongly, and I think the best analogy is
infectious disease. If you go back 100 years to the year 1901, Pasteur and
Koch and a lot of really wonderful scientists had determined that bacteria
caused some of the major diseases in our lives. The most common cause of
death in 1901 was pneumonia, and the second most common cause of death was
tuberculosis. And at that time, we'd identified the cause. Now it wasn't a
list out of 400, it was a list--pneumonia, there were half a dozen bugs that
caused most pneumonias, and tuberculosis, it's one kind of tuberculosis germ,
although it can deviate and get resistant.

And once that had been discovered, science got busy and said, `Let's make
targeted chemotherapy against those germs. Now that chemotherapy's called
antibiotics, and today, if you get pneumonia you go to the doctor and you
cough onto a plate, and the next day, a report comes back and tells the doctor
which germ caused your pneumonia, and in most cases--the cases of viruses we
don't have good treatment yet--but in most cases, which are bacterial, the
report tells you which antibiotic will work against that germ, and you treat
it, and pneumonia's no longer the first cause of death. It's down the list,
and tuberculosis is off the top 10 because we have specific treatments.

We'll never get rid of those diseases, but we've reduced their burden on
public health, and the same thing, I think, will be happening in cancer. It's
more complicated; the list is 400, we believe, and we could be off a bit, and
any one cancer has a number of genes that are malfunctioning, so we're going
to need a cocktail of targeted treatments to treat the cancer.

CONAN: My guest is cancer researcher Dr. John Mendelsohn. We'll be back
after a short break. This is FRESH AIR.

(Soundbite of music)

CONAN: I'm speaking with Dr. John Mendelsohn, president of the University of
Texas M.D. Anderson Center in Houston.

And, Dr. Mendelsohn, this is a story of these new cancer drugs that you,
amongst many others, are developing, that seems to involve--well, yes, bold
and innovative research, but bold and innovative entrepreneurs as well. Tell
us the story of C225.

Dr. MENDELSOHN: Well, back in 1980, I was on the faculty of the University
of California-San Diego, working with a colleague named Dr. Gordon Sato, and
at that time we were studying the epidermal growth factor receptor. Now just
briefly, there's--on the surface of cells, there are receptors that are like
locks, and around the cells there are stimulators of those receptors--those
are called growth factors--that are like keys. And the analogy I make is if
you get into a car, you got to put a key into the lock and turn the ignition,
and that sends a signal, an electric signal, that starts the motor and puts on
your power brakes and your power steering and the lights and everything goes,
but if you don't put that key in that lock, nothing happens. The same thing
controls the growth and proliferation of cells. There's locks on the surface
of the cell, and there's keys.

The locks are called receptors and the keys are called growth factors. What
we knew in 1980 was that there was--from the work of Dr. Stanley Cohen, who
won the Nobel Prize for this, we knew that there was a very important lock
called the epidermal growth factor receptor, and there was a key called
epidermal growth factor. So we had also learned from the scientific
literature that there were cancer cells that expressed very high levels of
this receptor, and...

CONAN: Now when you say that, you mean that this chemical shows up in excess
amounts when you've got a certain kind of cancer.

Dr. MENDELSOHN: Right. It turns out, many kinds of cancer. The data
subsequently have shown that in about one-third of all cancers there's huge
numbers of these locks on the surface of the cell, and, Dr. George Tedaro(ph)
and Dr. Michael Sporn published a paper in 1980 summarizing exciting data
showing that cancer cells produce their own keys, so the cancer cell produces
the key--epidermal growth factor. It excretes this key outside the cell, the
key latches on to the lock and turns the ignition, and the cancer cell
autostimulates itself to proliferate.

Now normally that key doesn't come from the cell. It comes from the
environment. You get a cut on your hand, the epidermal growth factor is
carried in in the bloodstream, and it stimulates the cells to proliferate and
your wound heals, and as everything heals up, the epidermal growth factor goes
away, and the cells stop dividing. But in the cancer case, there were models
that we had developed--we and others, many others, had done this; Dr. Tedaro
led this--had shown that cancer cells make their own keys and autostimulate
themselves.

So we decided we'd try to block this process by essentially creating a piece
of chewing gum that would stick into the lock so the key couldn't get in. And
we created an antibody to do this. It was called 225. It was the 225th
antibody we studied out of thousands. And this antibody binds to the
epidermal growth factor of the receptor the way antibodies bind to all kinds
of molecules. But we selected one that would bind to the very site where the
key goes in and blocked the function of the key. And that's why there's such
a variety of new drugs coming along. I mean, just attacking the epidermal
growth factor receptor, there are at least a half a dozen approaches now that
are all competing and looking in patient trials to see which will turn out to
be the most effective.

CONAN: Now yours turned out to be a terrific idea. But from your
description, this really does fit Thomas Edison's description of 99 percent
perspiration and 1 percent inspiration.

Dr. MENDELSOHN: Well, it was a lot of work to find this antibody. But I
think it was a confluence of information coming from many different scientists
that led to this idea. And I think it shows that science, from many different
directions--I mean, nobody would have guessed when epidermal growth factor was
discovered--it was discovered 'cause it helped the maturation of teeth in
embryos. OK. That's really pretty far away from cancer.

CONAN: Yeah.

Dr. MENDELSOHN: And Stanley Cohen worked on this. It was sort of far
outfield. Nobody really knew how important it was until 15 years later. And
by 20 years later he won the Nobel Prize for his work.

CONAN: Now as we pick up the story of C225, this new company ImClone Systems
is beginning production of it. What kinds of cancers does it attack, and how
successful is it?

Dr. MENDELSOHN: Well, ImClone has produced an awful lot of this antibody.
We've treated over 500 patients now. Well, answering your question, it turns
out that about a third of all cancers express high levels of EGF receptor.
Now we've concentrated on head and neck cancer, where 90 percent of the
cancers or more express high levels of EGF receptor. And we've looked at
advanced bowel cancer. That's in the colon and the rectum. And in that case,
probably a third to a half of the patients expressed high levels of EGF
receptor. And we've looked at pancreas, where the majority of patients
express high EGF receptor levels. But this could be relevant in lung cancer
for well over half. It could be relevant in about 20 percent of breast
cancers and 30 or 40 percent of ovarian cancers, in advanced prostate cancer,
in bladder cancer. So it doesn't matter where the cancer is. What matters is
if that cell depends on the EGF receptor as its key ignition to stimulate
proliferation.

CONAN: And how effective is it?

Dr. MENDELSOHN: Well, the initial trials have shown safety. And last May it
was at the meeting of the American Association for Cancer Research, three
clinical trials were reported looking at combining antibody C225 against the
EGF receptor with chemotherapy in head and neck cancer and in colon cancer and
in pancreas cancer. And in all cases, we were able to show that adding the
antibody increased the efficacy.

Now this isn't 100 percent, and the tumors didn't shrink forever. Some of
them were still responding, but some of the tumors escape. But this was proof
of principle, and this is how it works. You're taking advanced cancer, only
you're doing something with a new drug. This is proof principle that adding
C225 to chemotherapy can obviously improve the effect of chemotherapy alone,
'cause the patient served as his or her own control. They were finding the
tumor was growing. The tumor was responsive to the chemo. It had responded.
It was now escaping it. And then when we added the C225 again, the tumor was
responding.

CONAN: When this comes out, if it's as promising as you believe it will be,
who's going to make the money?

Dr. MENDELSOHN: Well, ImClone and its investors will make money.

CONAN: Among whom, we should say, are you.

Dr. MENDELSOHN: Well...

CONAN: You're on the board of ImClone Systems, right?

Dr. MENDELSOHN: I'm on the board. I joined the board of ImClone in 1996, as
I remember, and they have given me some stock options, so I do have way less
than 1 percent of the company, but I do have some interest. And I must say
that because of this, I am not treating any of the patients. I don't believe
that someone who has a potential financial gain from an experimental therapy
should be the person that's treating a patient. The patient has to feel that
there's no even possible conflict of interest and their health has to be the
primary thing. So that's why I've held back. But the University of
California owns the patent, and they will get funds through the license
agreement. And I think the money will go to those that have taken the risk
and have put up the capital. ImClone has invested well over $100 million, and
it probably will be $200 million in this project by the time everything is
signed and sealed.

And we don't know yet that this is going to be an approved drug. I want to
emphasize that. C225 is still an experiment. Obviously, the fact that we're
talking about it together is because there have been very exciting data
showing that it seems to be working well. But you haven't crossed home plate
until you cross home plate. So this is still an experiment, and the people
that are investing in this still are taking some risk.

CONAN: Dr. Mendelsohn, thank you so much. And I think on behalf of everybody
listening, good luck.

Dr. MENDELSOHN: Well, thank you very much. And you know you're wishing good
luck to thousands of investigators that are exploring these new approaches to
cancer diagnosis and treatment.

CONAN: Dr. John Mendelsohn helped create and develop C225, a cancer drug
that's currently in phase III clinical trials. He's president of the M.D.
Anderson Center in Houston, Texas, and a professor of medicine there.

Coming up in the second half of our show, an actor dodges taxis and buses to
re-enact the Revolutionary War's Battle of Brooklyn.

I'm Neal Conan. This is FRESH AIR.

* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *

Interview: Director-producer Joseph McCarthy talks about the making
of his new movie "The Brave Man" and about the Battle of Brooklyn
NEAL CONAN, host:

This is FRESH AIR. Terry Gross is on vacation. I'm Neal Conan.

Two hundred twenty-five years ago this month, the fledgling forces of
rebellion and an army of British professionals in the first pitched battle of
the American Revolution. It was very nearly the last. After the Battle of
Brooklyn, George Washington was lucky to evacuate his outnumbered and
inexperienced army across the East River to Manhattan. The key point on the
battlefield in Brooklyn was a stone house at a crossroads. In their first
taste of battle, a small group of soldiers from Maryland assaulted that house
three times. They couldn't hold it, but their gallant fight gave the rest of
Washington's men time to escape. The American army would live to fight
another day.

The Marylanders were led by General William Alexander, also known as Lord
Stirling. That largely forgotten commander and this neglected battle are
the subject of an unusual new movie called "The Brave Man." Here's an
excerpt.

(Soundbite of "The Brave Man")

Mr. GRAEME MALCOLM (As General Alexander, Lord Stirling): Our morning
started right about here at 4:00 AM, dawn, long before this became Greenwood
Cemetery. The date was August 27th, 1776, a Tuesday, just six weeks after
the Declaration of Independence had been read in Philadelphia. A British
fleet of more than 400 ships, including 30 ships of war, had gathered in the
harbor of Staten Island. Two days previously, thousands of redcoats had
crossed the narrows to Bay Ridge out there. When he heard, General Washington
reinforced the heights in Brooklyn back up that way to 10,000 men. This place
was called Martin's Pass(ph) back then. A track called the Shore Road
crossed it, parallel to the harbor on its way toward Brooklyn. Originally, it
had been an Indian trail. And now we call it Fourth Avenue.

CONAN: Actor Graeme Malcolm, who stars first as the narrator and gradually
evolves into the character of General Alexander, Lord Stirling. The writer,
producer and director of "The Brave Man" is Joseph McCarthy. He joins us from
NPR's bureau in New York.

Welcome to FRESH AIR.

Mr. JOSEPH McCARTHY (Director, "The Brave Man"): Thank you very much. I'm
glad to be here.

CONAN: When Graeme Malcolm points down Fourth Avenue, what we see is Fourth
Avenue. And later, as General Alexander, we see him dodging buses and taxis
as he moves his men around the battlefield. Why did you decide to set a
costume piece about the American Revolution in the streets of modern Brooklyn?

Mr. McCARTHY: Well, first off, I didn't have enough money for the 32,000
actors we'd need for the British side and 12,000 people we'd need for the
American side. And I guess I was interested in the way we see history. I
realized, as I walked down Fourth Avenue in the midst of working on another
film that you could actually see the landscape of the battle even in this
highly developed, urban environment. I mean, this was the first suburb and
this had been farmlands for New York. And now it has totally evolved into a
semi-industrial area. So, still, when you look down from the tops of the
small hills, you can see the valleys where the streams must have been. And I
realized that when you walk around Brooklyn, you can actually see the history
still there.

CONAN: You not only use Brooklyn, itself, as itself, you use toy soldiers,
kids riding on bikes to act as cavalry, a fleet of red rental cars as
standing in for the British army. This is all--you know, this is all pretty
experimental.

Mr. McCARTHY: I was trying to move from the present to the past. I was
trying to carry my audience with me. And I think I had the privilege, in a
certain sense, to substitute representations of equal power. So when the
narrator is looking out toward the British lines, which were approximately
down at 33rd Street and Fourth Avenue, he saw a red line of men--5,000 men
lined up against him. How could I represent that kind of force on the
streets today? And I decided that I could rent 16 red cars, line them up
across Fourth Avenue--which, if you're a Brooklynite, you know is not a
trivial undertaking--and have them lie, I guess, looming, waiting to attack.
And I felt that that would properly represent what we saw.

The same with the bicycles. He's still in modern dress. The British were
attacking on the right. I felt that a group of kids on--with red shirts
on--actually, you can't see it, but they're wearing Grant's Lobster
Shack(ph)--General Grant was the general of the British army--T-shirts. And
they come swooping around to the right. And that was a sense of what was
happening. That--so we're trying to move between the present and the past.

CONAN: I'm intrigued that in such a short film--and it's only 33 minutes
long--you do manage to bring out the character of your star, General William
Alexander.

Mr. McCARTHY: Well, thank you. I was trying to. And I guess I have to
credit Graeme Malcolm a great deal for helping to make that work. He really
took the words and made them his own. He--you see a man being revealed,
slowly. He starts out, arms length and distant. And you realize he was a
very substantial individual in the colonies. He'd at one time could probably
have been described as the richest man in America. And he pretended to
be--not pretended, but in the English sense--pretended to the earldom of
Stirling in Scotland. And he had distant connections that made that real. He
pursued that inheritance, which would have given him half of Long Island, most
of Maine and all of Newfoundland for 10 years and, essentially, bankrupted
himself. So when he goes into his battle, he's busted. He's living on the
imperiousness of his good name. And I think that's one of the motivating
forces that I was looking at when I found what I think is the answer to why he
decided to attack the British at that moment.

CONAN: Did you come to an answer to that question as to why this man decided
to go into battle against what he and, I'm sure, a lot of other Americans
still regarded as his king?

Mr. McCARTHY: It's complicated and I think there were a lot of reasons, but
I think there was real frustration. He'd pursued this inheritance, which, by
the right of primogeniture, should have been his in England for a number of
years. And finally it simply was not accepted. The Parliament chose not to
deal with it and, you know, this land grant had been given in 1604 and by
1773, there--the land was fully developed and there was no need for them to
have a--some nobleman claiming all the return on this investment. So I think
he was really frustrated and I think he was a man who had had a number of
failures in his life and this opportunity presented itself. He had the men.
The Marylanders were young men, age 15 to maybe 25, who had been training.
The militiamen were required to train once a year. And apparently these
young men were wealthy enough to afford real uniforms and they had modern
muskets. And they were trained in European fighting techniques and Stirling
found himself with them and with a responsibility and he accepted it.

CONAN: He also had a strong idea of what they were fighting for and the crux
of the battle and the crux of your film is a see-saw battle over a stone
house. Each side attacked, in turn; the 400 Marylanders steadily
whittled, as the much larger British numbers began to tell. The last charge,
the third charge, of the Marylanders--and, again, let's hear Graeme Malcolm,
the actor, as General Alexander.

(Soundbite of "The Brave Man")

Mr. MALCOLM (As General Alexander, Lord Stirling): Now, Marylanders, now is
the time to take what is ours. Prepare to charge. We will take that house
because it is ours! It does not belong to them. We have made this land.
We have cut these roads. We have built these houses. Charge, men, and take
it from them!

(Soundbite of rushing crowd)

Mr. MALCOLM (As General Alexander, Lord Stirling): Our charge caught them by
surprise as they were reloading. We drove them out of the garden. One group
entered the house and soon the redcoats they found inside were pushed from the
upper story windows and we killed them on the ground. Again, we found the
cannon loaded and turned them on the fleeing British. Through the cannon
smoke I could see General Cornwallis watching from a distance. Behind him,
rank after rank of fresh soldiers stood.

CONAN: General Alexander, as Stirling, was captured in the battle.
Actually, he surrendered.

Mr. McCARTHY: Oh, that's true. And then he was marched off and sat on
Admiral Howe's ship for six weeks, after which he was traded back to the
Americans for the governor of Florida and the Bahamas.

CONAN: It's quite common in those days for the opposing commander to be
offered the hospitality of his opponent's table.

Mr. McCARTHY: Very much so. He was--well, he knew a number of these people
from his pursuit of his earldom. And he would have fit in perfectly
comfortably. I mean, part of the reason we chose Graeme was his wonderful
Scots-British accent.

CONAN: Mm-hmm.

Mr. McCARTHY: And one of the things I hoped is that people would understand
that these were part of the same country. This was, in a certain sense, a
civil war. They were--they knew each other. Stirling knew Cornwallis.
Stirling had listened to Grant. They were part of the same country and it was
a big deal for them to break off.

CONAN: Our guest is filmmaker Joseph McCarthy. He's made a short film about
the Battle of Brooklyn called "The Brave Man."

We'll be back after a short break. This is FRESH AIR.

(Soundbite of music)

CONAN: My guest is Joseph McCarthy, writer, director and producer of the
short film "The Brave Man."

What was the significance of this particular battle, in your view?

Mr. McCARTHY: The first significance is Stirling Alexander stopped the
British. I like to say that it was like a--he was like a traffic accident on
the Brooklyn-Queens Expressway. The British were--the British--you've got to
understand this. Yes, he recognized 15,000 men coming from the backside that
was totally undefended, but those men were coming up a road that was the width
of a wagon with forests on both sides. So when he hit the front, Cornwallis'
advance, there, the grenadiers--I think there were 2,000 men--it stopped the
British army. And when an army stops, what does it do? It sits down. Then
once--to get an army started of that size takes a long time. Howe and
Clinton, who were the British generals, had hoped to arrive at the early part
of the day at the foot of Brooklyn Heights and overwhelm the 12,000 Americans.
I guess there were 9,000, because 3,000 were in the field at the time. But
because of the action of these men, he was unable to do that.

And then Washington was so impressed with what Stirling's men had been able to
do, he thought he'd stand and fight the best army in the world. Other minds
convinced him over the next day and a half that maybe being stuck with your
back to the water with the largest fleet in the world potentially being able
to come up the river behind you with the best army in the world in front of
you wasn't the best place to be. And he pulled off the most miraculous
escape, retreat that, I think, most--it's comparable to Dunkirk; that people
have not heard of anything like this before.

CONAN: With the great assistance of the men of Marblehead, the fisherman and
sailors.

Mr. McCARTHY: Yes, very much so. They--and people from up and down the East
River, who contributed their boats and their own skills, too. The
Marbleheaders, apparently--there's a description of one of them who crossed
the East River, which is nearly a mile wide, 20 times with boats loaded up to
the gunnels. Washington was able to get 9,000-plus men off Brooklyn Heights
with their supplies, with their weapons and their horses over the course of
the evening. Howe arrived at the Heights the next morning to find the embers
of the watch fires that they'd kept going throughout the night while they
stealthily sneaked across the river. I mean, it's just an amazing story.

CONAN: As you mentioned, the Howe brothers had arrived in New York with a
huge fleet and a huge army. Clearly, they hoped that this display of
overwhelming power and maybe one short, sharp shock would convince the
Americans to give up the rebellion. Despite the best efforts of General
Alexander and the Marylanders, they did quickly chase George Washington off
the Brooklyn Heights and onto Manhattan and chased him away from their
further. Why didn't that one short, sharp shock have the desired effect?

Mr. McCARTHY: Well, I think Washington survived with 9,000 men and his gear.
I think there is some sense that the Americans were heartened by the
resistance that Stirling and the Marylanders put up. I think, in a certain
sense, that they were not defeated. They were defeated in the Gowanus
Valley. But a strategic retreat is a perfectly legitimate, military
tactic. And that's what happened, was he pulled off a strategic retreat,
moved to Manhattan. There's a story that the Americans were marching up
Bloomingdale Road, which we now call Broadway, as the British were marching
down the Boston Post Road, which is Third Avenue. And there was forest in
between them as they--I mean, you may have to live in Manhattan to really get
this, but it would be--there were lots of trees and the two armies couldn't
see each other, so the Americans escaped north. I think their first fire
fight was up about 110th Street when the Americans were--resisted the British,
who were chasing them.

CONAN: Joseph McCarthy, we see an awful lot of Revolutionary War
battlefields memorialized at Saratoga; certainly Yorktown, Bunker Hill. What
happened in Brooklyn?

Mr. McCARTHY: Commerce. If you read Mike Wallace's book, "Gotham," which
everybody sees as daunting; this 1,400-page history of New York. But it's
really not. It's just a great read. You realize that New York was really
founded as a commercial enterprise, and it still is. That's the driving
force in the--this land where the Marylanders and the rest of the men who died
in the Gowanus Valley were buried in long, open pits, were--was described in
the deed for that land as a national treasure. And this la--and it said that
this land should not be built upon. But the--Mr. Litchfield, whose house
sits up in Prospect Park, bought the land down the hill from him along the
Park Slope and down to the Gowanus Valley and developed the whole area. You
see it now as sort of flat and paved and very urban, but at the time that this
battle was fought, it was rocky, hilly hillside with ravines and the farms
were along the side of an inlet called the Gowanus Creek.

CONAN: Far wilder than the rather--you know, the tamed views of Prospect
Park.

Mr. McCARTHY: Well, you can see the original landscape in Greenwood
Cemetery. The Greenwood Cemetery and Park Slope and Prospect Park and that
whole area, are the terminal moraine for the last Ice Age. And creeks and
springs ran down the side of this and it was just--it was really hilly. So
they scraped the tops off the hills and filled in the ravines. And that's how
you wind up with the beautiful Brownstone neighborhood, Park Slope.

CONAN: Joseph McCarthy's film is "The Brave Man."

Thanks very much for speaking with us.

Mr. McCARTHY: It's a pleasure to be here.

CONAN: A re-enactment of the Battle of Brooklyn will be held in Prospect Park
later this month. For more information on McCarthy's film, log on to his Web
site, www.thebraveman.com.

Coming up, a tribute to Mississippi John Hurt. This is FRESH AIR.

(Soundbite of music)

* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *

Review: Tribute album "Avalon Blues"
(Soundbite of "Stagger Lee")

Mr. MISSISSIPPI JOHN HURT: (Singing) Police Officer, how can it be? You can
arrest everybody, but cruel Stagger Lee. That bad man, oh, cruel Stagger Lee.

NEAL CONAN, host:

That's Mississippi John Hurt from a 1928 recording of his song "Stagger Lee."
Hurt faded into obscurity until he was rediscovered as a blues elder in 1963.
He recorded again and performed on the folk revival circuit until his death in
1966. A new tribute album shows that his appeal cuts across styles and
generations. Music critic Milo Miles has a review of "Avalon Blues."

(Soundbite of song)

Unidentified Singer #1: Well, make me a damn pallet on your floor. Make me a
damn pallet on your floor. Make me a pallet, down soft and low. Make me a
pallet on your floor.

MILO MILES reporting:

On the surface, everything about Mississippi John Hurt suggests he is just a
homespun entertainer eager to please. He spent most of his life as a hard
scrabble farmer and this blues musician stuff was just a bonus. But, in
fact, everything about Hurt's music is sneaky; the way he tells a story, the
way he finger picks guitar, the way he varies his themes. Sex, religion,
good food and bad breaks all creep in through the back door. No surprise
that the album "Avalon Blues," a tribute to Mississippi John Hurt, includes
covers by performers as diverse as Beck, Ben Harper, John Hiatt, Lucinda
Williams and Steve Earle, who does Hurt's most well-known tune.

(Soundbite of song)

Mr. STEVE EARLE: (Singing) Will all you ladies gather round good, sweet
candy man, candy man. Oh, candy man. Got a stick of candy that's nine-inch
long, sell as fast as ...(unintelligible). Candy man. Oh, candy man.

MILES: So you know the drill. The big names are meant to hook fans who know
nothing about Mississippi John Hurt, but "Avalon Blues" is more sprightly
and varied than many tribute projects. Because Hurt performed almost
exclusively solo, hearing his songs with more instruments is always a treat.
A masterful player like Chris Smither demonstrates how much press juice you
can get out of a straightforward rendition of "Frankie & Albert."

(Soundbite of "Frankie & Albert")

Mr. CHRIS SMITHER: (Singing) Frankie was a good girl, everybody knows. She
paid a hundred dollars for Albert to have a suit of clothes. He's a man;
ain't doing her wrong. Frankie went to the...

MILES: Victoria Williams, on the other hand, howls her way through "Since
I've Laid My Burden Down" in her best crazy-lady fashion. I think it's a
highlight of the album because it will offend the sensitive and tasteful
crowd, who enjoy John Hurt's decorum entirely too much.

(Soundbite of "Since I've Laid My Burden Down")

Ms. VICTORIA WILLIAMS: (Singing) Glory, glory, hallelujah, since I laid my
burden down. Glory, hallelujah, since I laid my burden down. No more
sickness. No more sorrow, since I laid my burden down. No more sickness.
No more sorrow since I laid my burden down.

MILES: "Avalon Blues" works fine as either an introduction to Hurt or as a
supplement to the original music. A generous selection of his 1960s work
appears on the album called "Rediscovered." But I wouldn't want to be
without his early side from a CD also called "Avalon Blues," but subtitled
"Complete 1928 OK Recordings."

(Soundbite of song)

Unidentified Singer #2: Ms. Collins weeps. Ms. Collins mourns to see her
son who is leaving home. The angels laid him away. The angels laid him away.
They laid him six feet under the clay. The angels laid him away.

MILES: Dick Waterman was Hurt's manager after his rediscovery and it seems
right to end by quoting this anecdote from Waterman's liner notes in "Avalon
Blues." Waterman was introducing Hurt at a college concert.

"I talked about his having been rediscovered in Avalon, Mississippi, by Tom
Hawskins in 1963. I talked about how he had made a sensational appearance at
the Newport Folk Festival shortly after that. As I talked on and on, I kept
glancing from side to side, expecting John to appear any time. I finally
looked up into the balcony and there was John sitting in the front row with
his face in his hands on the railing looking down at me. `John,' I sighed.
`You can't play from up there. You have to come down here.' After the show I
asked him why he had sat up there while I was talking so long. `Well, now,
Dick,' he said. `You got to be saying such nice things about me that I didn't
want to do nothing to cause you to stop.'"

CONAN: Milo Miles lives in Cambridge. He reviewed "Avalon Blues," a tribute
album to Mississippi John Hurt.

(Production credits)

CONAN: For Terry Gross, I'm Neal Conan.

(Soundbite of "Stagger Lee")

Unidentified Singer #3: Police Officer, how can it be? You can arrest
everybody, but cruel Stagger Lee. That bad man, cruel Stagger Lee. Billy
Lyons told Stagger Lee...
Transcripts are created on a rush deadline, and accuracy and availability may vary. This text may not be in its final form and may be updated or revised in the future. Please be aware that the authoritative record of Fresh Air interviews and reviews are the audio recordings of each segment.