Monthly Archives: July 2004

Susan T. Buffett, 72, Dies; Wife of Billionaire Investor

  • 7/30/2004
  • Cody, WY
  • By Matt Schudel
  • Washington Post

Susan Thompson Buffett, 72, the wife of billionaire investor Warren Buffett and, in her own right, the 17th richest woman in the world, died July 29 of a stroke while visiting friends in Cody, Wyo.

She and Buffett, whose net worth of about $41 billion makes him the second richest man in the world after Bill Gates, were married in 1952 but had lived apart since 1977. Her primary residence was in San Francisco, while he stayed in the house they had bought together in Omaha in 1958. They remained on friendly terms and often traveled together. Warren Buffett was with his wife at a Cody hospital at the time of her death.

Mrs. Buffett was a director of Berkshire Hathaway, her husband’s holding company, and was president of the Buffett Foundation, which has contributed millions of dollars for education, medical research, population control and other charities. The foundation was criticized by abortion protesters in the 1990s for funding the RU-486 “abortion pill” and groups supporting abortion rights.

She was known for her progressive views, had worked for civil rights and volunteered to help people in low-income housing. In evaluating organizations for possible contributions, Mrs. Buffett told the Omaha World-Herald last year in a rare interview, she sought people “who have heart and soul, the ability to organize and also to inspire — a rare combination.”

Her shares in her husband’s company have a current value of about $3 billion, which made her, according to Forbes magazine, the 68th richest person in the United States.

Last week, Mrs. Buffett and her husband contributed $6 million to five California doctors for the study of mouth cancer. In October 2003, Mrs. Buffett was diagnosed with mouth cancer and underwent surgery, radiation therapy and facial reconstruction. She had recovered enough to attend the annual shareholders’ meeting of Berkshire Hathaway in May, leading singalongs at cocktail parties.

She also attended her granddaughter’s graduation this spring from her alma mater, Omaha Central High School. She donated $5 million to the school two years ago for a new stadium and had given to many other institutions in her home town, as well.

Like her husband, Mrs. Buffett was born and raised in Omaha. Her father was a college professor and dean. Though their parents were acquainted, she did not meet Warren Buffett until her roommate at Northwestern University — his sister, Roberta Buffett — introduced them.

She occasionally performed as a cabaret singer and, in 1977, had a one-night performance at an Omaha theater. Soon after, she left her husband and moved to San Francisco, saying she wanted to pursue her singing career. She performed in New York and released several CDs. According to Roger Lowenstein’s biography, “Buffett: The Making of an American Capitalist,” her husband was heartbroken by her move. Since 1978, he has lived with Astrid Menks.

In a rare interview in 1999 with the Omaha World-Herald, Mrs. Buffett described herself as a “geriatric gypsy,” saying she spent only 20 percent of her time at her home in San Francisco.

She had been in line to inherit her husband’s fortune, but with her death nearly all of his wealth will go toward creating a charitable foundation. At current rates, the endowment of more than $40 million would make it wealthier than the Gates Foundation, which is currently the largest in the world.

Survivors include her husband, of Omaha; and three children; and several grandchildren.

July, 2004|Archive|

Patients who received three-drug combination show improved results

  • 7/30/2004
  • CHICAGO, IL
  • Journal Abstract
  • Journal of Hemotoogy

Adding paclitaxel to a cisplatin and 5-fluorouracil (5-FU) regimen led to significantly longer survival in patients with locally advanced head and neck cancer, according to a phase-3 study presented here at the Annual Meeting of ASCO. “This new chemotherapy combination may soon become the standard treatment option for some patients with head and neck cancer,” said lead researcher Ricardo Hitt, MD, from the Hospital ’12 de Octubre’ in Madrid. The expanded combination also halted tumor progression more effectively than the standard regimen, and patients who received the three-drug combination were more likely to retain the ability to speak and swallow, as well as exhibit less mucocitis.

The study involved 384 patients who had various types of head and neck cancer, particularly tumors of the oropharynx, larynx and oral cavity. All patients were treatment naive. In the standard arm, patients received 100 mg/m2 of cisplatin daily, and 1 gm/m2 of 5-FU on days 1 through 5 of a 21-day cycle. In the expanded regimen, patients received 100 mg/m2 of cisplatin daily, 500 mg/m2 of 5-FU on days 1 through 5, and 175 mg/m2 of paclitaxel on the first day of a 21-day cycle.

The trial “appeared to demonstrate a superior outcome and far better tolerability by adding paclitaxel to 5-FU and cisplatin for head and neck cancer in a dose schedule associated with less toxicity,” said Robert Mayer, MD, the director of the Center for Gastrointestinal Oncology at Dana-Farber Cancer Institute in Boston.

July, 2004|Archive|

TOBACCO CARCINOGENS, THEIR BIOMARKERS AND TOBACCO-INDUCED CANCER

  • 7/30/2004
  • By Stephen S. Hecht
  • Nature Reviews Cancer, Volume 3, #10

Preface

The devastating link between tobacco products and human cancers results from a powerful alliance of two factors — nicotine and carcinogens. Without either one of these, tobacco would be just another commodity, instead of being the single greatest cause of death due to preventable cancer. Nicotine is addictive and toxic, but it is not carcinogenic. This addiction, however, causes people to use tobacco products continually, and these products contain many carcinogens. What are the mechanisms by which this deadly combination leads to 30% of cancer-related deaths in developed countries, and how can carcinogen biomarkers help to reveal these mechanisms?

Summary

* Tobacco products cause a variety of cancers, including those of the lung, oral cavity, nasal cavity, larynx, oropharynx, hypopharynx, oesophagus, stomach, liver, pancreas, bladder, ureter, kidney and cervix, and myeloid leukaemia. The carcinogens contained in tobacco products are responsible for these cancers.

* There are more than 60 carcinogens in cigarette smoke and at least 16 in unburned tobacco. Among these, tobacco-specific nitrosamines (such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N’-nitrosonornicotine (NNN)), polycyclic aromatic hydrocarbons (such as benzo[a]pyrene) and aromatic amines (such as 4-aminobiphenyl) seem to have an important role as causes of cancer.

* Carcinogen biomarkers — DNA adducts, protein adducts and urinary metabolites — provide objective measures of carcinogen uptake and metabolic activation and detoxification in people who use, or are otherwise exposed to, tobacco products.

* DNA adducts are central to the carcinogenic process as induced by tobacco products.

* Among carcinogen biomarkers, DNA adducts potentially provide the most direct link to cancer, but there are still significant measurement problems. Protein adducts are useful alternatives to DNA adducts, and in some cases have provided significant mechanistic insights. Urinary metabolites are probably the most practical biomarkers and provide important information about carcinogen dose and metabolism.

* Carcinogen biomarkers are important in establishing carcinogen dose in people who are exposed to tobacco products and in understanding mechanisms of carcinogenesis, and might ultimately be useful in predicting cancer risk.

Source: Nature Reviews Cancer 3, 733 -744; doi:10.1038/nrc1190

July, 2004|Archive|

Sore throat was first sign of oral cancer

  • 7/29/2004
  • Oakland, MI
  • By CASEY CURTIS
  • The Daily Oakland Press

Dave Nilson’s sore throat lasted almost six months. Assuming it would go away without treatment was his biggest mistake.

The pain – which began to spread to his neck and caused a small lump in his mouth – stayed. Eventually, the 44-year-old Troy resident went to his doctor for an examination and was sent home with antibiotics for strep throat. When the lump grew larger over a two week period, Nilson’s doctor referred him to an oral cancer specialist who performed a biopsy. On Christmas Eve of 2002, Nilson received the devastating news that the lump was in fact stage three – almost the last stage – of squamous cell carcinoma.

Never having smoked, chewed tobacco or drank alcohol, Nilson was utterly overwhelmed. Just a couple of years earlier, Nilson had lost his sister to melanoma and feared the worst. “I was thinking, ‘Oh my God, you’re going to die, too,’ ” he says.

In February 2003, Nilson underwent a 15-hour procedure to have tissue, several lymph nodes and 60 percent of his tongue removed. His jaw was cracked in half to remove the affected areas and muscle from his chest was stretched upward to replace the tissue lost on the right side of his neck.

Everything seemed to be going well, but Nilson developed “deadbone” in his jaw. That meant blood was not flowing to the bone. It restricted him from talking, eating and sometimes breathing. Nilson was given feeding tubes and breathing tubes to help him.

Last month, Nilson had surgery to correct his jaw. Bone and tissue from his leg were transferred into his jaw area in hope of making it heal. Unfortunately, Nilson suffered a stroke after the procedure. His recovery now will be much longer, and much more difficult.

Most are unaware

The Oral Cancer Foundation says 30,000 Americans will be diagnosed with oral cancer this year, and yet many people believe oral cancer is a rare disease. As such, they hear little about it. Death rates for oral cancer are higher than death rates of cervical, and skin cancer, according to The Oral Cancer Foundation.

Dr. Richard Arden of the Ear, Nose and Throat Physicians center in Sterling Heights, who was also Nilson’s physician, says oral cancer doesn’t only effect smokers, tobacco chewers and drinkers. “There is a small percent of patients who get it for reasons we still don’t know,” he says.

Although he has been cancer free for a little over a year now, Nilson won’t be in the clear for another four years. Patients aren’t considered cancer free until five years after the last day of their final treatment or surgery.

The cancer has taken its toll on Nilson as well as his family. His two sons Ryan, 21, and Eric, 18, were devastated with the news. Ryan eventually dropped out of his classes at Western Michigan to come home and help with the family businesses.

Nilson and wife Cheryl, 46, own four 7-Eleven stores and a Chicken Shack. Staff at each of the stores kept the businesses going in Nilson’s absence. Because of this support, Cheryl was able to spend most of the day with her husband in the hospital. How did she make it through the really tough times? “To tell you the truth, I don’t know,” she says quietly.

Unnoticed symptoms

One of the real dangers of oral cancer is that it can go unnoticed in its early stages. It can be painless, and little in the way of physical changes may be obvious. Arden says most symptoms are throat soreness, a small lump in the oral cavity and red or white lesions that may appear in the mouth. Neck pain, hoarseness or any numbness that lasts over two weeks are also symptoms. In these cases, Arden says it’s important to get a check-up from either your primary care physician or through a dental exam where a biopsies can be performed.

Some dentists, such as Bloomfield Township dentist Dr. Timothy Reilly, can perform a simple and painless procedure called a brush biopsy. The brush resembles a mini toilet brush, which is swiped back and forth over the lesion. The brush extracts cells from the surface and a little below the surface, which are transferred onto a slide and sent for analysis.

Reilly says he always looks for abnormalities in his patient’s mouth, and urges dentists to do thorough exams of the tongue, cheeks and floor of the mouth. “Not only is it good for your mouth and your body, but it can save your life,” he says.

Although the support from his family and friends has been tremendous, Nilson also found hope at a Troy Beaumont group called Support for People with Oral and Head and Neck Cancer. The group meets once a month to share their experiences, hardships and advice on the disease. Nilson says the group has been a big help with his self-esteem and has no doubt about his future of being cancer free.

When all the surgeries are finished, wounds healed and victory is achieved, Nilson says he wants one thing: “A nice slice of pizza.”

July, 2004|Archive|

The Ultimate Cancer Survivor

  • 7/24/2004
  • The Washington Post

Lance Armstrong has seen what W.B. Yeats called “The Cold Heaven”. So even on the day that he is expected to cross the finish line in Paris, having beaten all the Spaniards, Italians and French, and after climbing peaks in the face of spitting Germans, sceptics, accusers and naysayers, what Armstrong will prefer that people remember him for was not his sixth Tour de France victory, but his near-death experience. It remains his most significant accomplishment: he lived.

Six Tour de France titles is an epic achievement. In 100 years, no one has ever done such a thing; in fact, there’s probably no other feat in sport to which it can be compared for sheer effort, pain, will and character. Armstrong rode more than 3200 kilometres over mountains, skirting oceans, in heat and hail, enduring physical and mental agonies.

But the size of the record makes it all the more important to see Armstrong in small ways. That phrase “best ever” threatens to detach him from his central humanity; the trouble with becoming a sports immortal is that it puts him at a remove.

That’s the last thing Armstrong wants, because to him, his most essential quality is his most ordinary one. What’s important about Armstrong is what binds him to the rest of us: he has suffered. He has been sick, wounded and tired with cancer.

“Listen, I was there,” he says. “I haven’t forgot it. And I still use it. It’s not always easy because there are days where I encounter people who are not well. I don’t have any miracles to provide anybody other than giving a sliver of hope while pedalling a bike.”

Armstrong has his detractors, but I’m not one of them. My view of him is coloured by affection: he’s my friend and he gave me a best seller. All I can do is tell stories about him, in the hope of explaining him. Most of our conversations lately have taken place via cryptic e-mails, like the one he sent just before the tour began. “Best legs ever,” he wrote. “Gotta stay safe. We’ll see.”

We did see. What happened during the past three weeks was that a 32-year-old man raced like a boy, with a kind of rediscovered pleasure and blew past his competition. The main thing you need to understand about Armstrong is that without a bicycle, he probably would have been a bar-room brawler, or maybe an arsonist.

When he was a boy in Texas, his mother, Linda, bought him a racing bike that she could hardly afford. He has often remarked that cycling probably saved him from petty crime. He was a hyperactive kid who never knew his father. He once invented a game called fireball, which involved soaking tennis balls in kerosene, lighting them on fire and playing catch with them. He set the roof of their house on fire that way.

He carried around an inner emotional switchblade, the result of childhood deficits. He once finished a race swinging his fists at another rider, and he’s been known to take on Texas truckers on the highways.

The other important event in Armstrong’s life was the onset of cancer.

Armstrong has an extraordinary heart, lungs, arms, legs and genes. But whatever natural physical abilities he possesses were as randomly awarded as the winning numbers on a roulette wheel. Lacking an organised will and discipline, those attributes are meaningless. When he was a young racer, they were just a collection of scattered characteristics, topped by a smart mouth. Cancer gave him his will.

“He makes competitors roll over and expose their throat,” his close friend John Korioth says. “You kind of want to think he’s a nice, happy-go-lucky guy, but that’s not the case. People don’t want to hear that, but that’s the reality of the situation.”

He’s contradictory. He’s an agnostic who nevertheless wears a crucifix and who lovingly restored a chapel in his home in Girona, Spain. When he needs peace, he strolls the ancient cathedral and wanders around in the cool stillness, looking at religious art. He’s sweet and profane, methodical and hot tempered, flippant and reverent, and he has all kinds of hidden chips and sensitivities.

Time is Armstrong’s obsession; he reflexively, desperately clutches at it.

It’s a quality that served him well both in cancer and in racing. The Tour de France to him is a matter of meticulously tabulating time v pain v self-denial, a kind of physical algebra. “It’s a mathematical equation,” he says. He rehearses each crucial climb in the tour until he understands exactly how many seconds he can gain, what his heart rate will be, how many calories he will burn, how much he needs to weigh, how many watts he can generate and how long his body can stand it at that rate.

And yet clutching at time doesn’t always serve him well in everyday matters. Last spring his marriage was failing, and he was frantic with worry over his children. “Cancer never kept me awake at night,” he says. “This keeps me awake.”

One afternoon we wandered up the winding cobbled streets of Girona to an old Roman wall that circled the city, offering views of the Pyrenees. It was just a few blocks from his house, but he had never seen it before. He was almost distraught at the discovery that something so beautiful was so close to him, and he hadn’t had time to notice it. “I can’t believe this has been here,” he said. “I’m an idiot.”

If there’s one thing Armstrong could wish for, it’s more time. Time with his kids, from whom he’s been away for the better part of three months in pursuit of his sixth tour win. “I’m not doing this again,” he says. “I don’t want to and I won’t. I love two things, my kids and cycling. I’ll find a way to make it work.”

Time to compete in other prestigious races that could complete his career, such as the Giro d’Italia. Time to take some of the intensity out of his life. Time to think about what to do next.

But it may well be that Armstrong is constitutionally incapable of an easygoing life of leisure. “I had this idea that if I could bang this one out, I’d say, ‘It’s been nice knowing you’,” he says. Now he’s not too sure, after the young-at-heart way he’s felt these past three weeks.

“The guys were joking with me, saying, ‘So you want to go for the field sprint on the Champs Elysees?’ Every day we laced it up, we were like, ‘We’re gonna get it today’. You can’t walk away when you got a boyish feeling like that.”

But for the moment, it’s time to rest. On the last night of the tour, his sixth title a virtual formality, Armstrong was no longer a slave to it. He abandoned his famous self-denial and enjoyed a luxurious French meal with red wine and “several desserts”. He planned to fly home and scoop up his children, and take them to an isolated beach for a vacation with his girlfriend, singer Sheryl Crow. For now, he has a sense of completeness.

“I feel like something is finished,” he says.

July, 2004|Archive|

Optical Wand used to detect cervical cancer

  • 7/24/2004
  • Austin, TX
  • By Linda Marsa
  • LA TIMES

An experimental imaging tool could lead to faster diagnosis, fewer false positive results and better follow-up than the current colposcopy.

For many women, suspicious results from a cervical cancer screening may be just the beginning of a lengthy, and anxiety-filled, diagnostic process. They often must undergo a couple of follow-up tests and wait several weeks before receiving a definite answer.

Not only could an experimental fiber optic device help doctors make a diagnosis much more efficiently than current methods, it also may eventually enable them to do on-the-spot treatment.

“This tool could be a real advance over what we have,” says Dr. Daniel C. Sullivan, head of the cancer imaging program for the National Cancer Institute in Bethesda, Md. “It has the potential to be cheaper, quicker, and more accurate.”

Every year, about 13,000 American women are diagnosed with cervical cancer, which has a 92% survival rate if treated in its early stages. The conventional screening for cervical cancer is a Pap smear, in which a swab of cervical tissue is examined under a microscope by a trained technician.

When abnormal cells are detected, gynecologists visually inspect the cervix using a colposcope, a large electric microscope attached to a bright light. If they see abnormal cells, they’ll perform a biopsy, in which a tissue sample is snipped from the cervix and shipped to a lab for further evaluation.

However, colposcopy results are prone to human error: Cancers can be missed, or, in half the cases, the colposcope gives false positive readings that prompt needless, costly and painful biopsies.

“Diagnosis is very subjective and relies on the doctor having very good visual recognition skills,” says Rebecca Richards-Kortum, a biomedical engineer at the University of Texas at Austin and a co-inventor of the new optical imaging tool.

In addition, the delay between the initial screening and the eventual diagnosis can be six weeks or more, causing a great deal of anxiety and uncertainty. Some women fail to return for follow-up visits, meaning they may not get the correct diagnosis or, if necessary, treatment.

The new optical wands-designed to replace the colposcope examination, not the routine Pap smear-could shorten the time required for diagnosis, decrease the false positive rate (thereby eliminating unnecessary biopsies) and ensure that women receive adequate follow up.

The diagnostic device works by shining natural and ultraviolet light onto the cervix. Precancerous and cancerous cells reflect these light waves differently than normal cells, says Sullivan.

The pencil-thin fiber optic probe can also pick up other telltale signs of cancer, such as higher metabolic activity (because cancer cells divide faster than normal cells) or the presence of more red blood cells (which indicates that new blood vessels have been formed to ferry the nutrients and oxygen tumors need to survive), experts say. All this information is fed into a computer, which can determine immediately whether cells are cancerous.

Early tests indicate that this device may be more reliable than visual exams by physicians.

In a study of more than 100 women last year at the University of Texas at Austin and the M.D. Anderson Cancer Center in Houston, the probe reduced the rate of false positives by 50%, which experts estimate could save more than $600 million annually in healthcare costs in the United States alone. A larger test of 800 women comparing colposcopy with the optical device was recently completed, and results will be released within the next year.

OCF Note: If this device proves to be valuable in cervical cancer, its applications in oral cancer will be following.

July, 2004|Archive|

Smoke signals

  • 7/30/2004
  • By Oliver Childs
  • Nature Biology, Voulume 4, Number 8

Smokers die an average 10 years earlier than non-smokers; so concludes a landmark study published in the British Medical Journal (26 June 2004). This and other findings of the now-famous prospective study of the long-term smoking habits of over 34,000 British male doctors are the culmination of 50-years research into the effects of cigarette smoking in this cohort.

“Since the study began in 1951, tobacco has killed around 100 million people globally”, commented Alex Markham of Cancer Research UK (http://news.bbc.co.uk, 25 June 2004). But quantification of the risk of smoking has been limited. The results of this study provide some sobering facts and figures for smokers: “It is clear that consistent cigarette smoking doubles mortality throughout adult life” (Reuters, 22 June 2004), remarked Richard Doll, the Oxford University professor who initiated the study and first discovered the link between smoking and lung cancer.

However, the news is not all bad: “… we also know that stopping smoking will significantly limit the harm” (San Francisco Chronicle, 23 June 2004), said Richard Peto, Doll’s 30-year colleague on the study. In fact, the study found that stopping smoking at age 50 added 6 years to life expectancy. Furthermore, stopping before the age of 30 avoids almost all hazard associated with smoking.

The study conclusions are stark for those who continue to smoke, but also signal to those who are keen on quitting that it is not too late to do so. As Peto remarked, “Smoking kills people and stopping works” (Reuters, 22 June 2004).

Source: Nature Reviews Cancer 4, 574 (2004); doi:10.1038/nrc1423

July, 2004|Archive|

Buffetts’ donation aids cancer research

  • 7/20/2004
  • Onaha, NB
  • BY STEVE JORDON
  • Omaha World-Herald

Omaha investor Warren Buffett and his wife, Susan, have donated $6 million for research in appreciation of the treatment for mouth cancer that Susan Buffett received last fall, resulting in her “remarkable recovery.”

“Mrs. Buffett is doing extremely well, and we’re all very pleased that she has been able to resume her normal life activities,” said Dr. David Eisele, professor at the University of California-San Francisco. Last October, Dr. Deborah Greenspan, a professor of clinical oral medicine at the university’s medical center, found a “disturbing growth” at the base of Susan Buffett’s mouth, the medical center said in a public notice.

Greenspan referred Buffett to Dr. Brian Schmidt, an assistant professor of oral and maxillofacial surgery, who diagnosed her condition as potentially life-threatening cancer. Buffett met with Eisele, chairman of otolaryngology and head and neck surgery, who set up a treatment plan involving surgery and post-operative therapy through the medical center’s cancer center.

“Because of the seriousness of her diagnosis, Buffett spoke with specialists at a number of renowned cancer centers across the country,” the medical center said. “She was relieved to learn that Eisele’s plan would provide her with top-quality care close to her home in San Francisco.” Eisele led the tumor-removal surgery, followed by surgery by Dr. Pablo Leon, an assistant professor of plastic and reconstructive surgery. Six weeks of radiation therapy conducted by Dr. Jeanne Quivey followed.

The medical center credited the treatment team and “Buffett’s own courage and fortitude” for her “remarkable recovery.” In May, she came to Omaha for the annual shareholders meeting of Berkshire Hathaway. The Buffetts said they established funds for each of the five doctors who coordinated Susan Buffett’s treatment to use at their own discretion in research. “UCSF should be proud to have these exceptional people on its staff,” Warren Buffett said.

ADDENDUM: Susan Buffett died suddenly from a stroke on July 29, 2004 at the age of 71. While the details of her death have not been released, pateints who receive large doses of radiation as a result of treament for oral and head and neck cancers have a higher risk of stroke after treatment.

July, 2004|Archive|

U of C scientist finds how herpes attacks cancer

  • 7/19/2004
  • Calgary, Canada
  • Nature Cell Biology

U of C professor Patrick Lee is working on using the herpes simplex virus to kill cancer cells. A common virus is proving to be a powerful agent in the fight against cancer. Patrick Lee, professor at the University of Calgary oncology department, has discovered how an engineered form of the herpes simplex virus kills cancer cells.

“This is a major conceptual breakthrough in the design of viruses against cancer,” he said. The study of viral therapy — the use of common viruses such as the herpes simplex virus to destroy cancer cells while keeping healthy cells intact — is not new. Cancer researchers have been studying the process for a decade, but before Lee’s discovery, researchers did not understand exactly why the herpes virus is a potent cancer killer. The discovery, suggests Lee, will speed research into viral therapies for cancers.

The article detailing the findings was published in the scientific journal Nature Cell Biology. “Lee’s work provides an important link in our understanding of how viruses can be genetically engineered to attack cancer,” said Dr. Robert L. Martuza, a professor of neurosurgery at Harvard University medical school. Martuza, who is not part of Lee’s research team, is a leading researcher in how the herpes simplex virus acts as a cancer-killing agent. He is conducting human trials on the use of the herpes virus as a cancer therapy. “What Dr. Lee has done is identify a cancer pathway, and there are numerous cancer pathways. This is one building block in the whole scheme of things, but ultimately in the next few years, what we would have are viruses that are specific to cancer pathways A, B or C,” said Martuza. “So, for example, if you had a tumour diagnosed in you, we would identify which pathway is wrong and we would have a virus that would attack that pathway. Dr. Lee has provided a mechanism in providing the specificity of these viruses that we are making for cancer therapy.”

Lee is known for his work with the reovirus, a naturally occurring bug that poses no threat to humans yet can destroy cancer cells with amazing accuracy. He became interested in the herpes virus because he was curious to see whether other viruses work the same way as the reovirus in fighting cancers. “The herpes virus kills cancer cells through the Ras pathway. To understand the Ras pathway, you have to know the difference between a normal cell and a cancer cell,” said Lee. “There is a biochemical process called the Ras pathway in all cells that regulates cell growth. In normal cells, this process is tightly regulated. “In cancer cells, because of mutation, this pathway becomes very active.” Lee compares the cell to a room and the Ras pathway to a light switch in the room. “In normal cells, the Ras pathway is a light switch that is turned on only part of the time, and most of the time it’s switched off, because this pathway regulates cell growth. But in a cancer cell, the Ras pathway is on all of the time. And that is why you get cancer: because the light can’t be turned off and the cancer cells don’t die and keep on growing.”

But Lee discovered the herpes virus “loves the Ras pathway. “That is why when herpes cells go into a normal cell, they say, ‘Hey I can’t do anything because the light is turned off. But when they get into a cancer cell, the light is turned on and they say, ‘I can use that’ and boom they infect the cancer cell. The herpes virus then takes over the cell by making use of its resources to replicate itself, the cell then ruptures releasing virus particles which rapidly infects neighbouring cancer cells, killing them all.”

An individual injected with the modified virus would not become infected with herpes because the virus has been disarmed. In discovering how the herpes simplex virus infects cells, Lee said that it will also help researchers explore new drugs to control herpes infections.

July, 2004|Archive|

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  • 7/18/2004
  • Houston, TX
  • See below for authors
  • Arch Otolaryngol Head Neck Surg. 2004;130:869-873.

Objectives : To compare the survival rates of patients 40 years or younger and diagnosed with squamous cell carcinoma of the head and neck (SCCHN) with those of patients older than 40 years who underwent the same treatment. In 2 previous matched-pair analyses, the patients had been matched for tumor stage, site, sex, and date of presentation but not type of treatment.

Methods: Between 1995 and 2001, 46 patients 40 years or younger participated in a prospective epidemiologic study that included more than 500 patients newly diagnosed with SCCHN. We matched each of these patients by sex, race, tumor site, overall stage, and treatment modality with 2 patients older than 40 years. Ultimately, 31 of the younger patients were matched with 62 of the older patients. Survival analysis was performed using Cox proportional hazard models and accounting for the matched trios.

Results: There was no difference in overall, disease-specific, or recurrence-free survival rates between the patients who were 40 years or younger and those older than 40 years. Furthermore, matched survival analysis did not demonstrate a difference in overall survival rate (risk ratio [RR], 0.71; 95% confidence interval [CI], 0.22-2.29; P = .56), disease-free survival rate (RR, 0.83; 95% CI, 0.20-3.33; P = .79), or time to recurrence (RR, 1.46; 95% CI, 0.50-4.23; P = .49), and was not affected by adjustment for medical comorbidities or the severity of cancer-associated symptoms.

Conclusions: We found no evidence of a difference in the survival rates of patients with SCCHN who were 40 years or younger or older than 40 years and underwent similar treatment at our institution.

From the Departments of Head and Neck Surgery (Drs Pytynia, Grant, Roberts, and Sturgis) and Epidemiology (Drs Etzel, Wei, and Sturgis), The University of Texas M. D. Anderson Cancer Center, Houston. The authors have no relevant financial interest in this article.

July, 2004|Archive|