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Schools aid teen in his fight for life

Tartan junior battles rare type of leukemia

BY TAMMY J. OSEID

Pioneer Press - March 28, 2005 - Like many neighboring schools, Oakdale's Tartan High and North St. Paul's North High are bitter rivals on sports fields and in the classroom.

But Aaron Fowler, a Tartan junior fighting a rare form of leukemia, has drawn the two schools' communities together as they try to raise money to fight his disease.

"It surprised me big time how many people actually care," Aaron said. "With so many people I didn't even know saying they were praying for me & I can pretty much take whatever comes at me."

Organizers hope an April 15 student drive at North to raise money for the 16-year-old athlete and an April 17 community fund-raiser at Tartan will bring in enough money to cover medical bills that insurance won't. They also hope to help his family renovate their home so Aaron can be comfortable when he returns from Fairview University Medical Center in Minneapolis.

"Once you meet him, you'll never forget him," said family friend Paula Oleson, who is helping with the Tartan benefit. "Aaron is the kid who sticks up for those who get picked on. He's the guy who helps everybody else. Now he needs help."

Aaron, a hurdler and a high jumper for the North track team, was feeling bad for several weeks early this year, said his father, Bill Fowler, a nurse at Edina's Fairview Southdale. Then on Feb. 7, at his fifth doctor's appointment in three weeks, he was diagnosed with acute myelogenous leukemia, or AML.

The cancer causes the body to produce too few normal red blood cells, white blood cells and platelets. Patients often feel tired, appear pale, bleed or bruise easily and heal more slowly than normal and experience frequent infections or mild joint pain.

Aaron has been hospitalized for almost two months, spending two days at home between chemotherapy sessions. Bone marrow transplants might follow depending on how chemotherapy turns out.

Almost immediately after Aaron was diagnosed, friends, teachers and people who barely knew him began posting supportive messages on his private CaringBridge health-update Web page. Aaron was bummed he was missing out on the track season, so a friend gave him his state track medal, which now hangs by Aaron's hospital room window overlooking the University of Minnesota campus.

When some of Bill Fowler's co-workers heard about Aaron, they began organizing the benefit at Tartan. The Oakdale community, the Fowlers' church and others soon joined in to plan an April 17 variety show with a silent auction, craft sale, book sale and concessions to raise money.

Then at North, one of Aaron's former teachers, Sara Paul, helped several students arrange a "Rally for Aaron Day" on April 15. North students will pay $2 so they can wear a hat a clothing item normally not allowed in school.

Aaron's parents are pleased so many are rallying to their youngest son's support.

"It's not what you go through in life, it's how you go through it," Bill Fowler said. "We're not angry at God, we're not upset, but we have the same questions every other parent would: Why us? Why Aaron? We may never know.

"But at this time of year, Christ had victory over death. We're praying for the same for Aaron."

AARON FOWLER

School: Junior at Oakdale's Tartan High School

Family: Parents, Bill and Mary Fowler of Oakdale, both nurses; sister, Amy Just, school social worker; brother, Jason Fowler, a second-year medical student; and a 1-year-old nephew, Bryce Just

Activities: Varsity track, football, National Honor Society, student council; he planned to start taking college courses this spring through Minnesota's postsecondary enrollment option.

Notable for: Drawing communities together as he fights a rare form of leukemia

IF YOU GO

" The Tartan fund-raiser will be from 3 to 8 p.m. April 17 at Tartan High School. Admission to the variety show is free, but the event also features a silent auction, craft sale, book sale and concessions. All proceeds will go to Aaron's family. Go to www.aaronsnight.com for more information.

" North High School teacher Sara Paul is coordinating that school's hat-day drive. Contact her at [email protected] or 651-748-6100 for more information.

" To donate directly to Aaron and his family, send checks payable to Bill and Mary Fowler to Lake Elmo Bank, 600 Inwood Ave. N., Oakdale, MN 55128.

ALL Leukemia resists treatment

Fri 21 Apr 2006 - TENNESSEE (myDNA News) - Investigators at St. Jude Children's Research Hospital in Tennessee have used mouse models to determine why some forms of acute lymphoblastic leukemia (ALL) are extremely aggressive and resist a drug that is effective in treating a different type of leukemia.

The investigators found that the combination of a mutation called Bcr-Abl and the loss of both copies of the tumor suppressor gene Arf in bone marrow cells triggers an aggressive form of ALL. Inactivation of both Arf genes facilitated the multiplication of leukemic cells that did not respond to the drug imatinib. Imatinib is already successfully used to treat chronic myelogenous leukemia (CML), another blood cell cancer caused by the Bcr-Abl mutation.

The St. Jude study provided evidence that imatinib resistance in mouse models of ALL did not depend strictly on the presence of Bcr-Abl and the loss of Arf genes in the cancer cells themselves. Rather, drug resistance reflected an interaction of the tumor cells with specific growth-promoting factors produced in the mice. After removal of leukemic cells from mice that had failed imatinib therapy, compounds inhibiting enzymes called JAK kinases restored the cells' imatinib sensitivity.

The study's findings suggest why imatinib may fail to cause remission of ALL in patients with the Bcr-Abl mutation and point to a strategy for overcoming this resistance. A report on this work appears in the April 17 issue of Proceedings of the National Academy of Sciences.

The Bcr-Abl oncogene (a cancer-causing gene) is formed when parts of two chromosomes switch places, leading to fusion of a fragment of the Bcr gene from one chromosome to a portion of the Abl gene from the other. Bcr-Abl encodes a type of enzyme called a tyrosine kinase, which then drives the abnormal, uncontrolled multiplication of leukemic cells.

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