Re: Interferon 101

[Guest guest]

Some CML, I do not know how many, are using a combination of low dose

interferon and a TKI, with excellent results.

I know of one patient who went into MR on interferon alone.

It would be interesting to learn how many patients are on interferon and how

they manage the side effects.

________________________________

From: Lottie Duthu <lotajam@...>

CML < >

Sent: Mon, October 18, 2010 11:20:20 PM

Subject: [ ] Interferon 101

'The immune system serves as your body's natural shield against infection. A

wondrously complex and multi-layered system, it was designed to protect you from

potential invaders, including viruses, bacteria, and allergens. Your immune

system is also able to recognize dangerous changes in your cells and destroy

these potential pre-cancerous cells. Part of this protection includes the

production of interferon.

" Interferon is activated by the immune system when a virus attacks a cell.

Interferon serves two important functions. It signals neighboring cells and

triggers their resistance mechanisms, and it activates other immune cells that

kill invading pathogens. Interferon is essential to the immune system and helps

protect us from the daily exposure to millions of germs that can lead to serious

infection.

http://www.excelwithus.com/nutriferon/new_page_1.htm

______________________________

THE HISTORY OF INTEFERON

" RNA virus in a cell inhibits the growth of any other viruses in that cell.

Alick Isaacs, born in Scotland of Jewish parents (1921 - 1967) found that this

interference seemed to be caused by something inside the cell. In 1957, while

working with the visiting Swiss scientist Lindenmann, Isaacs found that

chick embryos injected with influenza virus released very small amounts of a

protein that destroyed the virus and also inhibited the growth of any other

viruses in the embryos. Isaacs and Lindenmann named the interfering protein

interferon. " Note: Mr. Isaacs died while still studying interferon and it's

effects on viral influenza.

" Interest in interferon was revived in the late 1960s when Ion Gresser (1928-),

an American researcher in Paris, discovered that the protein stopped or slowed

the growth of tumors in mice and also stimulated the production of tumor-killing

lymphocytes. Gresser and the Finnish virologist Kari Cantell then developed a

way to make interferon in useful amounts from human blood cells.

" Gresser and the Finnish virologist Kari Cantell then developed a way to make

interferon in useful amounts from human blood cells. Monoclonal antibodies,

first produced in 1975, made large-scale purification ofinterferon possible, and

the mid-1980s saw the advent of genetically engineered interferon, the first

example of which was produced from bacteria by Swissscientist Weissmann

in 1980. Scientists now know that there are three major types of interferon:

alpha, beta, and gamma. They have also learned that interferons are not species

specific but can have activity in other species.

" It has beenused successfully against leukemia, osteogenic sarcoma (a bone

cancer), and as a therapy for delaying disease recurrence and prolonging

survival in patients with melanoma (skin cancer). Research also continueson the

use of interferon to treat viral diseases like rabies, hepatitis, andherpes

infections. In December 1997, researchers from the Duke University Medical

Center also announced study results that indicate interferon may be a way to

preserve donor livers longer prior to transplantation. " (more at website)

http://www.faqs.org/health/topics/87/Interferon.html

___________________

Edit

Mechanisms of resistance to tyrosine kinase inhibitors in chronic myeloid

leukemia and recent therapeutic strategies to overcome resistance.............

Dale Bixby, Moshe Talpaz

Given its relative rarity, it may at first seem surprising that chronic myeloid

leukemia (CML) has garnered so much attention over the last decade. Yet, the

advances in molecular pathogenesis that have been derived from studying this

leukemia have clearly benefited all of oncology. Moreover, the strides in drug

design and development that have also ensued around CML have given rise to what

others have called a molecular revolution in cancer therapy. While a majority of

patients with chronic phase CML (CP-CML) have an excellent durable response to

imatinib, a clear minority will unfortunately have signs of primary or secondary

resistance to therapy. Significant efforts geared toward understanding the

molecular mechanisms of imatinib resistance have yielded valuable insights into

the biology of drug trafficking into and out of cells, epigenetic control of

cellular processes, alterations in enzymatic structures, and the rational

structural-based design of small molecule enzyme inhibitors. This review will

describe the efforts at understanding the pathogenesis of imatinib resistance

and the molecular rationale for the development of second and now third

generation therapies for patients with CML. " This story was published in 2009.

http://tinyurl.com/23ytkke

____________________

FYI,

Lottie Duthu