Transformation of CML to ALL

[Guest guest]

A new study has identified an oncogenic lesion that accompanies the

transformation of chronic myelogenous leukemia (CML) to acute lymphoblastic

leukemia (ALL). The study, published online this week in Nature, found that

deletion of IKZF1 (a gene coding for the transcription factor Ikaros) in

patients with CML often occurs during progression to ALL.

In this " rogue chromosome, " part of the BCR (breakpoint cluster region) gene on

chromosome 22 winds up adjacent to a portion of the ABL (Abelson murine

leukemia) gene from chromosome 9. The gene product of this fused sequence

activates several proteins and enzymes that control the cell cycle and

accelerates cell division. In addition, it inhibits DNA repair, which

destabilizes the genome and may lead to the " blast crisis " in CML.

Approximately 5% of pediatric and 40% of adult ALL patients have the

Philadelphia chromosome and are described as being BCR-ABL1-positive. The new

study examined leukemic DNA samples from both adult and pediatric patients with

ALL (n = 304); these included 22 adult and 21 pediatric patients with BCR-ABL1

ALL. Samples from 23 adult patients with CML were also studied. Click on the

link to read entire article.

http://www.medscape.com/viewarticle/572939

Blessings,

Lottie

[Guest guest]

Sent from my BlackBerry® wireless device from Cable & Wireless bMobile

[ ] Transformation of CML to ALL

A new study has identified an oncogenic lesion that accompanies the

transformation of chronic myelogenous leukemia (CML) to acute lymphoblastic

leukemia (ALL). The study, published online this week in Nature, found that

deletion of IKZF1 (a gene coding for the transcription factor Ikaros) in

patients with CML often occurs during progression to ALL.

In this " rogue chromosome, " part of the BCR (breakpoint cluster region) gene on

chromosome 22 winds up adjacent to a portion of the ABL (Abelson murine

leukemia) gene from chromosome 9. The gene product of this fused sequence

activates several proteins and enzymes that control the cell cycle and

accelerates cell division. In addition, it inhibits DNA repair, which

destabilizes the genome and may lead to the " blast crisis " in CML.

Approximately 5% of pediatric and 40% of adult ALL patients have the

Philadelphia chromosome and are described as being BCR-ABL1-positive. The new

study examined leukemic DNA samples from both adult and pediatric patients with

ALL (n = 304); these included 22 adult and 21 pediatric patients with BCR-ABL1

ALL. Samples from 23 adult patients with CML were also studied. Click on the

link to read entire article.

http://www.medscape.com/viewarticle/572939

Blessings,

Lottie

[Guest guest]

This morning I felt a somthing inside my neck a ball like is slightly larger

than a BB.

Have a cold so am hoping is because of the cold. 

I realize you guys are not doctors but does anyone have any insight to this.

When I was first diagnosed the doctors were alwys checking my lymphnodes but I

haven's seen a Dr sept and have not had blood work for geez since maybe aug. The

lab lost a sample the lab/mail lost it ..The results were not correct. Have

heard all sort of excuses.

And have had hosp/Dr office change my last appt from Dec 21 to Feb 22.

i am so trying not to be worried. And No I donot have  a choice in my Dr care. I

get what they will give me.

I would appreciate any and all input.

Anita

________________________________

From: Lottie Duthu <lotajam@...>

CML < >

Sent: Friday, January 23, 2009 3:26:43 PM

Subject: [ ] Transformation of CML to ALL

A new study has identified an oncogenic lesion that accompanies the

transformation of chronic myelogenous leukemia (CML) to acute lymphoblastic

leukemia (ALL). The study, published online this week in Nature, found that

deletion of IKZF1 (a gene coding for the transcription factor Ikaros) in

patients with CML often occurs during progression to ALL.

In this " rogue chromosome, " part of the BCR (breakpoint cluster region) gene on

chromosome 22 winds up adjacent to a portion of the ABL (Abelson murine

leukemia) gene from chromosome 9. The gene product of this fused sequence

activates several proteins and enzymes that control the cell cycle and

accelerates cell division. In addition, it inhibits DNA repair, which

destabilizes the genome and may lead to the " blast crisis " in CML.

Approximately 5% of pediatric and 40% of adult ALL patients have the

Philadelphia chromosome and are described as being BCR-ABL1-positive. The new

study examined leukemic DNA samples from both adult and pediatric patients with

ALL (n = 304); these included 22 adult and 21 pediatric patients with BCR-ABL1

ALL. Samples from 23 adult patients with CML were also studied. Click on the

link to read entire article.

http://www.medscape .com/viewarticle /572939

Blessings,

Lottie

[Guest guest]

This is odd, because someone just told me that her mother was diagnosed with

CLL, and they told her mother she had the good one, and nothing had to be done

at present.  She went on not doing any treatment, then they told her she went

into AML.  I think she had CML to begin with, and with nothing being done she

went into the blast phase.  IT was too late.  She died.  Seeing this post,

really made me think

From: Lottie Duthu <lotajam@...>

Subject: [ ] Transformation of CML to ALL

" CML " < >

Date: Friday, January 23, 2009, 4:26 PM

A new study has identified an oncogenic lesion that accompanies the

transformation of chronic myelogenous leukemia (CML) to acute lymphoblastic

leukemia (ALL). The study, published online this week in Nature, found that

deletion of IKZF1 (a gene coding for the transcription factor Ikaros) in

patients with CML often occurs during progression to ALL.

In this " rogue chromosome, " part of the BCR (breakpoint cluster region) gene on

chromosome 22 winds up adjacent to a portion of the ABL (Abelson murine

leukemia) gene from chromosome 9. The gene product of this fused sequence

activates several proteins and enzymes that control the cell cycle and

accelerates cell division. In addition, it inhibits DNA repair, which

destabilizes the genome and may lead to the " blast crisis " in CML.

Approximately 5% of pediatric and 40% of adult ALL patients have the

Philadelphia chromosome and are described as being BCR-ABL1-positive. The new

study examined leukemic DNA samples from both adult and pediatric patients with

ALL (n = 304); these included 22 adult and 21 pediatric patients with BCR-ABL1

ALL. Samples from 23 adult patients with CML were also studied. Click on the

link to read entire article.

http://www.medscape .com/viewarticle /572939

Blessings,

Lottie