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Old 06-15-2009, 12:17 PM   #1
Lani
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IBC gene identified

NYU Langone Medical Center researchers identify key gene in deadly inflammatory breast cancer [New York University]
Aggressive, deadly and often misdiagnosed, inflammatory breast cancer (IBC) is the most lethal form of primary breast cancer, often striking women in their prime and causing death within 18 to 24 months. Now, scientists from The Cancer Institute at NYU Langone Medical Center have identified a key gene—eIF4G1—that is overexpressed in the majority of cases of IBC, allowing cells to form highly mobile clusters that are responsible for the rapid metastasis that makes IBC such an effective killer.
The new findings, Essential Role for eIF4G1 Overexpression in Inflammatory Breast Cancer Pathogenesis, scheduled for advance online publication on Nature Cell Biology's website could lead to the identification of new approaches, therapies and a new class of drugs to target and treat IBC. This would be a critical development in the fight against IBC, which respond poorly to chemotherapy, radiation or any other current treatments for breast cancer, according to the study's lead authors Dr. Robert Schneider, associate director for translational research at The Cancer Institute, co-director of breast cancer research, and the Albert B. Sabin Professor of Molecular Pathogenesis at NYU School of Medicine, and Dr. Deborah Silvera, a postdoctoral research fellow.
"The tragedy of IBC is that it is often misdiagnosed and misclassified. Rather than presenting as a 'typical' lump, IBC looks like an inflammation of the breast and is frequently mistaken for an infection. Physicians often prescribe antibiotics, losing valuable time for treating this fast-moving killer," says Dr. Schneider, noting that IBC accounts for several percent of all breast cancer cases but takes a high toll on mortality, with an incidence that is 50 percent higher in African American women. He adds that there has been little progress in treating IBC over the past two decades, and there are no drugs specifically for this form of cancer. "In fact, IBC has only recently been recognized as a unique, genetically distinct form of breast cancer."
Dr. Schneider and his colleagues found that the overexpression of the gene eIF4G1 reprograms how the IBC tumor cells make proteins. Other researchers have identified genes associated with IBC, but this is the first gene shown to orchestrate how IBC tumor cells form special structures—unique to this disease—known as "tumor emboli." These small clusters of highly mobile tumor cells are responsible for the rapid metastasis of IBC. Because these cell clumps are not stationary or fixed, they can quickly travel to other areas of the body.
"The good news is that we're beginning to understand IBC at both a molecular and genetic level," says Dr. Schneider. "We believe this gene is a target for new drug discovery, and we also believe it is possible to silence the gene without hurting normal cells. Our next step will be to focus on the genetic basis of this disease and look at the genetic changes underlying IBC to reveal more targets at the genetic level."
EARLY VIEW: ABSTRACT: Essential role for eIF4GI overexpression in the pathogenesis of inflammatory breast cancer [Nature Cell Biology]
Inflammatory breast cancer (IBC) is the most lethal form of primary breast cancer. IBC lethality derives from generation of tumour emboli, which are non-adherent cell clusters that rapidly spread by a form of continuous invasion known as passive metastasis. In most cancers, expression of E-cadherin, an epithelial marker, is indicative of low metastatic potential. In IBC, E-cadherin is overexpressed and supports formation of tumour emboli by promoting tumour cell interactions rather than adherence to stroma. E-cadherin, a surface component of adherens junctions, is anchored by interaction with p120 catenin (p120). We show that the unique pathogenic properties of IBC result in part from overexpression of the translation initiation factor eIF4GI in most IBCs. eIF4GI reprograms the protein synthetic machinery for increased translation of mRNAs with internal ribosome entry sites (IRESs) that promote IBC tumour cell survival and formation of tumour emboli. Overexpression of eIF4GI promotes formation of IBC tumour emboli by enhancing translation of IRES-containing p120 mRNAs. These findings provide a new understanding of translational control in the development of advanced breast cancer.
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Old 06-15-2009, 01:08 PM   #2
StephN
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Whoopee!
The next HER2 in successful treatment options???

Thanks, Lani!
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"When I hear music, I fear no danger. I am invulnerable. I see no foe. I am related to the earliest times, and to the latest." H.D. Thoreau
Live in the moment.

MY STORY SO FAR ~~~~
Found suspicious lump 9/2000
Lumpectomy, then node dissection and port placement
Stage IIB, 8 pos nodes of 18, Grade 3, ER & PR -
Adriamycin 12 weekly, taxotere 4 rounds
36 rads - very little burning
3 mos after rads liver full of tumors, Stage IV Jan 2002, one spot on sternum
Weekly Taxol, Navelbine, Herceptin for 27 rounds to NED!
2003 & 2004 no active disease - 3 weekly Herceptin + Zometa
Jan 2005 two mets to brain - Gamma Knife on Jan 18
All clear until treated cerebellum spot showing activity on Jan 2006 brain MRI & brain PET
Brain surgery on Feb 9, 2006 - no cancer, 100% radiation necrosis - tumor was still dying
Continue as NED while on Herceptin & quarterly Zometa
Fall-2006 - off Zometa - watching one small brain spot (scar?)
2007 - spot/scar in brain stable - finished anticoagulation therapy for clot along my port-a-catheter - 3 angioplasties to unblock vena cava
2008 - Brain and body still NED! Port removed and scans in Dec.
Dec 2008 - stop Herceptin - Vaccine Trial at U of W begun in Oct. of 2011
STILL NED everywhere in Feb 2014 - on wing & prayer
7/14 - Started twice yearly Zometa for my bones
Jan. 2015 checkup still shows NED
2015 Neuropathy in feet - otherwise all OK - still NED.
Same news for 2016 and all of 2017.
Nov of 2017 - had small skin cancer removed from my face. Will have Zometa end of Jan. 2018.
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Old 06-15-2009, 04:07 PM   #3
Midwest Alice
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Thanks Lani, Great news!!!!!
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Alice
04/08 age 50 III IBC Her2+++ ER/PR-8cm 14/14 Double M, Body and Brain CT/PET clear, ? on spine,Muga 53
06/08, 4 A/C, Neulasta
08/08, Herceptin/tax 12 every week
10/08, CT/PET clear, ? on pelvis, hips, MUGA 43, started Enalaprial for heart, Herceptin every 3 weeks
11/08 33Rads; 12/08 MUGA 48
2/09 MRI spine and bone scan, old mets to spine, Chest x-ray, blood work, IV NED,regular CPAP use,Zometa x6, first -flue like symptoms 2 days;Herceptin x3; stage 2 lymphoedema..sleeve and glove
4/09 Brain MRI - CLEAR; MUGA 54
7/09 chest ultrasound,
10/09 PET, brain and spin MRI NED Herceptin only. MUGA 59!!!
1/11 Hip replacement 7/11 Hip 2 replacement
4/12 4 years!! Herceptin
6/12 start reconstruction finish in 12/12
2/14 Herception - 6 years!!!

1 Corinthians 10:13 "No temptation has seized you except what is common to man. And God is faithful; he will not let you be tempted beyond what you can bear. But when you are tempted, he will also provide a way out so that you
can stand up under it."

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