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Old 11-25-2007, 05:56 PM   #4
Becky
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Join Date: Sep 2005
Location: Stockton, NJ
Posts: 4,179
I actually heard that about half will become resistant. If you think about the adjuvant Herceptin trial where it decreased recurrence by 52% then that number is about right.

However, I believe there are many, many paths that contribute to resistance (if you want to actually call it that). For example, if a woman were ER/PR+ but did not take an anti-hormonal but took Herceptin - her cancer would probably grow due to estrogen or progesterone as those pathways are not blocked. But lets say they are also blocked and the cancer still grows, I think it is because this woman is also positive for something else. Something that isn't tested for or even discovered yet. The Herceptin is working on the Her2, the Arimidex is working on the ER/PR but something else is not blocked (ie: Her 1 or Her 3, IGFR or something not yet even imagined).

Also, sometimes women have a Her2 receptor that is a different shape than normal or the external domain is missing. This is called the truncated version (H95) and then Herceptin doesn't fit or doesn't have a key to lock onto.
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Becky

Found lump via BSE
Diagnosed 8/04 at age 45
1.9cm tumor, ER+PR-, Her2 3+(rt side)
2 micromets to sentinel node
Stage 2A
left 3mm DCIS - low grade ER+PR+Her2 neg
lumpectomies 9/7/04
4DD AC followed by 4 DD taxol
Used Leukine instead of Neulasta
35 rads on right side only
4/05 started Tamoxifen
Started Herceptin 4 months after last Taxol due to
trial results and 2005 ASCO meeting & recommendations
Oophorectomy 8/05
Started Arimidex 9/05
Finished Herceptin (16 months) 9/06
Arimidex Only
Prolia every 6 months for osteopenia

NED 18 years!

Said Christopher Robin to Pooh: "You must remember this: You're braver than you believe and stronger than you seem and smarter than you think"
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