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Actually, they are not just passengers. The other receptors, it being ER, PR, HER2, HER1, IGFR - whatever you have there, communicate with each other. Every receptor needs another type to "get it on with" (so to speak). This excitation sends signals into the nucleus of the cell via phosphorylation and initiates cell division. Herceptin (or Tamoxifen) stop the receptor to receptor excitation via bonding with that receptor.
The only receptor that will communicate with a "like" receptor is Her2 (that they know of at this time). Her2 will communicate with another Her2. That said, this is the reason if a woman is ER+ but PR neg (or vice versa), but not HER2+, doctors are certain that something else is going on too since the ER likes to communicate with something different than itself to get excited and grow.
So they are not there for the ride. Its that if you cover the ER, HER2 is still left there. If you covered Her2 with Herceptin and did nothing more, ER and PR will run the show together. And most of us probably have other minor moities hanging around too. Secondly, being ER/PR+ is a good thing regardless of Her2 status. Even being ER+ only is better than nothing because something can be done about it and the cancer tends to be slightly lower grade.
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Kind regards
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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