why the recovery to damage of the airways or GI tract may be slower whileon herceptni

[Lani]

Sci STKE. 2007 Apr 10;2007(381):re3. Links
Sequestration and segregation of receptor kinases in epithelial cells: implications for ErbB2 oncogenesis.

Carraway CA, Carraway KL.
Department of Biochemistry and Molecular Biology, University of Miami School of Medicine, Miami, FL 33136, USA.
Cell behaviors are regulated by signaling pathways triggered by the activation of cell surface receptors. A key aspect of receptor signaling is the location of these receptors relative to their ligands and to other receptors, particularly in epithelia, whose cells are polarized by tight junction barriers into apical and basolateral membrane regions. In polarized epithelia, the co-receptor ErbB2 is often localized to the apical surface by its intramembrane ligand Muc4, thus segregating it from its partner ErbB3, which is sequestered at the lateral surface, co-localized with cadherin junctions. The ErbB2-ErbB3 receptor heterodimer, when activated, is a potent stimulator of cell proliferation; thus, the segregation mechanism helps maintain these cells in a differentiated state. Similarly, epidermal growth factor, the ligand for ErbB1, which is present in the apical fluid of some epithelia, is segregated from its receptor by the tight junction barrier. Loss of cell polarity and the tight junction barrier facilitates the interaction of ErbB2 with the hemidesmosome integrin alpha(6)beta(4). This integrin acts as a docking site for signaling pathways to promote cell proliferation and further disruption of cell junctions. The ultimate dissolution of tight junctions may result from activation of transforming growth factor-beta receptors, one subunit of which is directly associated with the junction. This activation triggers degradation of critical tight junction components. These sequestration and segregation phenomena provide a model by which overexpression of the ErbB2 receptor kinase may trigger oncogenesis by initiating junction breakdown. Equally important, these mechanisms may act as a sensor for epithelial damage that can activate repair mechanisms.
PMID: 17426346 [

[Diana1993]

I'm presently on Xeloda, after being on herceptin for two years. I was taken off herceptin when my CA15-3 count jumped to 295 after a flu bug. I'm on holidays and I had blood work done this week, here in San Antonio. Also, I've had back to back 'cold, flu' and my CA15-3 came back at 518. Do you think that the flu can effect the test? The past counts have been steady at 160 to 180 range. Have any of you had a similar experience? Also I always end up with a dry hacky cough for weeks. Any and all comments are welcome.

[Laurel]

Diana,

I do not have an answer for you regarding the elevation of your tests after the flu. However, may I suggest you make this a separate post, begin a new thread, to have as many members view it and provide you with responses? I think you will just get buried here.

I can respond to the severity of colds while on Herceptin. I caught a mild something which typically I am always able to fend off. This past month, though, my little something became full blown bronchitis and sinusitis requiring antibiotics. I still have a dry, hacky cough. My labs since recovery from chemo have been slowly dropping. I should be specific; it is my RBC's and WBC's that are low. I surfed around the net a bit and discovered that Herceptin does lower our counts.

Hang in there. I do not think your hacky cough is due to any lung metastisis. Of course, calling your onc. may be what gives you the necessary peace of mind. I sure wish you all the best.