Topetecan vs. Clinical Trial

BACKGROUND: Sept. 2005 Dx Stage IIIC OVCA. Opt. debulked.
1st chemo: Clinical Trial...Carbo-6 cycles; Taxol/Avastin q3wksx1yr; ended 10/2006
April 2007: began Femara due to increasing CA 125
July 2007: began Doxil due to PET scan showing hypermetabolic activity in 2 lymph nodes and peripheral liver foci. Also CA 125 cont. slow rise.

March 2008: Had 9th Doxil treatment Over the course of 9 Doxil tx. CA 125 went from 243 to 64

April 2008: CA 125 was 80 and CT scan showed para-aortic node increased from 0.6 X 1.6 X0.5 cm to 0.9 X 1.8 X 1 cm.  Unchanged stable 1.2 X 0.9 cm distal left external ileac node.

I have no persistent significant sx.  

Doctor suggested switching to Topetecan OR going on clinical trial of weekly Taxol 80 mg/m2 and  possibly AMG 386. With the clinical trial I have a 2 in 3 chance of receiving the AMG 386.

I would appreciate your thoughts on my tx. options as well as any insights you have about the meaning of the change in my lymph node.

I have posted before and always appreciate your response. Many thanks.

[Annekathryn Goodman, M.D.]

Hi There,
Thank you for your complete information.
You are getting great care.
You have many options and there is no wrong answer.
you could:
take a break for a month and rest your bone marrow
or consider the options outlined by your doctor.

-Your have a slowly growing lymph node and that is reflected in the slight change of your CA 125.

As far as the BRCA2 mutation.
three thoughts:
-let your family know and suggest that they get screened
-get a mammogram
-ask your doctor about Parp inhibitors which are a new class of drug that is designed to work for women with BRCA 1/2 gene mutations. I have pasted a blurb below
best wishes

Poly(ADP-Ribose) polymerase (PARP) is a nuclear enzyme involved in repairing DNA damage, mediating cell death and regulating immune response. PARP activation occurs when cells are damaged in instances such as during chemotherapy, radiotherapy radiation therapy, stroke, head trauma and heart ischema. The multiple functions of PARP make it an attractive target for a variety of serious conditions including various types of cancer and neurodegenerative diseases.

In cancer patients, PARP inhibition may increase the therapeutic benefits of radiation and chemotherapy. Targeting PARP may prevent tumor cells from repairing DNA themselves and developing drug resistance, which may make them more sensitive to cancer therapies. In preclinical testing, PARP inhibitors have demonstrated the ability to increase the effect of various chemotherapeutic agents (e.g. methylating agents, DNA topoisomerase inhibitors, cisplatin), as well as radiation, against a broad spectrum of tumors (e.g. glioma, melanoma, lymphoma, colorectal cancer, head and neck tumors).

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[abrite]

Forgot to mention that I recently tested postive for the BRCA 2 gene mutation. Any thoughts on what, if anything, I need to do? Thanks again.