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Wednesday, September 2nd, 2009

Test Results – Tumor Markers #4

I COULDN’T WAIT TIL THIS EVENING TO POST THIS!!!

Last Friday, I had the bloodwork drawn to track my tumor markers.  It was draw #4.   I’ve been having Very Good Results…

I now have the results of the August 27 draw… this draw was for both the monthly tests (most specifically my CEA Tumor Markers) AND for the 3-month tests, which include my HER2 and EGFR Numbers…

On April 15, my baseline CEA tumor markers were 63.1 ng/mL (nanograms per milliliter)

On June 03, my 2nd draw CEA tumor markers were 35.9 ng/mL

On July 03, my 3rd draw CEA tumor markers were 12.8 ng/mL

My CEA numbers from the August 27 draw are 3.9 ng/mL

3-POINT-FREAKING-9!!!!!!

Norm is 0.0 – 3.0 ng/mL; levels higher than 3 ng/mL are not considered normal.

3.9 is Pretty Freaking Close To Normal!!

The numbers Just Keep Dropping!  I can’t help but be excited!!  Still I wish I was confident with just how much this meant, but this (CEA: The Test) has answered Some questions…

I’m Still hoping that this all means Something Good… Please mean Something Good…

My Other Numbers as of Aug 27 2009 blood test results:
CA-1256 U/mL (Reference @ 0-35) – an 11 point DECREASE – down from 15 U/mL from July’s draw
CA 15-3: 16 U/mL (Reference @ <32) – a 17 point DECREASE – down from 33 U/mL from July’s draw
CA 27.29 (see CA15-3 above): 28 U/mL (Reference @ <38) – a 12 point DECREASE – down from 40 U/mL from July’s draw

I’m thinking those numbers are looking Pretty Dang Good!

More Numbers from the tests I take every 3 months:
I’m not sure about what are good levels here, but this is what I’ve got…

EGFR (Epidermal Growth Factor Receptor)
From August 2009 draw – 39
From April 2009 draw – 86
A drop of 47

HER2 (Human Epidermal Growth Factor Receptor)
From April 2009 draw – 2.8
From August 2009 draw – 8.0
An increase of 5.2, is this good…?  I’m thinking an increase can’t be good… and such a large increase, more than double…? I DO know that I’m HER2 negative, and that’s a good thing to be.  But can you go from negative to positive…?  Would that increase be an indication?

Still vizualizing my Dragons with their light-saber wielding Riders!

Rich – I know that you’re a nurse…
Molli – you work for MD Anderson..
Either of y’all have any input / insight…?
PLEASE…?

What Is HER2, How Is It Tested, And Is It Tested On Invasive And Non-Invasive Breast Cancer?

Is your breast cancer HER2+? Further your understanding of HER2.

Read about HER2 and the importance of knowing the tumor’s HER2 status.

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Saturday, August 15th, 2009

RESULTS! PET/CT #3 & Bone #1

Received the results of the PET/CT #3 and Bone Scan #1!  I got them confirmed on Friday morning, but with the infusion and all, I’ve not had a chance to post them yet.

So… here we go… The “Overall” News Is Good!  YAY!

FINDINGS:

(the tumor) “has diminished from 7.7 x 3.8 cm on the previous exam (April 16 2009) to the current measurements of 6.9 x 2.4 cm.

That’s a decrease of .8 x 1.4 cm!  (There are 2.54 centimeters in 1  inch…)

FDG (fludeoxyglucose) activity has also diminished from previous peak SUV (standardized uptake value) of 4.8 to the current value 2.37.”

The FDG is the radioactive tracer that they inject for the PET/CT scan, the cancer attracts the FDG, and – from what I understand – the higher the SUV, the more cancer activity

Also…

Size of the left axillary nodes extending to the subpectoral compartment have also diminished with no hypermetabolic FDG activity demonstrated presently…

I was told that this means there is no longer activity in my lymph nodes!!!

Not all gone, but is Less!

The fight is Not over yet, not anywhere near finished, but it is LESS!!

For Now, it appears that it is not spreading, and that the activity has decreased… Decreased!!

Unfortunately, the bone scan did confirm the presence of “osteoblastic lesions” in the spine and sacrum which are “suspiciously related to early metastatic disease“… “ localized (on the spine) to the T9, L3, L4 and L5 in a pattern that is most likely produced by early metastatic disease“…

So… while the bone metastasis has not decreased, it has also not increased… so That is a good thing.

And Finally, there is a firm statement of arthritis… “there is evidence of degenerative arthritis in multiple joint areas” “in the feet in the tarsal areas and metatarsal joints, spine, shoulders and knees“…

I am still very much worried… I have won this small battle, but the war is not over… is far from over…

However, as I said, overall, Good Reports for now!

I am doing a (tentative) Happy Dance!

Sunday, June 28th, 2009

NEWS: PARP Inhibitors Working Against Inherited Cancers

More UNBELIEVEABLE Information!  This has been a Very Special Week in the War Against Cancer!!

I NEED to find out if this cancer I have is inherited.  I’m guessing that it is Very Possible, since Mom had the Same type of cancer 26yrs ago…

June 25th, 2009
PARP inhibitors working against inherited cancers
Posted by Dana Blankenhorn @ 6:29 am

If a genetic condition leads to cancer there is new hope in a class of drugs called PARP inhibitors.

Poly (ADP-Ribose) Polymerase (PARP) is a protein cells use to repair genetic injuries naturally. But cancer cells also use this protein to repair their own DNA damage. Inhibiting this action allows chemotherapy and radiation to do its job against cancers resulting from genetic mutation.

In a study causing much excitement in the cancer-fighting world (CBS called this the “holy grail” of cancer research, thus the French Taunter above) scientists at the Institute of Cancer Research in Sutton, England gave 19 patients with advanced cancers caused by mutations in the BRCA1 and BRCA2 genes a PARP inhibitor and over half saw their tumors shrink or stop growing.

The drug had no effect on 41 patients whose tumors were not the result of the genetic defect.

The big excitement is that PARP inhibitors can be designed against other forms of inherited cancer. They are already being tested against a form of breast cancer. And there are few side effects — you take a pill twice a day and may get some indigestion.

The new drug has the name olaparib. The full article is now in front of the New England Journal of Medicine firewall.

The Royal Marsden NHS Foundation Trust, which worked with the Netherlands Cancer Institute and drug maker KuDOS Pharmaceuticals, now owned by AstraZeneca, is a charitable group affiliated with that nation’s National Health Service. They would welcome your contribution.

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Sunday, June 28th, 2009

NEWS: New Drugs Could Transform Cancer Treatment

OMG, the implications of this study!!!  I can’t stop crying, can’t stop hoping…  THANKS to Vicki for sharing this info with me at the Baby Shower yesterday!!!

I’ve GOT to find out if/how I can qualify for clinical trials!!!

PARP inhibitors appear to destroy disease, small but stunning study shows
Commentary
By Robert Bazell
Chief science and health correspondent
NBC News
4:13 p.m. CT, Wed., June 24, 2009

Just-released research about a new class of drugs called “PARP inhibitors” is the most exciting development in cancer research in a decade or more. In just a few years it could save thousands of lives.

In the longer term, the drugs could represent a transformational approach to understanding and treating several forms of the disease.

All this enthusiasm is based on a small report published today (June 24) in the New England Journal of Medicine. It focuses on one clinical trial in its earliest stage in 60 patients with breast, ovarian and prostate cancer. Some — but not all — of the patients whose cancers seemed hopeless saw them shrink drastically or disappear. Many avoided the typical side effects — nausea, hair loss — associated with cancer treatment.

Of course, as with any good science, it is not just that one report that generates such excitement. The new research builds on many years of solid basic science and on other clinical trials that are either completed or in progress, which appear to show similarly dramatic reduction of certain breast, ovarian and prostate cancers.

The story of PARP inhibitors began in the early 1990s, when some scientists realized that breast cancer ran in certain families, and that some of the women in those families had an extraordinarily high — as much as a 90 percent lifetime risk — of getting the disease. There was a frantic and well-publicized hunt for the “breast cancer gene.” The hope was that finding the gene could provide crucial information about the cause of breast cancer and how to treat it.

BRCA1, BRCA2 raise risk for breast cancer
In September 1994, scientists from a company called Myriad Genetics and government researchers simultaneously won the race. It turned out there were two genes called BRCA1 and BRCA2. As they studied the genes, the researchers learned that they account for between 5 and 10 percent of all breast cancers, as well as a similar percentage of ovarian cancers and prostate cancers in men who are born with the mutated gene.

The immediate result of the gene discovery was that families and individuals at high risk could find out when they were affected. That continues to this day. But for those at risk, the treatment options are limited: surgical removal or close monitoring of the organs that might become cancerous.

What initially eluded the scientists was how BRCA1 and BRCA2 caused cancer. “We found the breast cancer gene, but we don’t know how it causes breast cancer,” one scientist famously quipped.

Years of hard work eventually revealed the mechanism. BRCA1 and BRCA2 produce proteins that repair mistakes in DNA that occur continually as cells in the body multiply normally. If a person is born with one defective of copy of one of the genes, the cells continue to grow but there is a far greater chance that an error will occur in the DNA that will cause cancer to arise.

ARP inhibitors kill cancer cells
The next big discovery came in 2005 when scientists found in lab experiments that they could make a drug, called a PARP inhibitor, that would interfere with the normal copy of the protein made from BRCA1 and BRCA2 genes. If cells have defective genes, when the drug is added, the DNA cannot be repaired at all. As a result, the cells die. And that is how PARP inhibitors kill cancer cells.

In experiments so far, the drugs have worked only in people with BRCA 1 and BRCA2 mutations resulting in breast, ovarian and prostate cancers. But there is evidence they may work in people without the mutations — particularly in cases of ovarian cancer for which better treatments are desperately needed.

The story of the PARP inhibitors is fine example of how research can move from the laboratory bench to the bedside, and it also shows how long and difficult journey can be.

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