Saturday, August 29, 2015

7 year update

It has been a long time since I updated the blog but realized, just yesterday, that it had been exactly 7 years since Linda's last chemo treatment.  That brought me back to the blog and I realized that many people still stop by.  I thought I'd take a moment to update y'all on Our Life With Breast Cancer.

I am happy to report that my beautiful bride is still with us and cancer free.

A few years back, Linda decided to have a preventative hysterectomy to minimize the number of places her cancer might show up again.  Post surgery, upon routine examination of the removed ovaries, they found a handful of cancer cells, ovarian cancer cells (not metastasized breast cancer cells).

In the world of ovarian cancer, this cancer wasn't even stageable.  From my understanding, doctors rarely, if ever, get to see clear cell ovarian cancer in its early stages.  Linda's biopsy was sent to Johns Hopkins University and we were told it will be used for further studies on the initial stages of ovarian cancer.  There was no need for chemo and in fact there is no established protocol for such an early detection.  Linda gets to visit the ob/gyn oncologist for 5 years to keep an eye on it with an abundance of caution.

I started writing this blog as my own personal therapy.  During those hazy days, I would scour the internet looking for stories of positive outcomes.  If you are reading this, I hope this gives you some hope that there is a future and, believe it or not, there will come a day when your diagnosis will not be the center of every waking and sleeping thought.

Our story is not over and that alone is reason to be thankful every day.

Tuesday, April 26, 2011

Future of Personalized Cancer Care Is Promising and Near

Newswise — BIRMINGHAM, Ala. – Cancer survival rates could improve soon with whole-genome sequencing, according to two studies published in the April 20, 2011, issue of the Journal of the American Medical Association that describe the first clinical applications of the high-tech process in patients with cancer.
The papers are remarkable examples of the power that genomic data hold for patients with a cancer diagnosis, according to an accompanying editorial by Boris Pasche, M.D., deputy director of the University of Alabama at Birmingham Comprehensive Cancer Center and professor of medicine, and Devin Absher, Ph.D., of the HudsonAlpha Institute for Biotechnology.
Whole-genome sequencing is a high-tech process that essentially maps a person’s DNA and analyzes it for mutations. This has enabled cancer therapies to evolve from a standard therapy for all patients with a given type of cancer to a slightly more personalized treatment.
“Whole-genome sequencing gives us the ability to screen a much larger number of tumors and correlate them with the outcome of the patient, so it is very likely that our targeted therapy is going to be exploding in the next decade,” Pasche says.
Half of all men and one-third of all women in the United States will develop cancer during their lifetimes, according to the American Cancer Society; and few, if any, do not know someone who has had cancer or died because of it. This new advance could change that.
“In one study, a patient with leukemia had a poor prognosis, but through sequencing, this patient was found to have a gene that showed they would react favorably with a different therapy than originally recommended,” Pasche says. “If patients have certain genes, they may not respond to certain treatments. But whole-genome sequencing gives a full picture of the genetic make-up of the tumor and the patient, and it may allow the physician to target a new treatment.”
Pasche says the unbiased picture of the sequenced DNA enables physicians to look at tumors in a way not possible previously. Even when the technology finally was available, it was too expensive. Now, the cost to sequence a patient’s entire genome and the genome of their tumor is down by more than 100 fold, but still ranges from $30,000 to $40,000.
“Prices are still dropping very rapidly; in the next 10 years, it will cost less than $10,000, and it certainly will be more affordable in the next five years,” says Pasche, who believes having sequencing covered by insurance or otherwise is a work in progress.
At UAB, Pasche says whole-genome sequencing is being used in many projects, most notably in a clinical trial for women with triple-negative breast cancer.
“There is a high degree of expectation with whole-genome sequencing,” he says. “The hope is that it will help survival rates of those with cancer.”
About the UAB Comprehensive Cancer Center
The UAB Comprehensive Cancer Center is among the 40 cancer centers in the nation to meet the stringent criteria for the National Cancer Institute's comprehensive designation. The center is a leader in groundbreaking research, reducing cancer disparities and leading-edge patient care.
EDITOR’S NOTE: The University of Alabama at Birmingham (UAB) is a separate, independent institution from the University of Alabama, which is located in Tuscaloosa. Please use University of Alabama at Birmingham on first reference and UAB on all consecutive references.

Scientists Decoded DNA of 50 Breast Cancer Patients

St. Louis, MO (Scicasts) - Scientists at Washington University School of Medicine in St. Louis have sequenced the whole genomes of tumors from 50 breast cancer patients and compared them to the matched DNA of the same patients' healthy cells. This is the single largest cancer genomics investigation reported to date, the university claims, and has allowed researchers to find mutations that only occurred in the cancer cells through this comparison process.

The above Circos plot is a visual representation of the genomic disruptions in one of the breast cancers studied. Image by: Matthew J. Ellis, MD, PhD.

This research was presented at the American Association for Cancer Research 102nd Annual Meeting 2011. According to the press report, the researchers uncovered incredible complexity in the cancer genomes, but also uncovered a glimpse of new routes toward personalized medicine.
In all, the tumors had more than 1,700 mutations, most of which were unique to the individual, said Matthew J. Ellis, MD, PhD, professor of medicine at Washington University School of Medicine in St. Louis and a lead investigator on the project. "Cancer genomes are extraordinarily complicated," Ellis continued. "This explains our difficulty in predicting outcomes and finding new treatments."
To undertake the massive task, Washington University oncologists and pathologists at the Alvin J. Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine collaborated with the university's Genome Institute to sequence over 10 trillion chemical bases of DNA — repeating the sequencing of each patient's tumor and healthy DNA about 30 times to ensure accurate data.
"The computing facilities required to analyze this amount of data are similar in scale to those of the Large Hadron Collider, used to understand the workings of sub-atomic particles," said Ellis.
The DNA samples came from patients enrolled in a clinical trial that Ellis is leading for the American College of Surgeons Oncology Group. All patients in the trial had what is called estrogen-receptor-positive breast cancer. These cancer cells have receptors that bind to the hormone estrogen and help the tumors grow.
To slow tumor growth and make the tumors easier to remove, patients received estrogen-lowering drugs before surgery. But, for unknown reasons, this treatment does not always work. Twenty-four of the 50 tumor samples came from patients whose tumors were resistant to this treatment, and 26 came from patients whose tumors responded. Comparing the two groups might help explain why some estrogen-receptor-positive breast cancer patients do well with estrogen-lowering drugs, while others do poorly.
Confirming previous work, Ellis and colleagues found that two mutations were relatively common in many of the patients' cancers. One called PIK3CA is present in about 40 percent of breast cancers that express receptors for estrogen. Another called TP53 is present in about 20 percent.
Adding to this short list of common mutations, the researchers found a third, MAP3K1, that controls programmed cell death and is disabled in about 10 percent of estrogen-receptor-positive breast cancers. The mutated gene allows cells that should die to continue living. Only two other genes, ATR and MYST3, harbored mutations that recurred at a similar frequency as MAP3K1 and were statistically significant.
"To get through this experiment and find only three additional gene mutations at the 10 percent recurrence level was a bit of a shock," Ellis explained.
In addition, the team found 21 genes that were also significantly mutated, but at much lower rates — never appearing in more than two or three patients. Despite the relative rarity of these mutations, Ellis stresses their importance.
"Breast cancer is so common that mutations that recur at a 5 percent frequency level still involve many thousands of women," he said.
Ellis points out that some mutations that are rare in breast cancer may be common in other cancers and already have drugs designed to treat them.
"You may find the rare breast cancer patient whose tumor has a mutation that's more commonly found in leukemia, for example. So you might give that breast cancer patient a leukemia drug," Ellis explained.
But such treatment is only possible when the cancer's genetics are known in advance. Ideally, according to Ellis, the goal is to design treatments by sequencing the tumor genome when the cancer is first diagnosed.
"We get good therapeutic ideas from the genomic information," he said. "The near-term goal is to use information on whole genome sequencing to guide a personalized approach to the patient's treatment."
This work builds on previous collaborations between Washington University oncologists and the Genome Institute. In a study published last year in Nature, they reported the complete tumor and normal DNA sequences of a woman with "triple-negative" breast cancer, a particularly aggressive type that is difficult to treat and more common in younger women and African-Americans.
While many mutations are rare or even unique to one patient, Ellis highlighted that quite a few can be classified on the basis of common biological effects and therefore could be considered together for a particular therapeutic approach.
Ellis looks to future work to help make sense of breast cancer's complexity. But these highly detailed genome maps are an important first step. "At least we're reaching the limits of the complexity of the problem," he said. "It's not like looking into a telescope and wondering how far the universe goes. Ultimately, the universe of breast cancer is restricted by the size of the human genome."

Sunday, April 24, 2011

Scientists Find Promising Breast Cancer Therapy

A new combination of drug therapies may prove effective in treating triple-negative breast cancer in human patients, according to a recent study published by researchers at Harvard Medical School and Baylor College of Medicine.
Triple-negative breast cancer is one of three classes of breast cancers and the only one that currently has no readily accessible treatment, said HMS Professor Stephen J. Elledge, the principle investigator for the Harvard lab.
The only treatment option for patients with these tumors is chemotherapy, and the median survival rate for such patients is very low.
The research sought to identify classes of molecules that, when down regulated, cause a cell to gain cancerous properties.
The study, which was published last month in the journal Cell, reported that the absence of a tyrosine phosphatase enzyme called PTPN12 caused human mammary cells to gain cancer-like properties in vitro.
The researchers separately found that PTPN12 was inactive in more than 50 percent of the triple-negative breast cancers tested, showing that the enzyme plays a significant role in this class of breast cancer, Elledge said.
Thomas F. Westbrook, a former postdoctoral fellow in Elledge’s Harvard lab and currently leading the research group at Baylor, discovered the PTPN12 enzyme while still at Harvard.
That enzyme is known to deactivate another group of enzymes called receptor tyrosine kinases that are responsible for cell growth.
So when PTPN12 is inactivated, cells are free to grow and divide rapidly, like cancer cells.
The research group identified three tyrosine kinases that are specifically regulated by PTPN12. These results indicated that the misregulation of these three enzymes could be a leading cause of triple-negative breast cancer, according to the study.
“If we figure out how to inhibit different kinases together, we might be able to treat this disease,” said Elledge.
The researchers tested in mice a combination of two FDA-approved, on-the-market drugs that are already used to treat other cancers and that inhibit the desired kinases. One drug, Tykerb, is known to inhibit two of the enzymes, and another, Sutent, is known to inhibit the third.
The study found that tumors in mice that were treated with a combination of both drugs shrank by more than 90 percent, and life expectancy for these mice more than doubled.
The researchers are now in the process of negotiating with drug companies to design a Phase II clinical trial that will test the new therapy in humans.
Ellidge said, “It may take two to three years to set up a clinical trial and get results, and then we can determine whether there will be a therapy.”
Ellidge said that while the research group has identified some of the kinases that are activated in triple-negative breast cancer, there is still more research to be done in order to understand the disease mechanisms completely.

Wednesday, March 2, 2011

New peptide could be effective treatment for triple negative breast cancer

New peptide could be effective treatment for triple negative breast cancer

Using a mouse model of triple negative breast cancer, they tested the new leptin receptor antagonist peptide and compared it to conventional chemotherapy. The leptin receptor antagonist peptide extended the average survival time by 80 percent, compared to 21 percent for chemotherapy. The peptide was found to be non-toxic even up to the highest dose administered, said Sumacz.

Tuesday, February 1, 2011

The Disappearing Spoon

For me, high school chemistry was all about bunsen burner hi-jinx and natural gas flame throwers.  I honestly cannot remember a single learning moment from Mrs. Brownstein's 10th grade chemistry class and a solid D on my high school transcript is reflective of that.  High school physics was even less appealing...theory without the fun of blowing up shit.  College chemistry followed suit and was only a means to an end.  Three semesters of physics on the other hand, although somewhat more enjoyable, had the unenviable position of being a Friday 8am class, an equal and opposite reaction to my Thursday night pre-weekend binge drinking.  My father, who received his doctorate in chemistry from the University of Birmingham a decade before I was born not only failed to pass along the affinity for chemistry but also any trace of academic acumen.  That being said, he was quite fond of pointing out that the pretzels I was eating were made with lye, the same stuff in drain cleaner, the bread I was eating was legally allowed to have 10 insect thoraxes per loaf, and the 7 different layers of plastic needed to make a 2L soda bottle (I think he still has the original prototype bottle in the crawlspace from the late 70s)...tidbits of trivia I pass along to my kids.

So why then, almost 20 years out of college, would you find a printout of the periodic table on my desk this week and an electronic version on my phone?  Last week I finished The Greatest Show on Earth: The Evidence for Evolution by Richard Dawkins.  Whether it be a mid-life crisis, a reaction to our cancer fight, or some other reason, I began to question my own beliefs.  Dawkins' book was one step in reaffirming them but it did leave a hole.  Among other things, it delves as deep as DNA, proteins, enzymes, and amino acids but stops short of explaining the genetic code, the transcription process, and why molecules behave the way they do at the atomic level.  Dawkins did a fantastic job expaining his assertions in all other areas of the book but I was, probably out of my sheer ignorance of basic chemistry, left wanting more.  With that, I went looking for a book on chemistry.

Needless to say, textbooks, acedemia and I don't gel too well.  I need some narrative and backstory with my facts.  I need it delivered in entertaining, sugary, bite-sized chunks.  I'm sure everyone can recall a certain teacher who made the process of learning a real joy.  Someone who didn't teach from a textbook but taught from their experiences and love of the subject.  Such is a book called "The Disappearing Spoon" by Sam Kean.  Fascinating stories of the atrocities of war-time gases, and the people behind them.  Petty personal rivalries.  The battle between silicon and germanium for our electronic hearts.  We all know about Marie Curie but none of us know about the 16 year kid who attempted to build a nuclear reactor in his garden shed.  Cadmium, thallium, and mercury poisonings, oh my!  Along the way, you learn about protons, neutrons, electrons, shells, valences, spin, isotopes, radioactive decay, and a whole lot more.  Information that, in high school or college, likely went in one ear and out the other.

I'm only halfway through the book but am thoroughly engaged and impressed.  I am a little closer to understanding nuclear medicine (there is no doubt we fret over its results every 3 months) and a little closer to understanding the cancer that has been a part of our life for 3 years.

Monday, January 24, 2011

Triple Negative Breast Cancer makes the front page in the Austin-American Statesman

Great news from our local network of doctors.

Austin American Statesman article

"This is the most compelling development in breast cancer in the last five years," she said. "I had a patient come here from Puerto Rico to get access to this trial."

"Breast cancer experts not connected to the study greeted the results with excitement mixed with caution. For a cancer that is difficult to treat, iniparib shows great potential — provided the results are confirmed by the final, phase 3 trial, they said. Patients are still in that trial, and results will be out later this year, Patt said.

Thursday, January 20, 2011

Breast Cancer News

Trio of Drugs May Combat 'Triple Negative' Breast Cancer

In the new study, Johns Hopkins scientists began with a drug called Entinostat, which blocks an enzyme that unfolds DNA, providing regulatory molecules access to genes within and also reactivates a gene called retinoic acid receptor-beta (RARβ). Then, they added a drug called All Trans Retinoic Acid (ATRA), related to Vitamin A, which binds a protein made by the reactivated RARβ gene. Together, the ATRA drug and RARβ gene act as a brake on cancer cell growth.

Sporadic Breast Cancers Start With Ineffective DNA Repair Systems

Ultraviolet light, for example, can cause mutations, but a sophisticated system of nucleotide excision repair (NER) proteins trolls the DNA strands to identify problems and initiate repair processes. The same system repairs damage caused by many environmental carcinogens, including tobacco smoke.

"Even in healthy breast tissue, this system is only about one-fifth as effective as it is in skin,"

Potential New Target for Treating Triple Negative Breast Cancer Identified

Now researchers in Dublin (Ireland) have found that TNBC cells respond to compounds that disrupt the signalling processes of another receptor, EGFR (epidermal growth factor receptor), high levels of which are expressed in TNBC

Saturday, January 1, 2011

All The Small Things

We once again enter the new year with a clean bill of health *knocks on wood*.

Although it wasn't what we expected, we got some good news at the tail end of 2010.  After a trip to Johns Hopkins in Maryland, the cancerous ovary turned out to be clear cell, not the non-invasive borderline we had hoped for.  The good news is that the tumor was microscopically small.  So small in fact that they could count the individual cells.  So small in fact that a dissection of the biopsy 1mm to the left or right would have missed the tumor.  So small in fact that no one has ever seen a clear cell tumor at such an early stage.  So small in fact that there is very little chance that the tumor had spread anywhere.  So small in fact that the removal of the tumor alone is all the therapy Linda will require.

A complete PET and CT scan from head-to-toe confirmed what we had prayed for.

On December 13th, we also passed the 3 year mark which is a huge milestone, especially for TNBC survivors.

With that, as folks have dreams and aspirations for bigger and better in the new year, we welcome 2011 and will continue to appreciate the small things.

Sunday, December 19, 2010

Merry Christmas

Yesterday, we enjoyed a perfect holiday Saturday.  We woke up late, searched out and found a gluten-free wing joint, went to the movies and saw Tangled, came home to hot chocolate by the fireplace and decorated the Christmas tree.

When I prayed to my God to help get us through the past 3 years, it was a day just like yesterday that I asked for.  I am ever grateful for the life that I enjoy and ever aware of how fragile it can be.

May the warmth of the season bless your home and you have the opportunity to spend it with those you love.

Merry Christmas,

Wednesday, November 10, 2010

Third Time Is A Charm

In families with a long history of breast cancer, there commonly exists an inherited genetic mutation which increase a person's susceptibility to breast and ovarian cancers.  These are known as the BRCA1 and BRCA2 genes.  From my layman's point of view, these genes are responsible for ensuring that there are no defects in a cell's DNA after that cell divides.  If there is, these genes commit cell suicide and thereby prevent it from replicating the damaged DNA further.  In people with defects in the BRCA1 or BRCA2 gene, this tumor suppressive behavior is damaged and that allows for the unregulated growth of cells, which is how you would characterize cancer.

Not long after Linda was diagnosed with breast cancer, she was tested for the BRCA1 and BRCA2 mutations and it came back negative.  It was a huge relief not only for her but also for our daughter who would likely have inherited this trait also.  Had it come back positive, a bilateral mastectomy and complete hysterectomy, along with chemo and radiation, would have been the proper course of therapy to minimize her risk of recurrence.

In the absence of the BRCA defects, and the initial IIB staging, our course was neo-adjuvant chemo, a lumpectomy, more chemo and radiation w/ chemo.  However, when the cancer came back a second time in the summer of 2009, a full bilateral mastectomy was the right path to take.  At the time, due to the nature of the 2nd cancer, Linda's oncologist suggested that something "odd" was going on in Linda's body which was forming these tumors.  Although she was BRCA negative, there may be some other gene defect that science has yet to discover causing the cancer.  She suggested that Linda think about a hysterectomy to reduce her risk of ovarian cancer which is closely associated with BRCA+ breast cancers.

Never being one to shy away from a fight, Linda decided to have a hysterectomy in October of this year.  We were happy with our allotment of progeny and the baby factory had long since shut down after her first chemo so this decision was purely a prophylactic measure to remove the parts where this cancer could grow.

Two weeks after surgery, on Oct 16th, while enjoying our Saturday morning coffee in bed, we received a call from Linda's ob/gyn surgeon.  They found a 2mm cancer in her right ovary.  She said Linda must have someone looking out for her because by the time they usually find ovarian cancer, it is too late.  Her decision to have the hysterectomy may indeed be the best decision she's ever made (aside from her decision to mate with me of course).  Dr M. hooked us up with the city's top ob/gyn oncologist to discuss our next steps and set the appointment for early November.

We met with Dr. T yesterday.  The first thing we learned was that this cancer wasn't a metastasis of the breast cancer.  Over the intervening 3 weeks, the thought of a Stage IV breast cancer metastasis literally kept me up at night, so it was a relief to hear that.  The second thing we learned was that they almost never see ovarian cancers at this early stage.  It was so early in fact that they have had a hard time figuring out what kind of cancer cells these are.  The initial pathology has identified them as both "border-line" and "clear cell", which according to the oncologist doesn't make sense.  They are either/or, but rarely ever both.  He has sent the tissue to Baltimore for a second opinion.  From our 1 hour long meeting, we learned that "border-line" ovarian cancers are non-invasive whereas "clear cell" cancers are high-grade and aggressive.  He believes that the second pathology will come back as "border-line" but can't make a final diagnosis until he gets the results back in 2 weeks.  He also believes that even if it is "clear cell", we caught it early enough that it hadn't had a chance to, as he put it, "sprinkle its seeds around the abdomen like a dandelion".  In either case, he doesn't think chemo is in our future, unless it comes back as "clear cell" which may introduce that option.

So we sit here and wait to see what our future holds.  We have beat cancer twice before, and with Linda's courage and your thoughts and prayers, I have no doubt we will beat it again for a third time.

Tuesday, August 3, 2010

Thank You

After more than 2 years of writing about our life, I think the time has come to close the electronic cover of my blog.  In a world where a video of someone getting smacked in the nuts gets 3 million hits, my blog's 5,000 visitors seems tiny but it has made a huge difference for me.  Hopefully I have helped some people, made others laugh, and made others think.  It has been a great outlet for me and I've made some friends along the way and reacquainted with others.  Linda has just finished the final touches of her reconstruction and the results are incredible.  We have some preventative surgeries in our future but outside that, I am anxious to take what we have learned and move on to the next chapter of our lives.  We are not the same people we were on Dec 12 2007 and, for the most part, that is a good thing.  It took a while, but I found my God living in my heart where it had always been.  You won't read about my God in a book nor hear about my God on the TV and even if I tried, I couldn't explain my God to you.  It's all good :)

From the bottom of my heart, I thank you for spending the last 2 years with me online and in my heart.

God Bless,

Tuesday, June 29, 2010

Summer, uninterrupted

It was July 3rd last year when we learned that the cancer was back.  4 days shy of that anniversary, we learned today that Linda's semi annual scans all came back normal.  Hold on a sec...there is no such thing as "normal" when talking about recurrent breast cancer scans.  There is "super shitty" and "friggin awesome".

I do declare June 29th to be Friggin' Awesome Day!

Thanks for all your support.  You are friggin awesome!

Thursday, May 27, 2010

Do the right thing

The drive-thru at McDonalds was too long this morning so I decided to pull in and order in the lobby.  On my way there, I found a $5 bill wrapped in a $20 in the parking lot.  I looked around, picked it up and slid it into my pocket.  Sweet!  As the guy in front of me started to order, he began searching his pockets for 'something'.  He told the cashier to wait and ran out to his car to get his wallet and returned to pay for his meal.  While we waited for our breakfasts, I asked him if he had lost something outside.  In a thick Eastern European accent he said 'I zink I lost twenty-fi dolla'. I reached into my cargo pocket, grabbed the fold of bills between my index and middle fingers and extended it out to him. 'Zank you wery much' he said.

Man that felt great!

So my question is...why the hell did I do that?  Don't get me wrong, I'm glad I did, but why?  Was it a completely selfish act knowing that it would 'feel better' to return the money than keep it?

Part of my left brain says it is a simple biological event engineered to release a cocktail of endorphins and dopamine that 'feels good'.  Over 4 billion years of fine-tuning, evolution has preferred variants/decisions that lead to the preservation of the species and it is that 'wiring' that makes us know what is the 'right' thing to do, because we are rewarded with 'feel good' drugs.  Caveman want food, caveman steal food, caveman beat on head with club for stealing food, end of line for caveman (and his potential offspring).  I think even Laplace's demon would have a hard time correlating 4 billion years of events with my McDonalds moment.

The other part of my left brain says this is environmental conditioning.  40+ years of personal interaction and societal influences (which themselves have been fine tuned over 10,000 years of civilization) yielded that moment in McDonalds.  The meaning of right at that particular moment was a personal one.  Someone else may believe the right thing to do is to keep the money.  Are right and wrong just shaped personal biases?  I hope R v. W is something bigger than that.

My right brain, which has been getting a lot of attention lately, is more confused than the left side but luckily doesn't require the same level of clarity than the left side does to operate properly, nor does it need to adhere to the scientific method, but I suppose that is why we have 2 halves (evolved or otherwise).  Good vs evil, right vs wrong, Nacho vs Cool Ranch.  Epic questions...none of which was answered in the LOST finale :)

It has taken me 40 years to find Hope, at least I think I found it.  Perhaps it will take another 40 years to find Faith and for me, I suspect right and wrong will play a big part of that.

Anyhow back to my McDonalds I'm driving out of the parking lot in my hail damaged 7 year old VW Jetta, I look in my rear-view to see the guy getting into his late model 7 series BMW.  I had to laugh :)

Sunday, May 16, 2010

It's All Relative

Linda: Daddy can install the light fixture when we get home.
Daughter: But Daddy cut his finger on the hedge trimmer.  He's laying down.
Linda: I just had my nipples sewn on and I was doing laundry the next day.  He can suck it up.

How can I argue with that?  I can never be sick again....*sigh*

Friday, April 16, 2010

Fallen Soldier

Linda just called to tell me we lost another Pink Ribbon Cowgirl today.  She was 29.

Linda seems fine, however I am hiding out in my office waiting for my eyes to dry.  This shit is fucked up.

Sunday, March 21, 2010

829 Days

It has been 829 days since Linda was diagnosed with breast cancer.  Since then, I have shared 829 sunrises with her and 829 sunsets.  We have tucked our kids in 829 times and told them we love them (at least) 829 times.  I am thankful for every day I get to spend with her.  I have stopped asking why and simply accept the gift that is given to us every morning.  Tomorrow will be 830 and I will treat the day with the reverence it deserves.

Tuesday, February 16, 2010

The Wonder Drug: Not Just For Hangovers Anymore

Incredible news, and applicable to TNBC, which in previous studies wasn't proven.

...It affected both estrogen-positive tumors and those not fueled by the hormone...

Aspirin cuts death risk after breast cancer

Large study of nurses showed 50 percent lower risk cancer would spread

WASHINGTON - Breast cancer survivors who take aspirin regularly may be less likely to die or have their cancer return, U.S. researchers reported Tuesday.

The study of more than 4,000 nurses showed that those who took aspirin — usually to prevent heart disease — had a 50 percent lower risk of dying from breast cancer and a 50 percent lower risk that the cancer would spread.

"This is the first study to find that aspirin can significantly reduce the risk of cancer spread and death for women who have been treated for early stage breast cancer, " said Dr. Michelle Holmes of Harvard Medical School, who led the study published in the Journal of Clinical Oncology.

"If these findings are confirmed in other clinical trials, taking aspirin may become another simple, low-cost and relatively safe tool to help women with breast cancer live longer, healthier lives," Holmes added in a statement.

Holmes and her team studied 4,164 female registered nurses taking part in the Nurses' Health Study, an ongoing analysis of a wide range of health issues.

They started in 1976, looking at who took aspirin, watching for breast cancer and all causes of death until 2006.

Over this time, 341 of the nurses died of breast cancer.

Women who took aspirin two to five days a week had a 60 percent reduced risk of their cancer spreading and a 71 percent lower risk of breast cancer death. Six to seven aspirins a week lowered the risk of spread by 43 percent and the risk of breast cancer death by 64 percent.

Most of the women were taking low-dose aspirin to prevent heart attacks and stroke.

Ibuprofen and naproxen appear to lower risk too

Other drugs in the same class as aspirin also apparently lowered the risks, too. These drugs, called non-steroidal inflammatory drugs or NSAIDs, include ibuprofen and naproxen but not acetaminophen, also known as paracetamol.

But there was not enough data on these drugs to give a clear answer.

The researchers said they are not sure how aspirin and other NSAIDS may affect tumors but it could be by lowering inflammation. Other studies have shown that aspirin and ibuprofen can lower colon cancer risk, for instance.

"Aspirin has relatively benign adverse effects compared with cancer chemotherapeutic drugs and may also prevent colon cancer, cardiovascular disease, and stroke," the researchers wrote. It affected both estrogen-positive tumors and those not fueled by the hormone.

Holmes' team stressed that patients should not take aspirin while undergoing radiation or chemotherapy because of the risk of side effects.

And aspirin can cause stomach bleeding so it should not be taken without a doctor's supervision.

Friday, February 5, 2010

Nothing to report

All is going as planned, no complications at all.  Aside from some minor fix-up tweaks, the results are great.  We are eager to get going on a running/exercise plan once we are given the go ahead and Linda feels up to it.

This central Texas winter has been extraordinarily long and cold (by Texas standards) and we are anxiously waiting for spring/summer to arrive.  Life is good and it is full speed ahead :)

Thursday, January 21, 2010

The Null Process

If you've spent any time around a PC, at some point you've come across the Task Manager. The Task Manager tells you what processes are running on your computer.

You will probably also have noticed a process called the "System Idle Process" which seems to take up an inordinate amount of processing cycles.  The truth is, most modern computers and operating systems *have* to be doing something all the time.  When they have nothing to do, they do the "System Idle Process".

Your brain is pretty much the same.  I call it the 'null process'.  When you are not thinking or processing the task at hand, your brain reverts to the null process.  If you were to come by office at around 4:30 in the afternoon, and I'm staring at my desk with a line of spit running from my chin to the keyboard, that would be the null process in action. 

Everyone has different null processes and in all likelihood they have changed over time.  At age 12 my null process changed from thinking about cartoons, comics, and Star Wars to thinking about other things that occupy a young man's mind...

Actually from age 12 to 25, thinking of vaginas and related accessories (butts, boobs, etc) was pretty much a foreground process the whole time.  At 25, I married my favorite vagi...errr...Linda and the null processes started to lean towards family and career.  How do we get ahead?  Is this the right move?  Should we have kids?  Should we have more kids?  How do we make more money?  Getting started is pretty tough, so the majority of the early years were directed toward my career.

Then, around 35, after establishing myself in my career, I started to realize that we were not only supposed to raise kids, we were supposed to raise 'good' kids.  That required a shift in priorities and my null processes started to flip-flop

and, I think you know where this is going.  On Decemeber 13, 2007,  my process table changed forever

and that's how it stayed for all of 2008. When all you do 24x7 is think about cancer, your mind tends to take you to some pretty dark places.  What's worse, at least in my case, is there was no outlet.  As the caregiver, I couldn't very well burden the caregivee with what I was dealing with.  That's when I started writing about it.  Sure I was still thinking about it *all* the time, but instead of letting my null process take me to those places where my fears and insecurities live,  I instead focused on telling our story and hopefully injecting some much needed humor along the way.

I think 2009 was our way of coping with 2008.  Our stated goal for 2009 was to have as much fun as possible and to make up for 2008.  We surely did, and I have the scars to prove it!  Subconsciously, or maybe consciously, I believe the unstated goal was to keep the null process at bay.  If you are busy doing other stuff, the null process never gets a chance to run.  When the cancer came back in July, we really overclocked ourselves, far beyond the manufacturer's (and definitely the credit card company's) recommended settings.  It really was all cancer, all fun, all the time.

and then, just this past weekend, an interesting thing happened.

It wasn't a huge event, but enough so that I noticed.  I think that is a pretty healthy sign.

My stated goal for 2010 is to devote some active and null processes to my career, which has definitely been a background process for the past 2 years.  Thankfully, I have had more support from my company than anyone could ask for.  2010 calls for a healthy mix of family, fun and career, and who knows, if I play my cards right...