Outliving Cancer: Surviving Even the Deadliest Forms of Cancer

My book of the same title (Outliving Cancer, Basic Health 2013) is an exploration of cancer biology through the lens of individual patients.

The conceptual framework within which my laboratory operates, reflects the basic premise that cancer doesn’t grow too much it dies too little. Thus, effective cancer therapy (regardless of contemporary wisdom) provides benefit only when the drugs induce cell death. While the forms of cell death may vary from necrotic, to apoptotic, autophagic and others, it is, in the end, the death of the cell that heralds a successful outcome.

We, along with a small group of collaborators, have pioneered the concept of individualized cancer care using each patient’s tumor as the study model. Fresh biopsies exposed to chemotherapies and signal transduction inhibitors, live or die depending upon their relative sensitivity to the drugs in question.

The simple elegance of our platform has provided immense insight into cancer biology, insights we describe in the book, which may ultimately lead to a greater understanding of all human diseases.

Having successfully applied this approach in many diseases, we have published findings in leukemia, breast, ovarian, and most recently, in lung cancers. We are now very excited by observations in one of the most difficult cancers – pancreatic. Ongoing work in this disease will be the subject of upcoming clinical trials.

One patient with pancreatic cancer comes to mind. Steve Lockwood presented to medical attention in the Spring of 2010 with weight loss, abdominal pain, and unrelenting low back pain. He was seen by a local medical oncologist after a CT scan revealed a large mass in the pancreas, extensive liver metastases and disease throughout the abdomen. He then sought the opinion of UCLA and the City of Hope.  Neither institution could offer any solutions. Luckily his wife, a nurse, had heard about our work and brought him to Rational Therapeutics.

His tumor markers were doubling every week. He couldn’t eat and required daily intravenous hydration, as well as high dose narcotics to get through each day. He was deteriorating so rapidly that I had concerns that he might be too ill for me to help. We decided to conduct an open liver biopsy. As his tumor markers, CA19.9, climbed into the multiple thousands, we found a three-drug combination to be the most active for his tumor.

Within a week, the pain began to subside. After two weeks, it was demonstrably better. By the time we began treatment cycle two, he had begun to gain weight and came off pain medications entirely.

Two cycles later, his tumor markers were normal and his PET CT remarkably improved. An additional cycle later, his PET CT was normal.

While there are many difficult cancers, metastatic pancreatic cancer figures among the worst. The fact that we could find a treatment was cause for celebration. The fact that Steven now remains in remission, after three years, is nothing short of a miracle. As I have written before, there are two kinds of cancer patients: those we can treat and those we can’t. Steve Lockwood turned out to be one of those patients we could.

Like Niebuhr’s Serenity prayer, oncologists need the serenity to accept the cancers they cannot treat, the courage to treat those that they can, and the wisdom to know the difference. It is our use of laboratory assays to select treatments that provides us with that particular form of wisdom.

Phar Lap and the Treatment of Leukemia

Phar Lap (1926-1932) was a thoroughbred horse bred in New Zealand. After winning the Melbourne Cup and 37 other races, his victory at the Agua Caliente racecourse in Tijuana, Mexico, established the track record in 1932.

With each victory, his detractors became more strident. He was even the target of an assassination attempt. To prevent him from winning (and thereby disrupting the betting odds) officials would add lead bricks to his saddle. On the occasion of the Melbourne cup of 1930 he carried 138 pounds of lead, yet won the race. A quote from the Sydney Morning Herald dated Wednesday, November 5, 1930, read, “The question was not which horse could win, but could Phar Lap carry the weight. Could he do what no other horse before him had done?”

It appeared that the one thing that race officialdom feared above all else, was a horse that could consistently beat the field and win the race.

The tale of Phar Lap was brought to mind after a colleague forwarded a paper published in the journal Leukemia on August 10, 2012: “The use of individualized tumor response testing in treatment selection: second randomization results from the LRF CLL4 trial and the predictive value of the test at trial entry.” (E Matutes, AG Bosanquet et al, Leukemia, Letter to the Editor.)

Published as a letter to the editor, the paper describes correlations between the TRAC (tumor response to antineoplastic compounds) assay, a short-term suspension culture cell death laboratory assay (very similar to our work) and clinical response, time to progression and overall survival in patients with chronic lymphocytic leukemia (CLL) who received chemotherapy as part of the LRF CLL4 trial conducted in England between 1999 and 2004.

The initial trial was a blinded correlation between laboratory assay results and patient response to one of three treatment regimens. An examination of the data reveals a clear and statistically significant correlation between drug sensitivity and overall survival (p = .0001). The 10-year survival of drug sensitive patients was 28 percent, while the 10-year survival for drug resistant patients was 12 percent.

Significant correlations with survival were observed for known prognostic factors like 17p and 11q deletion, as well as IGHV mutational status. Correlations were also observed between the TRAC assay results and these prognostic factors.

The report goes on to describe a second randomization that took place at the time of disease progression, either failure of first-line therapy or reoccurrence within 12 months. In this part of the study, 84 relapsed patients were allocated to standard therapy and their outcomes were compared with 84 patients allocated to treatment guided by the TRAC assay. The drugs tested in the assay-directed arm included chlorambucil, cytoxan, methylprednisolone, prednisolone, vincristine, doxorubicin, mitoxantrone, 2CDA, fludarabine and pentostatin. In vitro resistance for combinations was defined as resistance to all constituent drugs in the combination, while drug sensitivity was defined as TRAC-assay sensitivity for any of the drugs used in combination. No discussion of synergy analysis was included.

In examining this study, I cannot help but be reminded of Phar Lap. First, marshaling a study of 777 CLL patients, and conducting 544 TRAC analyses, is a phenomenal undertaking for which these authors should be commended.

Second, the observation of a significant correlation between laboratory assay results and overall survival, as well as the biological implications of this platform’s capacity to correlate with molecular markers is a demonstrable and noteworthy success, however unheralded.

Where the analogy with poor Phar Lap’s struggles, weighted down with lead, becomes most poignant is the final portion of the study wherein 84 patients received assay-directed therapy. To wit, we must remember that in 2012, drug refractory CLL remains an incurable malignancy (with the exception of a small subset of successfully transplanted patients) and that no chemotherapy-alone trial has provided a survival advantage in this group. But this only begins to explain this trial’s results.

Among the virtually insurmountable hurdles that these investigators were forced to confront was the fact that fully 52 percent of the standard treatment arm group were destined to receive fludarabine. This drug, the current gold standard for previously treated patients who fail chlorambucil (constituting 73 percent of the patients in this part of the trial), has an objective response rate of 48 – 52 percent in this population. As the drug would likely be identified as active in vitro as well, this had the impact of pitting the assay arm and the standard arm against one another, frequently using exactly the same treatment.

While this does not mean that the assay arm could not succeed, it does have an enormous impact upon the sample size calculations used to determine the number of patients required to achieve significance.  No pharmaceutical company would ever allow a registration trial to be conducted against an “unknown” control arm, particularly one using the same therapy as the study arm – not ever! Despite these burdens, the assay-directed arm had a superior one-year survival, while virtually all other trends favored the group who received assay-selected therapy. The results of this study are worthy of recognition and further support the clinical relevance, predictive validity and importance of functional analyses. Yet, this interesting study in CLL is unceremoniously relegated to the status of a Letter to the Editor in Leukemia. Perhaps, like Phar Lap, no one really wants to upset the odds.

November is Lung Cancer Awareness Month

With November designated as Lung Cancer awareness month we have the opportunity to focus national attention on this disease, the leading cause of cancer death in America.

It may come as a surprise to many that lung cancer causes more deaths than prostate, breast and colorectal cancer combined. Lung cancer is the big kahuna. And up until the last several years, no one seemed to be paying much attention. It may be that people considered lung cancer a disease associated with cigarette smoking and therefore, in some way, the individual victim’s fault. However, we are now witness to a changing biology wherein the predominant histology of lung cancer, previously squamous cell, has transitioned to adenocarcinoma.

While the incidence in males has fallen, the incidence in females has risen. Strikingly, the incidence of lung cancer in non-smokers is rapidly climbing. Indeed, up to 20 percent of lung cancers today do not appear to be directly related to cigarettes or known exposures at all.

Our recent publication of a clinical trial in lung cancer patients was highly instructive. First, we were able to double the response rate and nearly double the survival through functional profiling (EVA-PCD®).

Second, there was no “right” treatment for patients. Different treatment combinations worked best for each patient with no single combination working for all.

Third, many patients did well with first line targeted agents. In fact, several long-term survivors have never received any form of cytotoxic chemotherapy, despite widely metastatic disease at presentation.

Several questions remain. Among them, the role of the repeat biopsies in patients with recurrent disease.  Several patients under my care have undergone additional biopsies each time a recurrence was documented with the new assay findings guiding us to a different treatment regimen. It is not impossible to imagine a day when cancer treatments will be modified and changed the way contemporary internists switch antihypertensives or cholesterol lowering drugs. That is, lung cancer like these maladies is becoming a chronic disease.

With several patients out over five years this strategy has served us well in select cases. A second issue surrounds the early introduction of experimental agents. Should we not have the opportunity to utilize drugs that have succeeded in Phase I trials, (and are thereby known to be safe for human administration), for patients whose cancer tissue reveals a favorable profile ex-vivo? I, for one, would relish the opportunity to administer second-generation EGFr-TKIs to c-MET inhibitors, to appropriately selected candidates. Smart drugs need smart mechanisms to get to market.

With the advent of lung cancer awareness month we have the opportunity to educate the public and expand awareness of the desperate need for advances in this disease. The disparity in funding for lung cancer patients compared with ovarian or breast cancer patients is disturbing. For every lung cancer death, there are five to 10 times more dollars expended on research to prevent breast and ovarian cancer deaths. While we applaud the successes in breast and ovarian cancer treatment we encourage lung cancer patients to call your congressperson to make lung cancer a front burner issue.

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One of our most gratifying success stories is Pat Merwin, now four years since diagnosis. Pat has organized a local (Long Beach, CA) observance of the national lung cancer awareness vigil to be held on Tuesday, November 13. I could not be happier than to be the invited speaker for this important occasion and to be with many of my patients.

The Tumor Micro Environment

As I was reading the October 1 issue of the Journal of Clinical Oncology, past the pages of advertisement by gene profiling companies, I came upon an article of very real interest.

While most scientists continue to focus on cancer-gene analyses, a report in this issue from a collaboration between American and European investigators provided compelling evidence for the role of tumor associated inflammatory cells in metastatic human cancer. (Asgharzadeh, S J Clin Oncol 30 (28)3525–3532 Oct 1, 2012) Through the analysis of children with metastatic neuroblastoma, they found that the degree of infiltration into the tumor environment by macrophages had a profound effect upon clinical outcome. This study confirmed earlier reports that macrophage infiltration is an integral part and potential driver of the malignant process.

Using immunohistochemistry and light microscopy the investigators scored patients for the number of CD163(+) macrophages, representing the alternatively activated (M2) subset within the tumor tissue. They then examined inflammation related gene expressions to develop a “high” risk, “low” risk algorithm and applied it to the progression free survival in these children.

Highly significant differences were observed between the two groups. This report adds to a growing body of literature that describes the interplay between cancer cells and their microenvironment. Similar studies in breast cancer, melanoma and multiple myeloma have shown that tumor cells “co-opt” their non-malignant counterparts as they drive transformation from benign to malignant, from in-situ to invasive and from localized disease to metastatic. These same forces have the potential to strongly influence cellular responses to stressors like chemotherapy and growth factor withdrawal. While we may now be on the verge of identifying these tumor attributes and characterizing their impact upon survival, these analyses represent little more than increasingly sophisticated prognostics.

The task at hand remains the elucidation of those attributes and features that characterize each patient’s tumor response to injury toward ultimate therapeutic response. To address this level of complexity, we need the guidance of more global measures of human tumor biology, measures that incorporate the dynamic interplay between tumors cells, their stroma, vasculature and the inflammatory environment.  These are the “real-time” insights that can only be achieved using human tissue in its native state. Ex vivo analyses offer these insights. Their information moves us from the realm of prognostics to one of predictives, and it is after all predictive measures that our patients are most desperately in need of today.

Systems Biology Comes of Age: Metastatic Lung Cancer in the Crosshairs

Cancer therapists have long sought mechanisms to match patients to available therapies. Current fashion revolves around DNA mutations, gene copy and rearrangements to select drugs. While every cancer patient may be as unique as their fingerprints, all of the fingerprints on file with the federal AFIS (automated fingerprint identification system) database don’t add up to a hill of genes (pun intended), if you can’t connect them to the criminal.

To continue the analogy, it doesn’t matter why the individual chose a life of crime, his upbringing, childhood traumas or personal tragedies. What matters is that you capture him in the flesh and incarcerate him (or her, to be politically correct).

The term we apply to the study of cancer, as a biological phenomenon is “systems biology.” This discipline strikes fear into the heart of molecular biologists, for it complicates their tidy algorithms and undermines the artificial linearity of their cancer pathways. We frequently allude to the catchphrase, genotype ≠ phenotype, yet it is the cancer phenotype that we must confront if we are to cure this disease.

Using a systems biology approach, we applied the ex-vivo analysis of programmed cell death (EVA-PCD®) to the study of previously untreated patients with non-small cell lung cancer. Tissue aggregates isolated from their surgical specimens were studied in their native state against drugs and signal transduction inhibitors. This methodology captures all of the interacting “systems,” as they respond to cytotoxic agents and growth factor withdrawal. The trial was powered to achieve a two-fold improvement in response.

At interim analysis, we had more than accomplished our goal. The results speak for themselves.

First: a two-fold improvement in clinical response – from the national average of 30 percent we achieved 64.5 percent (p – 0.00015).

Second: The median time to progression was improved from 6.4 to 8.5 months.

Third: And most importantly the median overall survival was improved from an average of 10 – 12 months to 21.3 months, a near doubling.

These results, from a prospective clinical trial in which previously untreated lung cancer patients were provided assay directed therapy, reflects the first real time application of systems biology to chemotherapeutics. The closest comparison for improved clinical outcome with chemotherapeutic drugs chosen from among all active agents by a molecular platform in a prospective clinical trial is . . .

Oh, that’s right there isn’t any.

Type I Error

Scientific proof is rarely proof, but instead our best approximation. Beyond death and taxes, there are few certainties in life. That is why investigators rely so heavily on statistics.

Statistical analyses enable researchers to establish “levels” of certainty. Reported as “p-values,” these metrics offer the reader levels of statistical significance indicating that a given finding is not simply the result of chance. To wit, a p-value equal to 0.1 (1 in 10) means that the findings are 90 percent likely to be true with a 10 percent error. A p-value of 0.05 (1 in 20) tells the reader that the findings are 95 percent likely to be true. While a p-value equal to 0.01 (1 in 100) tells the reader that the results are 99 percent likely to be true. For an example in real time, we are just reporting a paper in the lung cancer literature that doubled the response rate for metastatic disease compared with the national standard. The results achieved statistical significance where p = 0.00015.  That is to say, that there is only 15 chances out of 100,000 that this finding is the result of chance.

Today, many laboratories offer tests that claim to select candidates for treatment. Almost all of these laboratories are conducting gene-based analysis. While there are no good prospective studies that prove that these genomic analyses accurately predict response, this has not prevented these companies from marketing their tests aggressively. Indeed, many insurers are covering these services despite the lack of proof.

So let’s examine why these tests may encounter difficulties now and in the future. The answer to put it succinctly is Type I errors. In the statistical literature, a Type I error occurs when a premise cannot be rejected.  The statistical term for this is to reject the “null” hypothesis. Type II errors occur when the null hypothesis is falsely rejected.

Example: The scientific community is asked to test the hypothesis that Up is Down. Dedicated investigators conduct exhaustive analyses to test this provocative hypothesis but cannot refute the premise that Up is Down. They are left with no alternative but to report according to their carefully conducted studies that Up is Down.

The unsuspecting recipient of this report takes it to their physician and demands to be treated based on the finding. The physician explains that, to his best recollection, Up is not Down.  Unfazed the patient, armed with this august laboratory’s result, demands to be treated accordingly. What is wrong with this scenario? Type I error.

The human genome is comprised of more than 23,000 genes: Splice variants, duplications, mutations, SNPs, non-coding DNA, small interfering RNAs and a wealth of downstream events, which make the interpretation of genomic data highly problematic. The fact that a laboratory can identify a gene does not confer a certainty that the gene or mutation or splice variant will confer an outcome. To put it simply, the input of possibilities overwhelms the capacity of the test to rule in or out, the answer.

Yes, we can measure the gene finding, and yes we have found some interesting mutations. But no we can’t reject the null hypothesis. Thus, other than a small number of discreet events for which the performance characteristics of these genomic analyses have been established and rigorously tested, Type I errors undermine and corrupt the predictions of even the best laboratories. You would think with all of the brainpower dedicated to contemporary genomic analyses that these smart guys would remember some basic statistics.

Beyond Our Borders

I recently returned from Brazil where I participated in a cancer symposium. During my visit I encountered many highly skilled physicians with expertise in breast, thoracic, gastrointestinal and orthopedic oncology. The degree of collegiality and enthusiasm was palpable. The most exciting aspect of my visit was the warm reception and extremely high level of interest in the clinical application of our laboratory platform. It was a refreshing reminder that the parochial thinking of the American oncology community is not the norm throughout the world.

Upon my return, I had the pleasure of meeting a charming 61-year-old woman from New Delhi, India. In review of her chart I recognized her name as a patient for whom we had conducted a study in February of 2012. Her husband, an accomplished businessman, had learned of our laboratory and worked diligently to obtain, process and transport a portion of his wife’s tumor from the surgical suite to our lab. Despite multiply recurrent disease and numerous prior treatments, this patient’s ovarian cancer cells revealed exquisite sensitivity to a drug combination in the laboratory. Her physicians at the Apollo Hospital of New Delhi delivered the treatment exactly as outlined by our lab, and here sitting across from me was the patient in complete remission six months later. The family had traveled from India to meet me and express their thanks.

Each of these experiences speaks volumes for the globalization of cancer care. Cancer patients, whether from Brazil, India or China are more alike than different. Each confronts a seemingly insurmountable adversary. Each in their own way seeks out the best information and advice. And each can be best managed with those treatments found uniquely effective for their tumor. Perhaps once we have conquered cancer in India and Brazil, the EVA-PCD® assay will be ultimately accepted in the United States of America.

Empowering Patients Towards Personalized Cancer Care

We have one more guest blogger to introduce during Dr. Nagourney’s absence: Patricia Merwin. Pat just celebrated her fourth anniversary of wellness after receiving a diagnosis of metastatic lung cancer.

In July of 2011, I attended a local TEDx conference in Long Beach, CA where Dr. Robert Nagourney gave a compelling talk about the nature of his work and the future of cancer care. TED is a global organization with a mission to “share ideas worth spreading,” a very appropriate forum for Dr. Nagourney to share his insights into cancer and how to defeat it.

Just three months earlier, at another TEDx event in the Netherlands, Dave deBronkart also gave a talk about the future of cancer care.  Dave deBronkart, better known as “E-patient Dave,” was diagnosed in January 2007 with a rare and terminal kidney cancer.  Given a dismal prognosis, Dave refused to cede his life to “standard care.”  Instead, he turned to a group of fellow patients online and found the information that eventually led to a treatment that saved his life. Dave deBronkart has since become a prolific online patient advocate and an internationally renowned speaker on the subject of patient empowerment and participatory medicine.

Like e-Patient Dave, I was given a “dismal prognosis” when I was diagnosed in 2008 with advanced metastatic lung cancer.  I too refused to cede my life to the standard protocol of the day. But it was not my health care providers who led me to Dr. Nagourney, it was a close friend.  Empowered with the knowledge that it was possible to improve my odds for survival, I chose functional profile testing (EVA-PCD®) to help determine my personalized treatment plan. It was a wise, informed decision resulting in the best possible outcome.  I have since become an online patient advocate, spreading the word to thousands of other patients so that they can become knowledgeable about this important test that could save their lives.

According to Dr. Nagourney, “Every system performs exactly as it was designed to perform. The current system of medical oncology provides adequate care for the average patient. There is little room for true, individualized care, for it disrupts the norm.”  But every patient with cancer has the same objective. To find the treatment that will work for “me.”  With a system skewed toward averages and away from the individual, the path to personalized medicine must be to empower the person with the most at stake – the patient. Dr. Nagourney says, “Today’s patient must become his or her own best advocate.”

More and more, patients are turning to online forums and other patient groups, not just for support, but to seek and share the latest news and information about treatments, side effects, tests, etc. If two heads are better than one, then thousands of engaged patients should, at the very least, provide good food for thought, “ideas worth spreading.”

Dr. Nagourney believes that “it’s in the online trenches where the real, personal war of cancer is being waged.  The old paradigm, that knowledge runs downhill from academics to practitioners to patients is being turned upside down as empowerment goes from the bottom up, not just from the top down.”  I’m sure e-Patient Dave would agree, along with countless other e-patients like him.

Cancer Treatment – A Husband’s View

Guest blogger – Gary Brutsch

Dr. Nagourney is currently attending an international conference where he is an invited speaker. During his absence we will have guest bloggers sharing their views on chemosensitivity testing and the EVA-PCD® assay. Our first guest is Gary Brustch.

Five years ago, my wife of otherwise good health was diagnosed with Stage IV uterine cancer. Following a surgical “solution,” we commenced our search for the next best alternative to just waiting for the disease to take its course.

We settled on a protocol supervised by a major cancer treatment center in Texas. For a total of six months, my wife, Tina, was treated with a combination of chemotherapies. During this treatment we continued to look for medical care that was more scientific-based.

At the conclusion of their protocol, we were notified that the course of treatment had not been successful. At this time Tina’s cancer marker numbers were approaching 800. Two days after this notification we decided that our final option was to contact Robert Nagourney, MD, at Rational Therapeutics in Long Beach, CA.

Our decision was based on the belief that his tumor sensitivity based chemo architecture was probably a more effective method to treat her tumor growth.

After obtaining a tumor sample from Tina and subjecting it to a laboratory process (assay testing), Dr. Nagourney prescribed a specific chemotherapy cocktail for her treatment. After one month of supervised treatment, Tina’s cancer marker number was under one hundred.

We are now into our fourth year of maintenance supervised by Dr. Nagourney. Our united opinion seems to say that, as health challenged individuals we must demand that caregivers treat our health challenges on a focused, individual basis.

We cannot accept that one category of chemotherapy is good for all.

The Good, the Bad and the Good

Two years ago, almost to the day, I met a charming gentleman who had been diagnosed the preceding month with metastatic non small cell lung cancer.

The work-up that confirmed his diagnosis also identified an EGFR mutation. This mutation enabled him to receive the targeted agent erlotinib (Tarceva®) as first line therapy and it provided immediate benefit. An incidental finding in his work-up was a meningioma (a benign brain tumor that often arises in the midline of the brain, in an area known as the falx).

Follow up MRI showed no growth of the meningioma. The patient remained on the same therapy for three months at which time his treating physician decided to consolidate him with chemotherapy. The patient’s tolerance could not have been worse: nausea, malaise, fatigue and a 30 pound weight loss. He requested that I assume his care. After careful consideration, I put him right back on what worked in the first place – erlotinib.

With the exception of a few minor toxicities the patient did beautifully. As we approached his restaging with PET/CT and MRI of the brain, scheduled for August 2012 (his two-year point), he presented to a university medical center with disturbing neurological symptoms. An MRI revealed the meningioma to be much larger than originally found two years earlier. Surgery was scheduled for the following day.

The patient and I discussed his situation by phone as he sat in his hospital room awaiting the surgery. If this were a meningioma, it could be removed. However, if this was related to his lung cancer, then there was an opportunity at hand to determine (using the EVA-PCD® platform) whether the cancer was still responsive to erlotinib or had developed mutations that might confer resistance (e.g., T790M). On the one hand, high dose pulse erlotinib can be effective for CNS disease, so long as resistance has not developed. On the other hand, newer classes of drugs that target T7090M might be required.

We needed tissue for testing, so we could create a functional profile of the tumor, and the surgery was 12 hours away. The patient wanted us to do the study. I wanted to do the study. The problem was that I needed to arrange to get tissue to the lab and time was running short.

With an admirable degree of sleuth work, we identified the surgical resident on duty that evening. We explained our need and he proceeded to explain in great detail that this would never happen. Above and beyond the protocols and standards by which he delivered care, he had 45 other patients to cover, as well as consults to conduct. I hung up disappointed that this opportunity would be missed.

The next morning as I finished hospital rounds I noticed a 6:40 a.m missed call on my cell phone. It was from the hospital where the patient was undergoing surgery. I then received a second call from the same number. It was the attending senior surgeon. He was about to scrub in for the scheduled surgery and offered to assist me in any way he could. He explained that they hoped and believed that this was a benign meningioma. If it was, he would remove it and there would be no need for our involvement. An hour later, communicating via speakerphone in the OR, the surgeon explained that this was indeed adenocarcinoma consistent with the patient’s lung cancer diagnosis. He promised to process the tissue carefully, and then provided his cell phone number so we could communicate. I felt a sense of great relief.

While I cannot say what our laboratory tests will find, the story is both educational and inspirational. The patient is an example of a breakthrough in medical science that provided him an excellent and durable response with comparatively little toxicity. That was the good.

The bad reflected the overworked resident’s insouciance. He was busy, it was late and it appeared that we had confused him with someone who cared. After all, there is no payback to perform above-and-beyond-the-call-of-duty medicine. That was sad, for we are now training physicians who are technicians and not healers. They play by the rules and never extend themselves. No one can ding them for doing their job and no one applauds them for doing more.

The really good news was the response of the attending physician. This individual whom I have never met, evidenced an admirable degree of patient advocacy, commitment and compassion. This patient’s good outcome mattered to him and if there was something that I could bring to the table to help this person in need, then he was all there.

We are at a crossroads in medicine. Will we sponsor the healers or promote the technicians? In our laboratory we do everything in our power to provide all the science that we can bring to bear for every patient. The one component that we cannot offer as a service is the art of medicine. That is up to each individual physician.