Avastin Lucentis Update 9 A Disturbing Report about the Upcoming Trial Between Avastin and Lucentis

In my ongoing efforts to keep the public informed about the status and availability of Avastin and the upcoming clinical trial comparing Avastin to the already approved Lucentis for battling age-related macular degeneration, I have received permission from the editors of Executive Laser Report to reprint their disturbing findings about these drugs from the recently concluded American Academy of Ophthalmology meeting held in Las Vegas.

Retina Report from the 2006 AAO meeting in Las Vegas, November 12-14, 2006
Published in the November 30th issue of Executive Laser Report

Industry entities (pharmaceutical and device companies in general – not just Genentech) reportedly are attempting to prevent the newly announced head-to-head trial sponsored by the National Eye Institute (NEI) of Genentech’s Lucentis and Avastin in AMD. Dr. William Rich, an American Academy of Ophthalmology legislative expert, said, “We are very concerned about an intervention of industry into getting this trial carried out…We are monitoring it very carefully…We do anticipate some interference with the start of this trial by industry…Industry is going to petition not to see this trial carried out…I wouldn’t be surprised (to see the trial stopped). And public interest groups (e.g., AARP) around the country are going to be watching carefully, too.”

Asked how industry could interfere with the NEI trial, Rich said there may be petitions that (1) the trial is not necessary, so the government shouldn’t pay, or (2) the government shouldn’t pay because the treatment (Avastin) is experimental. He added, “I think Genentech is classy enough that I don’t think they would interfere in Washington. The company is known for its ethics, but the entire pharmaceutical and device industry is threatened (by the trial). I would be shocked if there aren’t discussions going on in Washington now about this trial.”

There was a strong emphasis at AAO on the price differential between Lucentis and Avastin and the impact of that cost difference on the US economy (about $5 billion more than if Avastin were used). Other countries simply will not use Lucentis, experts emphasized, so Avastin has to be studied as a public health issue, because that is what other countries will use. Dr. Rich emphasized that the NEI trial is not a “cost-based” trial because cost is not a factor in Medicare coverage today, rather the trial is to resolve “public health issue” because of the non-US countries that will be using Avastin.

Currently, Avastin is covered by Medicare for AMD in 48 states. The co-pay cost to a Medicare patient is roughly $60 for Avastin vs. about $440 for Lucentis. Most retina surgeons said they are giving patients a choice between the two drugs, asking them what they want to pay or how often they want to come in (monthly with Lucentis or once every 6-8 weeks with Avastin).

How many patients are choosing Avastin? Sources indicated the split is about 50/50. That was also the finding of a Retina Society survey. So, why are Lucentis sales strong? There are doctors who don’t want to use an off-label product. There could be some stocking, but retina specialists didn’t think that was a major factor.

Genentech has created a lot of ill will in the ophthalmology community. There is a definite negative attitude by retina specialists toward Genentech. Their attitude is reminiscent of the way interventional cardiologists felt several years ago toward Johnson & Johnson because of its monopoly (and perceived high price) for the Palmaz-Schatz cardiac stents – and for which they punished J&J for years after competitors were available.

This article was reprinted with permission from the November 30th issue of Executive Laser Report, published by Emerging Trends in Medicine. For information on subscribing to Executive Laser Report, please contact Emerging Trends in Medicine, by clicking on the connecting link.

Author’s Note on Avastin

Since posting the original article on January 31, 2006, I have now posted ten updates on this important drug for treating age-related macular degeneration. In addition to the posting you are reading, here is a listing (with links) to the others:

Avastin: A New Hope for Treating AMD (January 2006)

Avastin Update: Medicare not Likely to Cover its Use (March 2006)

Avastin Update II: AAO supports Medicare Coverage for Off-label Avastin Use (April 2006)

ARVO 2006: A Further Update on Both Avastin and Lucentis for Treating AMD (May 2006)

Avastin/Lucentis Update 4: FDA Approves Lucentis for Treating Wet AMD (July 2006)

Avastin Update 5: NIH Considers Comparing Lucentis and Avastin (August 2006)

Avastin/Lucentis Update 6: Latest Results Published in NEJM and Another Call for a Trial Between Them (October 2006)

Avastin/Lucentis Update 7: BREAKING NEWS – NEI/NIH Will Fund Comparative Study (October 2006)

Avastin/Lucentis Update 8: A Report of the Latest News from the 2006 AAO Meeting (November 2006)

Avastin Lucentis Update 6 Latest Results Published in NEJM and Another Call for a Trial Between Them

Avastin/Lucentis Update 6: Latest Results Published in NEJM and Another Call for a Trial Between Them

This week’s issue (October 5, 2006) of the New England Journal of Medicine (NEJM) contains several articles on the use of Lucentis to treat age-related macular degeneration (AMD). The lead article, “Ranibizumab and Age-Related Macular Degeneration”, relates the latest test results that led to the drug’s approval on June 30th of this year, while a second article, "The Price of Sight -- Raninbizumab (Lucentis), Bevacizumab (Avastin), and the Treatment of Macular Degeneration" calls for a clinical trial between them because of the price differential.

Genentech, the manufacturer of both drugs, commented about the release of the first article:

Genentech, Inc. (NYSE: DNA) announced today the publication of data from the two randomized, controlled pivotal Phase III clinical trials of LUCENTIS (ranibizumab injection) in the New England Journal of Medicine. The published findings include two-year efficacy and safety data from the MARINA trial and one-year efficacy and safety data from the ongoing ANCHOR trial. Based on these studies, LUCENTIS was granted U.S. Food and Drug Administration (FDA) approval on June 30, 2006 for the treatment of patients with the neovascular (wet) form of age-related macular degeneration (AMD), a leading cause of blindness in people over 55.

The MARINA and ANCHOR clinical trials met the primary efficacy endpoint of maintaining vision (defined as a loss of less than 15 letters in visual acuity) at one year in patients with wet AMD. In these studies, nearly all patients (approximately 95 percent) treated with LUCENTIS maintained or improved vision at one year compared with 62 percent of patients in the MARINA control group and 64 percent of patients in the ANCHOR control group. Importantly, up to 40 percent of patients experienced an improvement in vision of three lines (15 letters) or more on the study eye chart compared with 5 percent and 6 percent of patients in the MARINA and ANCHOR control groups, respectively. The improvement in visual acuity endpoints among patients treated with LUCENTIS in the MARINA study was maintained at year two, while patients in the control group continued to decline.

"The results of these Lucentis studies have changed the way we approach the treatment of wet AMD by demonstrating, for the first time, improvements in vision in more than one-third of patients treated," said David Brown, M.D., lead author for the ANCHOR study and retina specialist at Vitreoretinal Consultants, The Methodist Hospital in Houston, Texas.

"What makes this publication particularly significant is that the visual acuity benefits after one year of treatment in the MARINA study were maintained through two years and associated with anatomic improvements consistent with the changes in visual acuity observed," said Philip J. Rosenfeld, M.D., Ph.D., professor of ophthalmology, Bascom Palmer Eye Institute in Miami and lead author for the MARINA study. "In this study, Lucentis had a favorable safety profile and did not appear to put patients at an additional risk for systemic adverse events and the ocular adverse event rates were similar to what we would expect among people in this age group who receive an injection in the eye."

However, perhaps more importantly, Dr. Robert Steinbrook commented in his article, "The Price of Sight -- Raninbizumab (Lucentis), Bevacizumab (Avastin), and the Treatment of Macular Degeneration" on the need for a direct clinical trial between Lucentis and Avastin because of the price disparity between the two drugs, as I have related previously in my web Journal. (See the Author’s notes at the end of this article.)

As Doctor Steinbrook noted in his “Perspectives” article, “Before the FDA approved ranibizumab, some ophthalmologists began using another monoclonal antibody, bevacizumab, that is closely related to ranibizumab to treat patients who have neovascular macular degeneration or other chorioretinal diseases mediated by vascular endothelial growth factor. Marketed as Avastin and also manufactured by Genentech, bevacizumab is a full-length antibody that is derived from the same mouse monoclonal antibody precursor as ranibizumab (see Figure 1), neutralizes vascular endothelial growth factor, and costs considerably less than ranibizumab when administered as an intraocular injection.”

Figure 1. Relationship between Ranibizumab and Bevacizumab.

Ranibizumab is a recombinant humanized monoclonal IgG1 kappa-isotype antibody fragment (with a molecular weight of about 48 kD). It is produced in an Escherichia coli expression system (and thus is not glycosylated) and is designed for intraocular use. Bevacizumab is a recombinant humanized monoclonal IgG1 antibody (with a molecular weight of about 149 kD). It is produced in a Chinese-hamster-ovary mammalian-cell expression system (and thus is glycosylated) and is designed for intravenous infusion. Both the antibody fragment and the full-length antibody bind to and inhibit all the biologically active forms of vascular endothelial growth factor (VEGF) A and are derived from the same mouse monoclonal antibody. However, ranibizumab has been genetically engineered through a process of selective mutation to increase its affinity for binding and inhibiting the growth factor. The Fab domain of ranibizumab differs from the Fab domain of bevacizumab by six amino acids, five on the heavy chain (four of which are in the binding site) and one on the light chain. Not all the intermediate Fabs between the mouse monoclonal antibody and ranibizumab are shown.


“In February 2004, the FDA approved bevacizumab for the treatment of metastatic cancer of the colon or rectum. Although the typical price of bevacizumab as part of a chemotherapy regimen is $4,400 a month, a 4-ml vial containing 100 mg has a wholesale acquisition cost of $550. Thus, physicians and compounding pharmacies can prepare small aliquots in syringes for intraocular injection at a cost to the physician of $17 to $50, depending on the dose and the efficiency of the process. In some instances, charges to patients may be considerably higher. On a molar basis, the typical dose — 1.25 mg (0.05 ml) — of bevacizumab is similar to the approved dose of ranibizumab.”

“Intraocular administration of bevacizumab is entirely off-label; the drug is formulated for intravenous infusion, not intravitreal injection. Nonetheless, and though data from controlled trials are lacking, bevacizumab appears to be safe and effective in the short term. And ophthalmologists frequently use medications off-label.”

“As of mid-September 2006, ranibizumab had been approved in the United States and Switzerland (where it is marketed by Novartis, which has commercialization rights outside the United States). Bevacizumab has already brought Genentech billons of dollars in sales; ranibizumab will soon do so as well.”

“The good news for patients is that there are two new medications for neovascular age-related macular degeneration, both of which appear to work better than the alternatives. But since they have never been directly compared, physicians can only speculate about which drug is superior with regard to safety, efficacy, and frequency of administration. The price difference is also too big to ignore.” (Emphasis added by this author.)

“In many parts of the world, a medication that costs $1,950 for a monthly injection is unaffordable. In the United States, under Medicare, ranibizumab is covered through Part B; patients are responsible for a 20% copayment for each injection. In some instances, supplemental insurance, Medicaid, or support programs for the poor or uninsured that are funded by the manufacturer or others cover most or all of the patients' costs. But regardless of who pays the bill, sales of ranibizumab generate revenue for Genentech, the drug's high price contributes to the overall cost of health care, and the drug may sometimes still be unaffordable.”

“It is possible that bevacizumab would prove to be superior for neovascular age-related macular degeneration. For example, the molecule is about three times as large as ranibizumab and may remain in the eye longer, decreasing the frequency with which injections are required. At present, intraocular pharmacokinetic data are lacking. However, ranibizumab could also prove to be better. In addition to its smaller size, ranibizumab is genetically engineered to have greater affinity for vascular endothelial growth factor and is formulated for intraocular use; more of the drug may therefore penetrate all the layers of the retina. Moreover, ranibizumab that leaks out of the eye into the circulation has a half-life of hours; the half-life of a full-length antibody such as bevacizumab is longer. For this reason, ranibizumab could theoretically be associated with less systemic toxicity than bevacizumab, but it is not known whether this is in fact the case. As an antibody fragment, ranibizumab lacks an Fc portion, so it may be less likely to induce inflammation within the eye. However, according to Rosenfeld, no apparent inflammation has been seen with bevacizumab, even with the highest dose that has been administered.”

“Since late 2005, the National Eye Institute has been considering a proposal for a prospective multicenter trial that would compare ranibizumab directly with bevacizumab. Although the institute has signed off on the need for a trial, as of mid-September it was still considering the research design and how to pay for the study, which would probably cost tens of millions of dollars. If the study is to go forward, the federal government will probably have to buy both drugs from Genentech. And the investigators will probably have to submit to the FDA an investigational new drug application for intravitreal bevacizumab. Such a comparison might not ultimately affect the difference in price between the drugs, but it is certainly the only way to determine which drug is better for patients.”


In addition to the two articles noted above, two additional articles are included in this week’s edition of the NEJM. They are:

Ranibizumab versus Verteporfin in Age-Related Macular Degeneration, a discussion of the clinical trial showing the differences between using Lucentis and verteporfin PDT in treating AMD; and a general discussion of AMD: Age-Related Macular Degeneration.

All of the articles can be found at:

http://content.nejm.org/cgi/content/full/355/14/1409

however, only Dr. Steinbrooks article can be read in full without a subscription to the NEJM.


Author’s Note on Avastin

Since posting the original article on January 31, 2006, I have now posted eight updates on this important drug for treating age-related macular degeneration. In addition to the posting you are reading, here is a listing (with links) to the others:

Avastin: A New Hope for Treating AMD (January 2006)

Avastin Update: Medicare not Likely to Cover its Use (March 2006)

Avastin Update II: AAO supports Medicare Coverage for Off-label Avistan Use (April 2006)

ARVO 2006: A Further Update on Both Avastin and Lucentis for Treating AMD (May 2006)

Avastin/Lucentis Update 4: FDA Approves Lucentis for Treating Wet AMD (July 2006)

Avastin Update 5: NIH Considers Comparing Lucentis and Avastin (August 2006)

Newer Updates:

Avastin/Lucentis Update 7: BREAKING NEWS – NEI/NIH Will Fund Comparative Study (October 2006)

Avastin/Lucentis Update 8: A Report of the Latest News from the 2006 AAO Meeting (November 2006)

Avastin/Lucentis Update 9: A Disturbing Report about the Upcoming Trial Between Avastin and Lucentis (December 2006)

Stem Cells in Ophthalmology Update 23 Maurie Hills’ Story More Details About The Stargardt’s Clinical Trial Patient

Back in early August, I wrote about Maurie Hill, a Stargardt’s disease patient who is undergoing stem cell treatment as part of the Advanced Cell Technology clinical trial in which an injection of retinal pigment epithelial (RPE) cells derived from human embryonic stem cells, was injected into her retina in an attempt to stop the progression of her disease and, hopefully, restore some vision that she has lost.

That first posting, A Stargardt’s Clinical Trial Patient’s Story – In Her Own Words, told Maurie’s story, taken from the blog she is writing about her experiences in this clinical trial.

Last week, Ricki Lewis, the author of The Forever Fix: Gene Therapy and the Boy Who Saved It, an excellent book about the gene therapy trials ongoing at Children’s Hospital in Philadelphia to treat Lebers Congenital Amaurosis, wrote more about Maurie Hill and the clinical trial.

Back in early summer, when Maurie first contacted me about the possibility of her taking part in the ACT clinical trial, I introduced her to Ricki. I thought that Ricki might be interested in writing another regenerative medicine book, this time about the use of stem cells. Ricki was interested, and made contact with Maurie, and this story is the result of that introduction.   

Human Embryonic Stem Cells Finally Reach Clinical Trials: Maurie’s Story

By: Ricki Lewis, PhD

Posted: September 27, 2012

DNA Science Blog in PLOS One Blogs

On July 11, Wills Eye Institute ophthalmologist Carl Regillo delicately placed 100,000 cells beneath the retina of 52-year-old Maurie Hill’s left eye. She was rapidly losing her vision due to Stargardt disease, an inherited macular dystrophy similar to the much more common dry age-related macular degeneration (AMD).

Maurie’s disease was far along, the normally lush forests of photoreceptor cells in the central macula area severely depleted, especially the cones that provide color vision. Would the introduced cells nestle among the ragged remnants of her retinal pigment epithelium (RPE) and take over, restoring the strangled energy supply to her remaining photoreceptors? They should, for the cells placed in Maurie’s eye weren’t ordinary cells. They were derived from human embryonic stem cells (hESCs).

I’ve waited 15 years to see human embryonic stem cells, or their “daughter” cells, make their way through clinical trials. And thanks to Maurie’s sharing her story, I’m witnessing translational medicine.

On September 29, 1997, The Scientist published my first stem cell article, Embryonic Stem Cells Debut to Little Media Attention. Alas, the public was still too enamored with Dolly the cloned sheep to pay much attention to cells that could both spawn specialized cell types and “self-renew,” maintaining a perpetual stream of hard-to-derive cells that could be used to both observe embryonic development and replace abnormal adult tissue. Over the years, public interest seemed to surface only on slow news days. And still the media report that the cells can “turn into” every cell type in the body – ignoring the very quality that defines the cells: the capacity for self-renewal, making more of themselves as their daughters specialize.

Partly because deriving hESCs until just a few years ago required destroying early human embryos, research using less objectionable stem cells accelerated. And while so-called “adult” and induced pluripotent stem cells (iPSCs) don’t require embryos and match patients so that the immune system isn’t provoked, embryonic stem cells remain the “gold standard” for scrutinizing a disease’s beginnings as the ball-of-cells early embryo folds into layers, contorts, develops organs, and grows. For example, hESCs recently glimpsed how the drug thalidomide harms embryos. The second use of hESCs is to generate useful specialized cells, such as sensory neurons to restore hearing. It’s this second application – hESCs as a source of implants – that is the focus of clinical trials for Stargardt disease and dry AMD.

Using hESCs could be incredibly economical. Just one can yield many millions of cells, the characteristics of the cells coaxed by the cocktails that researchers choose. And embryos can be returned to the freezer, unharmed. The RPE cells in Maurie’s eye came from an hESC line derived in 2005 by Robert Lanza and colleagues at Worcester, Mass.-based Advanced Cell Technology, one of five cell lines called NED for “no embryo destroyed.”

NED cells come from a protocol similar to pre-implantation genetic diagnosis (PGD), in which one cell of an 8-celled embryo is sampled to screen for genetic disease, and if all is well, the remaining 7-celled embryo is implanted in a uterus. PGD has been around since 1989. The ability to pluck out a cell at this stage without damaging the whole is a characteristic of our branch of the animal kingdom called indeterminate cleavage, for those who recall Zoology 101.

For a time, the first clinical trial to use hESC-derived cells — oligodendrocytes to treat spinal cord injury – was sponsored by Menlo-Park, CA–based Geron Corp. That effort ended in November 2011, due to cost. But eye diseases are perhaps a better first choice, because the retina is naturally shielded from the immune system.

I never expected to befriend one of the first people to be in an hESC clinical trial. But this past June, an email friend, Irv Arons, connected Maurie and me. She and her older sister Cindi would soon be on their way back from the Wills Eye Institute in Philadelphia, where they were being evaluated for the clinical trial to treat Stargardt disease. They’d be at the Albany Amtrak station on their return to Vermont, near my home.

The sisters have become so adept at using their peripheral vision to see around the central abyss in their visual fields that I couldn’t, at first, tell that anything was wrong with them. They were as excited as if they’d just won the lottery.

“Twelve people are participating. When I saw something about the clinical trial a year ago I thought yeah, right. But things just lined up,” Maurie said. She works 12 hours a week blogging for Ai Squared, maker of ZoomText software, and has a young daughter, a husband, and an associate’s degree in electronics and engineering technology.

Cindi agreed. “I was thinking this will never happen. There were too many barriers, too many things had to fall into place.”

The visual loss of Stargardt is slow. “In 3rd grade I‘d read very fast, but by 5th, I knew I should be able to read faster,” Maurie recalled. She struggled, not realizing anything was wrong, and didn’t even have an eye exam until her physical for college. “The doctor saw something and he sent me to an eye specialist who sent me to another eye specialist, but still I had no diagnosis.”

   

Eyechart: This is what Maurie Hill sees with her right eye covered when observing the eye chart from a meter away. (credit: Derek Bove)

At age 30, Maurie needed a physical for work, and again made the rounds of referrals. “I could still see pretty well, but some things bothered me: night driving and the lights coming at me and then disappearing, and being unable to recognize faces. I’d have trouble going from light to dark and vice versa.” By age 35, yet another job required a physical, and she went again to retinal specialists, but by this time she’d lost enough visual function to meet the diagnostic criteria for Stargardt. With every month, she could see less.

Meanwhile, Cindi’s vision was going downhill. “I went to my doctor, and I said ‘my sister has this, do I have it too?’ He ran out to open his textbook to see what it was, and said ‘yes, I think you have it,” Cindi said. She taught special ed for 14 years before she had to leave, no longer able to do the visual tasks required for her job, even with the adaptive technology that had helped for a decade.

The sisters have four other siblings. True to Mendel’s first law for single-gene inheritance, their older brother has Stargardt too, although his case is so mild that until recently he could read normal-sized print, although slowly and with great eyestrain.

In 2009, the siblings heard about successful gene therapy for Leber congenital amaurosisamaurosis  another inherited retinal disease. Could they have gene therapy too?

In May 2009, the family went to the National Eye Institute to confirm Maurie’s 1995 diagnosis, which had been based on clinical findings. But genetic test results indicated that the family didn’t have a mutation in the ABCA4 gene, as 40% of those diagnosed with Stargardt do, or any other mutation. “That was a little disappointing, since we knew the mutation would have to be known to do gene therapy,” recalled Maurie.

But what about stem cell therapy?

Maurie read (by zooming her text and using her peripheral vision) a news release from Advanced Cell Technology announcing that their researchers had derived RPE cells from hESCs. The first two applications would be dry age-related macular degeneration and Stargardt disease. Mice and rats had responded well.

So Maurie called her siblings, and her brother called ACT immediately, but got nowhere. The timing just wasn’t right.

By late 2010, FDA had approved ACTs testing the RPE cells for safety, and clinicaltrials.gov officially announced the upcoming experiments in late April 2011. Four cohorts of three Stargardt patients each would receive escalating doses, starting with 50,000 RPE cells. The AMD trial would proceed in parallel.

Results came very quickly, published online in January 2012’s Lancet. And the news was good. The cells hadn’t harmed the first two patients, a woman in her 70s with AMD and a 51-year-old woman with Stargardt, both treated at the Jules Stein Eye Institute in Los Angeles.

A fear of using embryonic stem cells is that they can give rise to teratomas, which are bizarre tumors festooned with bits of specialized tissue such as teeth and hair. If an ES cell lurked among the RPE cells put into a patient’s eye, a teratoma might sprout. But since this hadn’t happened by three months, and neither woman had inflammation or immune rejection, the therapy passed the first safety hurdle. (A year out, the 9 patients treated so far report more vibrant color vision and improved visual acuity. The first woman treated, for example, could detect only hand-waving before the procedure, but can now read three lines on an eye chart.)

After the sisters heard the two LA patients on NPR January 23, Maurie called the clinical trial director at the nearest participating center, the Wills Eye Institute. When she finally got through, she learned that the center would consider only local patients, so they’d be easier to follow. But a month later, her local eye doctor urged her not to give up.

So Maurie called back, and finally the timing was right. “The research coordinator answered and was flowing with information.” Elated, Maurie sent her medical records right away – she had fortuitously just had a colonoscopy (cancer is grounds for exclusion due to the teratomas), mammogram, Pap smear, cholesterol test, and more.

Dr. Regillo liked Maurie’s test results. She was the ideal clinical trial participant – healthy except for the condition under study, a rarity. When Maurie got the good news, she asked if she could bring Cindi along. Both sisters agreed to foot the Amtrak bills. They told me about the visit when I met them in the Albany train station. Maurie was in; Cindi is still being evaluated.

The big day came in just a month. On July 11, Maurie and Cindi arrived a little before noon, surprised at the video cameras. Every step of the procedure had been meticulously choreographed and practiced, with trial runs to identify the time with the lightest traffic on a midsummer Wednesday between New Jersey, where the precious cells were on ice, and Philadelphia.

The cells arrived in a red cooler, the clock ticking down the 3 hours they could survive. Testing for viability and contamination took 30 minutes, and then the procedure itself took just 3 minutes.

Maurie hadn’t expected to be awake and aware as the descendants of human embryonic stem cells flooded her eye, although she’d chosen local anesthesia. “I actually saw the needle come in the inside of my eye! Dr. Rigello said, ‘Can you see that?” I said I clearly saw the needle coming in from the left, and he said, ‘Yup!’ I could see the fluid coming out and forming a little puddle. It was the coolest thing. And everyone was so excited that I saw it!”

Maurie Hill, shortly after having 100,000 retinal pigment epithelium (RPE) cells derived from human embryonic stem cells (hESCs) placed in her left eye

And so Maurie Hill joins the brave and selfless individuals who have volunteered to participate in clinical trials, who make new treatments possible for many. But Maurie’s going one huge step farther: she’s blogging about her progress.

To be continued …

The Author

Ricki Lewis is a science writer with a PhD in genetics. The author of several textbooks and thousands of articles in scientific, medical, and consumer publications, Ricki's first narrative nonfiction book, "The Forever Fix: Gene Therapy and the Boy Who Saved It," was published by St. Martin's Press in March 2012. In addition to writing, Ricki provides genetic counseling for parents-to-be at CareNet Medical Group in Schenectady, NY and teaches "Genethics" an online course for master's degree students at the Alden March Bioethics Institute of Albany Medical Center.