ACKC e-Newsletter Volume 1 Number 2

Sunitinib (Sutent) Survival Data

Of the targeted therapy drugs that have so far been approved by the Food and Drug Administration (FDA) for metastatic renal cell carcinoma, only temsirolimus (Torisel) was approved (May 2007) based on increase in survival time. The FDA approved sunitinib (Sutent) (January 2006) on its ability to shrink tumors and sorafenib (Nexavar) (December 2005) on its capacity, over that of a placebo, to increase the time it takes for metastases to progress after initiation of therapy. The temsirolimus trial upon which the FDA approval was based evaluated kidney cancer patients who were in advanced stages of their disease (over 70% classified as poor risk), however the other two therapies were administered to patients who had “good performance status”, i.e. they were in much better condition than the temsirolimus patients, therefore, survival data were not mature enough to be available for evaluation.

Progression-free survival figures had previously been reported for the Phase III randomized trial of sunitinib versus interferon-alpha with 11 months for sunitinib patients and 5 months for interferon-alpha patients. Dr. Robert Figlin of City of Hope Cancer Center reported, at the ASCO 2008 Conference, on the overall survival data for sunitinib, based on matured data for that trial. 750 clear cell patients were in trial, half randomized to each arm, with the sunitinib patients receiving 50 mg daily, four weeks on and two weeks off. At a certain point in the trial, the protocol was amended to allow interferon-alpha patients who progressed to “cross-over”, i.e. to switch to sunitinib.

In addition to patients who crossed over from interferon-alpha to sunitinib, when patients on either arm progressed and left the trial, over half proceeded to take other therapies, specifically other VEGF inhibitors (sorafenib, Avastin), cytokines (interleukin-2, interferon-alpha), mTOR inhibitors (temsirolimus), and chemotherapy.

The cross over patients and the post-treatment therapy complicate the overall survival calculation, but to simplify it, we can look at only those patients who did not take any post-study treatments. In this case, the data are as follows:

Overall Survival Patients Evaluated Median Months
inteferon-alpha 193 14.1
sunitinib 162 28.1
NB: sunitinib row includes 20 patients who crossed over to sunitinib on the study

Here there is a clear advantage for sunitinib over interferon-alpha for first-line treatment for metastatic kidney cancer. No other targeted therapy has shown comparable results in either first-line or second-line settings.

Dr. Figlin also charted survival benefit versus presence of selected markers. Oncologists have been trying to predict survival of metastatic kidney cancer patients based on biologic markers. Some of these markers presented below overlap with those used by Dr. Robert Motzer of Memorial Sloane-Kettering Cancer Center in his risk factor model that is used by several oncologists to categorize patients upon entering clinical trials. This confluence of factors is understandable since Dr. Motzer was the principal investigator on the first-line sunitinib trial.

Overall Survival
Factor HR 95% CI P-value
ECOG PS (0 vs 1) 0.515 0.417-0.636 <0.0001
Hemoglobin (>=LLN vs <LLN) 0.504 0.401-0.634 <0.0001
Time from diagnosis to tx (>=1 yr vs <1 yr) 0.574 0.461-0.715 <0.0001
Corrected calcium (<=10 vs > 10 mg/dL) 0.466 0.327-0.664 <0.0001
Alkaline phosphatase (<=ULN vs >ULN) 0.676 0.542-0.844 0.0005
LDH (<=1.5 vs > 1.5 x ULN) 0.500 0.337-0.742 0.0006
No. of metastatic sites (1 vs >=2) 0.664 0.503-0.876 <0.0037
Treatment (sunitinib vs interferon-alpha) 0.764 0.623-0.936 0.0096
Notes: HR: hazard ratio, CI: 95% confidence interval; P-value: statistical significance
ECOG Performance Status of 0 or 1 is either fully active or able to carry out light work
LLN: lower limit of normal; ULN: upper limit of normal; tx: medical treatment;
LDH: lactate dehydrogenase

The hazard ratio (HR) is the relative risk of dying for two comparison groups of patients. If the hazard ratio were equal to 1, there would be no advantage of one group over another. The lower the hazard ratio, the higher is the advantage. So in the above table, for example, patients having corrected calcium levels <= 10 mg/dL have a significantly lower risk of dying than patients whose corrected calcium levels are > 10 mg/dL. The P-value indicates statistical significance, the lower the value the higher the significance. Note that the HR for sunitinib vs. interferon-alpha of 0.764 includes patients who first received a placebo and were then crossed over to sunitinib. For patients who received only sunitinib, the HR = 0.647 indicating a higher survival advantage for these patients.

American Society for Clinical Oncology (ASCO) Conference

The ASCO Conference, the leading oncology conference in the world, took place in Chicago, May 30-June 3. Over 30,000 oncologists and others attended to hear the latest developments in cancer therapeutics. We have posted summaries of six presentations from the conference entitled: Cediranib, Interleukin-21, Pazopanib, Sutent and Brain Metastases, Temsirolimus (Torisel), and TroVax. They will be found at http://www.ackc.org/ under Kidney Cancer Info->ASCO Reports->Report from ASCO 2008. Further reports will be added on a flow basis.

Kidney Disease and Kidney Cancer Survivors

25 million Americans suffer from kidney disease. After a nephrectomy, the second kidney usually grows and takes over the filtration function of the missing kidney. However, this is not always the case, and many kidney cancer survivors also suffer from early stage kidney disease. We hear a lot about creatinine level as being a marker for kidney disease, but it is only one factor. The normal creatinine level varies depending on one’s individual characteristics, so the standard measure of kidney function is GFR, or Glomerular Filtration Rate, which is a combination of creatinine level, age, gender, and ethnicity. GFR is measured in milliliters per minute of blood clearance by the kidneys with 100 mL/min considered normal. For example, a GFR of 50 would indicate a 50% filtration or kidney function rate.

Kidney disease is broken down into five stages, with Stage 1 defined as a GFR greater than 90 mL/min (close to a normal) to Stage 5, with a GFR of less than 15 mL/min, indicating kidney failure and requiring dialysis. The GFR normally decreases with age and it is higher in men and African-Americans based on the same creatinine level because men and African-Americans have higher muscle mass, which normally produces a higher creatinine molecule than say women would. Of the 20 million Americans who have kidney disease, based on the GFR definition, only 300,000 have Stage 5. For many people kidney disease is asymptomatic so a blood test revealing a high creatinine level is often the first indicator of a problem. When the GFR falls into the Stage 3 level, i.e. 15-59, it is time to see a nephrologist. To see whether your GFR falls below 60, go to the following URL to calculate GFR or filtration rate, http://nkdep.nih.gov/professionals/gfr_calculators/orig_con.htm.

After a nephrectomy, the remaining kidney usually takes over the body’s filtration burden leading to normal or near-normal kidney function. However, in some cases, the remaining kidney is not able to handle the added responsibility and the creatinine level shoots up and the GFR level falls. Risk factors for lower kidney function after nephrectomy are hypertension, diabetes, and proteinuria (high levels of protein in the blood). Anyone diagnosed with kidney cancer who has these risk factors, should consider having nephron-sparing surgery, i.e. a partial nephrectomy, if possible, in order to preserve kidney function.

Ken Youner, ACKC Board Member

Dr. Kenneth Youner, ACKC Board member, and his wife Cecile have been busy this summer advocating for cancer causes. Here is Ken’s brief summary of some of their activities.

Cecile and I are both cancer survivors battling stage 4 cancer, Cecile with breast cancer and me with kidney cancer. We were both invited to speak in Washington on July 22nd for the NCCS (National Coalition for Cancer Survivorship). NCCS is the oldest survivor-led cancer advocacy organization in the US. It advocates, at the federal level, for changes that will advance cancer research and the delivery of cancer care in the US. NCCS is currently promoting a federal bill (The Comprehensive Cancer Care Act S. 2790/H.R. 1078) that will allow Medicare to pay physicians for a detailed, written cancer survivorship plan for patients. This will enable patients to have a written portable summary of their cancer diagnosis, test results, treatment plans, side effects profile and need for follow-up and surveillance plans. Since this is currently not readily available for most cancer patients we felt that it is very important to support this bill.

Cecile and I spoke in front of a room crowded with congressional aides and reporters. Cecile spoke first and related how she had been diagnosed in 1993 with a small, early breast tumor. Her nodes were negative, and we believed that she had been cured with surgery. Ultimately, however, the cancer came back with metastatic disease in her lungs and then her bones. She did not have a written summary with recommendations for follow-up care which may have led to better and earlier surveillance.

I spoke of my battle with metastatic kidney cancer. Since being diagnosed, I have become a member of ACKC’s Board of Directors and have been active on ACOR (Association of Cancer Online Resources), the major kidney cancer listserv in the U.S. As the only active physician on the list, I see the daily struggle of people who do not have the medical understanding and access to resources that I have and I try to provide them with information and support. A written cancer treatment plan, treatment summary and follow-up medical plans would greatly advance the quality of cancer care for these people and for other cancer patients in this country.

Two days after returning from Washington, DC, I boarded a plane to Columbus, Ohio to take part in the 2008 Livestrong Summit, where over 1000 cancer advocates met and joined in advocacy training sessions organized by the Lance Armstrong Foundation (LAF). I participated in sessions to improve my ability topersuadedecision makers, to take joint action with other advocates, and to mobilize others. There were panel presentationsfrom leaders in the political, medical oncology and governmental spheres. Lance Armstrong was there for the entire 4 days and it was apparent to me how committed he is to making cancer a major priority for the incoming administration. We discussed the need for improved federal support for the National Cancer Institute as its budget has been flat for the past 3 years. I met many advocates who are cancer survivors and was energized by their dedication and spirit.

Editor’s note:

The LAF is forming a nationwide force of advocates called the Livestrong Army. Ken is the leader of the Northern NJ Army. Anyone in that area wishing to work with Ken can contact him at livestrongsrmyNNJ@gmail.com.

Interviews with Two Leading Oncologists

At the ASCO Conference, ACKC interviewed two nationally prominent kidney cancer oncologists to get a sense of the patient-client relationship with respect to a “specialist” oncologist who usually sees patients after they have previously consulted with their local or “community” oncologist. Following are the interviews, which were with Dr. Brian Rini who is Associate Director for Clinical Research at the Cleveland Clinic Taussig Cancer Institute and Dr. Janice Dutcher, a member of the Department of Oncology at Montefiore Medical Center in the Bronx, NY.

Interview #1:

ACKC: How do you decide which therapy to use for your patients, e.g., from the literature, conferences, your own trials, etc? Do you lean towards FDA-approved therapies or investigational drugs?

Dr. Rini: it’s a combination of my own experience, which is largely a clinical trial experience. We lean as a center, towards investigational drugs, but obviously use FDA-approved agents as well. I don’t think there’s any one clear path for any patient in terms of which therapies to pick.

ACKC: Do you prefer one drug to another?

Dr. Rini: Not necessarily. I think sunitinib (Sutent) has the strongest prospective Phase III data, so if there’s a drug that we use more often I’ll say it’s Sutent, but not exclusively.

ACKC: What percentage of your patients are informed about the therapeutic options before they come to see you?

Dr. Rini: I would say a large percentage, 60-70%. We obviously have a select group of patients that seek us out for our expertise so they are generally more well informed.

ACKC: Do your patients see you for a second opinion?

Dr. Rini: Yes, probably nowadays they will be seen locally and then they will seek us out through the Internet or the Kidney Cancer Association and then come see us. But not always. We get a lot of patients from our urologists as well and they may not have seen somebody on the outside.

ACKC: Do you prefer that your patients do independent research about treatment options and participate in the treatment decision, or do you prefer that they leave it entirely up to you to decide the appropriate treatment?

Dr. Rini: I don’t know if I have a preference one way or the other. Usually patients have a preference, either they’re the type of patient who does a lot of independent research that I’m happy to talk about and come to some treatment recommendations, and some people want me to entirely make the choice. I don’t think one or the other is right or wrong, it’s just personal style and I’m really happy to do either.

ACKC: What types of questions would you most want your patient to ask you?

Dr. Rini: You want mostly that patients understand their situation, the severity of the disease, the fact that they’re likely to die from the disease, the fact that these drugs have toxicities, to be realistic about the benefits. You worry when patients don’t come into it with that realism.

ACKC: What do you tell someone who is terminal?

Dr. Rini: That’s where it gets into the art of medicine in terms of deciding how much can I tell this patient at one time. We don’t have four hours with each patient so I can’t have a full counseling session with each patient for somebody who comes in unaware of what is going on. You introduce it in sequential visits over time. That’s just a doctor-patient relationship type issue that’s a tough one though, about people who don’t have an understanding and how you bring them to one.

ACKC: Sometimes it’s impossible to get through to them?

Dr. Rini: It is and everybody accepts it on some level. Some people accept it within a week and some people don’t ever.

ACKC: If you weren’t constrained by lack of funding for research, what would you study?

Dr. Rini: Probably the same things I’m studying now but perhaps in more quantity. We can’t do every trial because we don’t have enough data mangers and research nurses and budget people and contract people. If we could do every trial we’d open every single trial out there and study everything properly.

ACKC: Are you restricted by what the drug companies make available to you?

Dr. Rini: Well we can do studies through the cooperative groups of through CTEP (Cancer Therapy Evaluation Program, an NCI program). It’s not that I’m dying to put two agents together but can’t because there’s no money. I don’t think that there’s one thing there that’s so promising as a combination that hasn’t already been studied that’s simply being held up by funding.

ACKC: Why do tumors become resistant to anti-angiogenic therapies?

Dr. Rini: I have no idea.

ACKC: If someone progresses on a therapy do you immediately remove them from the therapy?

Dr. Rini: My personal belief is that you know when someone is getting worse. It might be a hard thing to quantify in a scan or a number or to teach people but in general you know when someone is no longer benefiting from therapy. That might be RECIST PD (progressive disease by RECIST tumor measurement standards), it might be clinical worsening, or some combination – that’s a difficult one. But I think at the end of the day you kind of know when people are getting worse. It’s not a great answer but we don’t really have any other way of measuring.

ACKC: Where do you see the future development of anti-angiogenic or targeted therapies?

Dr. Rini: Hopefully, it’s novel targets. We have a lot of anti-angiogenics now so it’s novel drugs in that category and novel drugs in a completely different category. I’m looking for some other target that we haven’t talked about.

ACKC: Is there room for immunotherapy?

Dr. Rini: I think there’s still room for it. It’s a smaller room than it was before. As part of a trial that’s maybe looking at a combination or a novel selection, I think that’s reasonable.

ACKC: One of the criticisms of targeted therapies is that they have not yet shown to have complete responses.

Dr. Rini: Well, people always say that. I have people in my clinic who have been on them for four and five years. Are they complete responses? They’re still on drugs. Do they have radiographic abnormalities? Probably. Does it matter that they have radiographic abnormalities? I’m not sure. So if they live for 10 years and die of something else, well that’s a long term CR (complete response). It’s not as radiographically dramatic as high-dose interleukin-2, but I just don’t think that we know yet.

ACKC: Do you think the complete response will come via the targeted therapies or do we need another paradigm?

Dr. Rini: That’s a tough question to answer. It may be through combinations of targeted therapies. It may be through targets that we don’t yet have drugs for.

ACKC: Do you have further comments on recommended therapies for other types of kidney cancer (clear cell was well-covered in the sessions)?

Dr. Rini: For anything that’s not clear cell, there’s no obvious first-line therapeutic choice. You couldn’t be faulted for putting someone with papillary or chromophobe on a totally novel agent as first-line therapy. Because, in all likelihood, they’ll be able to get Sutent or whatever second-line.

ACKC: So you would put them on a trial?

Dr. Rini: I might. If I had one that I thought was a reasonable mechanism. If the patient had a high tumor burden then I might lean towards Sutent although it’s not definitively proven in that setting. Statistically, I think it’s more likely to work than some novel agent that hasn’t been tested.

ACKC: What about collecting duct?

Dr. Rini: Mostly cisplatin chemotherapy. We don’t see that much of it. That’s not kidney cancer. That’s totally different. That’s really bladder cancer.

ACKC: What about poor prognosis patients?

Dr. Rini: We don’t see many, but the data support temsirolimus (Torisel), not that other agents are wrong, but the evidence indicates temsirolimus as the agent of choice until proven otherwise.

ACKC: For second line therapy?

Dr. Rini: I don’t think there’s one second-line agent of choice.

ACKC: Thank you very much.

Dr. Rini: Your welcome.

Interview #2:

ACKC: How do you decide which therapy to use for your patients, e.g., from the literature, conferences, your own trials, etc? Do you lean towards FDA-approved therapies or investigational drugs?

Dr. Dutcher: For new patients, the first thing I do is assess them for eligibility for high-dose interleukin-2 because I think that’s probably the best thing to give first. There are some data from Boston to suggest that after TKIs (tyrosine kinase inhibitors like Sutent) there may be some problems, so if someone is really eligible for IL-2 I would like to do it up front. In terms of other options, if we have a clinical trial I’m still strongly in favor of continuing to do clinical trials even in untreated patients. We do have an IL-2 clinical trial looking at biological markers of response to IL-2. We also have clinical trials with new angiogenesis drugs in new combinations and we’re very much committed to the ECOG’s (Eastern Cooperative Oncology Group) BeST trial looking at combinations of targeted therapies (bevacizumab, sorafenib, and temsirolimus). Beyond that, it’s really not easy to make a decision. You’ve got four drugs now that are available for kidney cancer other than cytokines (IL-2 and interferon-alpha) that have activity, so it’s really in some degree dependent upon logistics, dependent upon practical issues like payment, reimbursement, distance from the institution, whether they can come every week if they want to take an intravenous drug. So it’s not clear that there’s a 1-2-3 approach.

ACKC: What percentage of your patients are informed about the therapeutic options before they come to see you?

Dr. Dutcher: Probably more than 75% have had some introduction to the treatments that are available. They often come having been referred by the ACOR listserv, i.e. they come self-referred essentially. Some come referred by surgeons, some have been to a medical oncologist and have gotten one of the other new drugs and want to know what else is out there. I’ve seen more people who are actually on treatment and they want to know what to do next or how they go about looking for something new. So it’s more on treatment than it used to be. It’s a small percentage who really don’t have a clue about the treatment options. But the other problem is that earlier, they did their whole literature search so they knew what all their options were, and now they’re being told ‘this is what I would do’ so they don’t do the search that they probably should do.

ACKC: Do you prefer that your patients do independent research about treatment options and participate in the treatment decision, or do you prefer that they leave it entirely up to you to decide the appropriate treatment?

Dr. Dutcher: No, I prefer that they interact and that they understand what the options are. I think that my job is to filter the information, and to put it into perspective. The more they know the better off they are. I don’t think that they have a complete medical background to understand all of it, and that’s what I feel that my position should be.

ACKC: What types of questions would you most want your patient to ask you? How do you see your role?

Dr. Dutcher: I think it’s pros and cons of approaches. I think in addition to systemic treatments there are a lot of localized treatments that people are undergoing such as RFA (radiofrequency ablation), cryosurgery, surgery. When do these things fit into the therapeutic armamentarian? For example, if patients have a solitary metastasis, then surgery is probably a better option than any systemic treatment. When do you start systemic treatment? If somebody’s rock stable, maybe you don’t. So these things need to be discussed as well. Sometimes people come to me and say I should start Sutent, and I say why don’t you get that removed and we’ll see you in 6 months with a new scan. I think that what I have to offer people now is different than just providing a new trial, but it’s a 20-year prospective on the disease because it’s not like other solid tumors and medical oncologists who are used to solid tumors are not used to this disease and are not used to the new treatments. So I don’t mind that people get treated locally, I think that’s good. But I think they need a back-up person who knows the disease and the drugs.

ACKC: If you weren’t constrained by lack of funding for research, what would you study?

Dr. Dutcher: I think the key is still new drug development. We are trying to get to the molecular basis of the disease, but it’s not clear that with all of the drugs that that’s changed how we approach clinical trials. Yes, we’re doing anti-angiogenesis, but all of a sudden the oncogene in papillary also feeds into the angiogenesis pathway, the Met oncogene. And TKIs are actually working in papillary renal cell, so it’s not like this goes to this disease and that goes to that disease, it’s not that straightforward.

ACKC: Why do tumors become resistant to anti-angiogenic therapies?

Dr. Dutcher: I’m not sure it’s resistance. I mean they become refractory to it, they overcome that driving force and they use something else and then when you stop the drug, sometimes they can back off and you can re-start it a little bit later. So that’s a major question and it is a major focus of research right now.

ACKC: What’s the difference between refractory and resistance?

Dr. Dutcher: Resistance suggests that you disable the pathway and I think that the pathway just becomes less important than another pathway – the tumor finds a different way to stimulate growth. And then when you take away the angiogenesis drug, then I think it goes back to the same pathway again.

ACKC: If someone progresses on a therapy do you immediately remove them from the therapy?

Dr. Dutcher: That really depends on how aggressively progressive and over what period of time. If somebody’s on an anti-angiogeneis drug and they’ve got a little bit of growth every two or three months, I might keep them on it for a while. I think that there’s more pressure to change now because there are more drugs out there. But my basic approach is to push it as far as you can push it, so if there’s a millimeter or two change, I won’t stop the drug.

ACKC: Where do you see the future development of anti-angiogenic or targeted therapies?

Dr. Dutcher: Well, clearly angiogenesis is a big deal. There are at least three more drugs in development right now, two of which are very close, although they’re looking at other tumor types because the renal field is so crowded. I think this next year will be the year of the combinations, and people will see if they’re better, safer, or more toxic. The ECOG trial is one of those. Wyeth is pursuing an mTOR plus bevacizumab (Avastin) study. There are some cytokine plus sorafenib (Nexavar) studies out there. And then the new kinds of drugs that will be coming out are Met inhibitors, MEK inhibitors, possibly RAS/RAF inhibitors. But do we know if those pathways are important? The nice thing about renal cell is that we know the VEGF pathway is important. We also know that EGFR is up-regulated in renal cell, but erlotinib (Tarceva) is not particularly effective in renal cell, but we have the SWOG (Southwest Oncology Group) study with erlotinib in papillary renal cell where survival was improved over historical controls. This was a small study where although survival improved there were not a lot of responses, so I think we have to go back and see if there are things that will target that pathway in papillary. I would like to see an EGFR inhibitor plus a Met inhibitor in papillary renal cell.

ACKC: Is there any new immune therapy in renal cell?

Dr. Dutcher: There are a couple of things. There’s ipilimumab, which is a big thing for melanoma right now. It’s a CTLA-4 antibody and has activity in renal cell. They sort of backed off because when they did the study at the National Cancer Institute, it was early on in the development of the drug and one of the side effects was an auto-immune colitis and they had a lot of complications from that because the patients weren’t staying at the NIH and being watched closely. Now that they’ve learned this in the melanoma study, it’s very manageable, so I think they need to go back and look at it again in renal cell. The other drug, which is not an immunotherapy, is Pfizer’s drug axitinib, which has activity, will go into Phase III (ed. Note It already has.)

The other immunotherapy is IL-21 and sorafenib in combination. We’ll see. IL-21 has some, small amount of activity on its own.

ACKC: Is there any vaccine in kidney cancer?

Dr. Dutcher: Not that I’ve seen.

ACKC: How about adjuvant therapy?

Dr. Dutcher: Just the two studies that are ongoing, the Wilex monoclonal antibody G250 study, which is still ongoing, and the ECOG study (sorafenib/sunitinib/placebo). That’s it right now.

ACKC: Further comments on recommended therapies for types of kidney cancer?

Dr. Dutcher: I would say starting with collecting duct we’re still starting with chemotherapy or with a clinical trial. But I don’t think that there are enough patients with this disease to be able to say that. I’ve had people with this disease who responded to Sutent. I had a man who had a very nice response on Sutent then we switched to Torisel, which didn’t work, then we switched him back to Sutent, which is still working. But it’s going to be a handful of people and the others are going to be on chemotherapy. The chromophobe and papillary people I would not give cytokines to.

ACKC: Not even chromophobe?

Dr. Dutcher: Well chromophobe I’ve seen responses, mostly stabilization. But I probably would still start them with a TKI, although if I thought they might respond to IL-2, I would enroll them in the SELECT trial to look at the biomarkers first to see if it’s real.

For poor prognosis patients I would probably go with an mTOR inhibitor (Torisel). But I’ve had responders with the others as well. So I think some of that’s going to depend upon if they can come every week, etc. it’s very well tolerated so in some ways it’s a very good choice. For example, I have a patient who’s a golfer and he’s had renal cell for over 20 years. He had a big hiatus and then it came back and he had IL-2 and then he sat for five years and then it came back. He didn’t want to take sorafenib or sunitinib due to the hand-foot syndrome because he like to golf. So we started Torisel and he had a very nice response to it.

ACKC: Would you recommend anything for second-line therapy?

Dr. Dutcher: I know that’s what they’re doing with those algorithms, but I don’t think we should put them in boxes because I think the choice is more personal and except for IL-2, you’re actually closing some doors if you say ‘this is first-line’ or ‘this is second-line’.

ACKC: You remarked initially about there being a problem with respect to sequencing IL-2 and TKIs.

Dr. Dutcher: Yes, there was a poster presentation by Schwarzberg which showed in a retrospective study that they treated 23 people with TKIs and then IL-2 and 6 of the 23 or 26% experienced cardiovascular toxicities (ed. Note: this was compared to 8.5% in the landmark Phase III trial of 192 patients reported by McDermott in 2005. This study suggest that eligible patients should start with IL-2 before tackling TKIs).

ACKC: Thank you.

Dr. Dutcher: You’re welcome.

Cancer Wars MAARS Journey

Gerald White, a 10-year kidney cancer survivor of a metastatic 20-pound tumor, sent me a note that he recently updated his website http://cancerwarsmaarsjourney.com/. Gerald is a proponent of Guided Imagery, which is a method to enable the body’s immune system to recognize the tumor as foreign, i.e. antigen recognition, thereby facilitating its destruction.

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