The OBR Blog

October 25, 2016 - 05:10 pm Posted in Featured comments0 Comments

I have extensive experience in “real world” policy-setting and decision-making and I am puzzled about the motivations regarding the attempt to transfer and recast the failed Quality Adjusted Life Years-based NICE program in the UK to the USA. Among other things, this concern is based upon the findings (Oct. 2014) of the EchOutcome Committee appointed by the European Commission whose chairman concluded that:

“The research provides robust scientific evidence that Quality Adjusted Life Years produce hugely inconsistent, wrong results on which important decisions are being made.”

I add that it has been noted that these wrong NICE-driven decisions have been correlated with decreases in OS across tumor types driving the UK to the “Bottom of the Barrel” in terms of OS across many tumor types compared to other developed Western European countries. Why do we want such a life-threatening process to be transposed to the US by ICER?

Further I note the points (OBR Green on Oct.19) made by 5 eminent Key Opinion Leaders who treat lung cancer every day.

“For us as practicing oncologists and lung cancer researchers, this report has raised serious concerns regarding ICER’s ability to interpret clinical evidence and reach conclusions on drug value that are scientific, comprehensive, and unbiased. ICER appears to represent a perspective that is less oriented toward patient benefit than toward motivations that would limit patient access to new therapeutic options. ICER’s clinic-economic methods include approaches and metrics that, due to their singular focus on population level health, would likely fail patients on an individual clinical needs basis!”

In looking at the roster (Drs. Ettinger, Schwartzberg, Otterson, Jahanzeb, Waterhouse) of experts, I am in full agreement with them. Further, I see many more points that bear extensive examination and discussion. These points include:

  • Across Value Metric Frameworks, including ICER, the failure to use or at least recognize the “Real Price” (e.g., minus 340B and Medicaid discounts) leaves an important piece out of the ICER analysis.
  • Making comparisons and valuations across disparate patient populations (e.g., PD-L1 expression levels) leads to almost absurdly different and misleading comparative values.

Finally, and most importantly, here is a critical lesson that I learned at Aetna making real world decisions daily that directly impacted the lives of 15 million people and that should be duly noted.

“Those who engage in the development of assessments of Evaluation and Valuation must be willing to live with, in an ABSOLUTE manner, (e.g., no appeals, no nothing) the decisions based upon their own assessments realizing that someday such assessments (e.g., ICER) may drive and direct decisions about the treatment of their mother, sister, brother, spouse, children etc.”

by William McGivney, PhD, Managing Principal for McGivney Global Advisors, and former long-time CEO of the NCCN, VP for Clinical and Coverage Policy at Aetna, and Member of the Medicare Coverage Advisory Committee

October 10, 2016 - 02:10 pm Posted in Featured comments0 Comments

By Emily Benesh, Ph.D., Analyst, Clinical & Scientific Assessment, Kantar Health and Stephanie Hawthorne, Ph.D., Vice President, Clinical & Scientific Assessment, Kantar Health




Faslodex® (fulvestrant, AstraZeneca) was approved in 2002 for the treatment of postmenopausal metastatic hormone receptor (HR)-positive breast cancer patients following prior anti-estrogen therapy. To date, utilization of Faslodex has favored second- and third-line settings for this indication, while aromatase inhibitors (AI) are generally favored in the first line for postmenopausal patients. Unlike AIs, which inhibit estrogen biosynthesis, Faslodex is an estrogen receptor antagonist (a selective estrogen receptor degrader (SERD)) that competes with estrogen to bind to estrogen receptors.  Since Faslodex acts through a different mechanism than AIs, it may represent an attractive treatment option in the first line for physicians concerned about bone loss caused by AIs. AstraZeneca previously marketed the AI Arimidex® (anastrozole), but since it lost patent protection in 2010 AstraZeneca has been looking to reestablish a branded agent (Faslodex) in the first-line postmenopausal setting. Indeed, AstraZeneca supported the FIRST trial, an open-label randomized Phase II study that evaluated Faslodex (500 mg) versus anastrozole (1 mg) as first-line hormone therapy in 205 women with postmenopausal HR-positive, locally advanced or metastatic breast cancer; notably, 72% and 78% of patients in each arm, respectively, have received no prior endocrine therapy. Faslodex was superior to anastrozole in both time to progression (23.4 versus 13.1 months; HR: 0.66, P=0.01) and overall survival (54.1 versus 48.4 months; HR: 0.70, P=0.04),1,2 prompting further evaluation of Faslodex in the first-line setting.

The objective of the Phase III FALCON trial was to confirm the superiority of Faslodex over anastrozole in postmenopausal HR-positive and HER2-negative patients with locally advanced/metastatic breast cancer who had not received prior endocrine therapy. FALCON was a double-blinded international trial that randomized patients to either Faslodex (500 mg subcutaneous injection on Day 0, 14 and 28, then every 28 days) or anastrozole (1 mg oral once daily).  The primary endpoint was progression-free survival (PFS), with several secondary endpoints including overall survival and objective response rate. Patients were included had WHO performance status of 2 or better and greater than one measurable or non-measurable lesion. Exclusionary criteria included prior endocrine therapy, systemic estrogen-containing hormone-replacement therapy use six months or less prior to randomization, presence of life-threatening metastatic visceral disease, and prior systemic treatment except one line of chemotherapy or radiotherapy.

AstraZeneca announced via press release in May 2016 that FALCON met its primary endpoint, but the data outcomes remained unknown until presented today at the 2016 European Society of Medical Oncology (ESMO) conference.3 Median PFS was improved by 2.8 months in favor of Faslodex (16.6 months for Faslodex versus 13.8 months for anastrozole; HR: 0.797, p = 0.0486). Overall survival was not significantly different between the arms (HR: 0.88, P=0.428), although the study had reached just 31% maturity. No significant differences were found in overall response rate, clinical benefit rate, or median time to deterioration by FACT-B total score. Immature duration of response endpoints showed promise (20.0 versus 13.2 months, Faslodex and anastrozole, respectively) as did duration of clinical benefit (22.1 versus 19.1 months, Faslodex and anastrozole, respectively); although statistical significance was not reported for these endpoints, the authors noted that they were trending toward significance. Overall safety profiles were generally similar between the two arms, with modestly higher signals in the Faslodex arm for arthralgia (16.7% versus 10.3%), myalgia (7.0% versus 3.4%), and ALT increase (7.0% versus 3.0%).

Interestingly, subgroup analysis found that PFS more strongly favored the Faslodex arm in patients lacking visceral metastatic disease. In the subpopulation of 208 patients, only 53.7% had a progressive event in the Faslodex arm, compared with 69.9% of patients in the anastrozole arm (22.3 months versus 13.8 months median PFS, respectively; HR: 0.592). No difference was observed in PFS between the Faslodex and anastrozole arms in patients with visceral metastatic disease. The generalizability of these findings was strengthened by similar PFS improvements in the Faslodex arms of the FIRST1,2 and CONFIRM4,5 trials.

Despite the fact that the FALCON trial met its primary endpoint, Faslodex will have hurdles to overcome in order to gain utilization in the front-line setting for this patient population. The largest hurdle faced by Faslodex in the first line is competition with the CDK 4/6 inhibitors. Ibrance® (palbociclib, Pfizer) is already U.S. FDA-approved in combination with letrozole in the first-line setting and in combination with Faslodex in AI-pretreated metastatic breast cancer, and a European approval is currently pending. Given the exemplary data that Ibrance/letrozole demonstrated in first line in comparison to letrozole alone (PFS: 24.8 versus 14.5 months, respectively, HR=0.58, p<0.000001)6, the 2.8-month benefit for Faslodex demonstrated in the FALCON trial in a very selective group of hormone-naïve first-line patients is not expected to unseat current use of the Ibrance/letrozole combination. Where Faslodex may find use in first-line is in those patients who don’t currently receive an Ibrance combination. Metastatic breast cancer patients with very indolent disease that has demonstrated strong sensitivity to endocrine therapy may be treated with a single agent hormone therapy upon first metastatic recurrence; the superiority that Faslodex demonstrated over anastrozole may support its use in first-line in some of these patients. However, that displacement may not be widespread given the small degree of benefit (2.8 months median PFS, PFS HR 0.797, and no overall survival benefit). Where Faslodex may find a niche role in first-line is in patients with bone-only disease (non-visceral), patients at risk for bone complications, or in patients who are not compliant with oral therapies.

The FALCON results suggest that for the vast majority of metastatic breast cancer patients, Faslodex will continue to play a strong role in the second- or third-line settings. Several Phase III trials in the relapsed setting that have combined Faslodex with targeted agents are underway, and indeed the Phase III PALOMA-3 trial has already reported impressive results for the combination of Faslodex plus Ibrance in AI-pretreated patients.7 Knowing that Ibrance plus Faslodex is superior to Faslodex alone in the second-line setting, there has been speculation that positive results in FALCON could spur use of this combination in the first-line setting. However, the small magnitude of benefit actually observed in FALCON will likely limit use of this combination in first-line in clinical practice.

The positive results from the FALCON trial will be viewed as an important advance for a select group of metastatic breast cancer patients (HR-positive, HER2-negative and endocrine therapy-naïve). While the FALCON results will allow Faslodex to take flight into first-line for this niche patient group, ultimately this bird of prey can’t out-compete a bird of peace8


  1. Robertson JF, Lindemann JP, Llombart-Cussac A, et al., “Fulvestrant 500 mg versus anastrozole 1 mg for the first-line treatment of advanced breast cancer: follow-up analysis from the randomized ‘FIRST’ study,” Breast Cancer Res Treat, 136(2): 503-11, 2012.
  2. Robertson JF, Llombart-Cussac A, Felti D et al., “Fulvestrant 500 mg versus anastrozole as first-line treatment for advanced breast cancer: Overall survival from the Phase II ‘FIRST’ study,” Abstract S6-04, SABCS, 2014.
  3. Ellis MJ, Bondarenko IM, Trishkina E, et al.; “FALCON: A phase III randomised trial of fulvestrant 500 mg vs. anastrozole for hormone receptor-positive advanced breast cancer;” Annals Oncol, 27 (s1):  Abstract LBA 14_PR, 2016.
  4. Di Leo A, Jerusalem G, Petruzelka, et al.; “Results of the CONFIRM Phase III Trial Comparing Fulvestrant 250 mg With Fulvestrant 500 mg in Postmenopausal Women With Estrogen Receptor–Positive Advanced Breast Cancer;” J Clin Oncol, 28 (30): 4548-4550, 2010.
  5. Di Leo A, Jerusalem G, Petruzelka L, et al., ” Final Overall Survival: Fulvestrant 500mg vs 250mg in the Randomized CONFIRM Trial,” J Natl Cancer Inst, 106 (1): djt337, 2013.
  6. Finn RS, Martin M, Rugo HS, et al.; “PALOMA-2: Primary results from a phase III trial of palbociclib (P) with letrozole (L) compared with letrozole alone in postmenopausal women with ER+/HER2– advanced breast cancer (ABC);” J Clin Oncol 34, 2016 (suppl; abstr 507).
  7. Turner NC, Ro J, Andre F, et al.; “Palbociclib in Hormone-Receptor–PositiveAdvanced Breast Cancer;” New  Engl J Med,  2015, DOI: 10.1056/NEJMoa1505270.
  8. PALOMA is derived from Latin “palumbus” which means Dove; a symbol of Peace.

October 10, 2016 - 02:10 pm Posted in Featured comments0 Comments

By Tari Awipi, Ph.D., Associate Consultant, Clinical & Scientific Assessment, Kantar Health and Stephanie Hawthorne, Ph.D., Vice President, Clinical & Scientific Assessment, Kantar Health




Tesaro’s PARP inhibitor, niraparib, has generated a lot of excitement in recent weeks. On September 12, Tesaro announced that it had received an FDA fast track designation for the treatment of patients with recurrent platinum-sensitive ovarian, fallopian tube or primary peritoneal cancer. In addition to the initiation of a rolling submission of a New Drug Application (NDA) for niraparib to the FDA that Tesaro intends to complete during the fourth quarter, the company also announced plans to submit the Marketing Authorization Application (MAA) for niraparib to the European Medicines Agency (EMA) in the fourth quarter. These plans were driven by the promise of the NOVA data that were presented today at the 2016 European Society of Medical Oncology (ESMO) meeting in Copenhagen1 and published in the New England Journal of Medicine.2 NOVA (ENGOT-OV16) was a randomized, placebo-controlled, Phase III trial conducted by the European Network for Gynecological Oncological Trial groups and investigators in the United States, Canada and Hungary. This trial compared single-agent niraparib versus placebo as maintenance therapy following second-line induction therapy in platinum-sensitive ovarian cancer patients who have either germline mutation in breast cancer susceptibility gene 1 or breast cancer susceptibility gene 2 (gBRCA) or a tumor with high-grade serous histology. One thing that sets the NOVA trial apart is the large number of patients included who do not have a gBRCA mutation (350 of the 553 total enrolled patients). The non-gBRCA mutation patients were further stratified according to tumors with homologous recombination deficiency (HRD), defined by the myChoice HRD test (Myriad Genetics).

The primary endpoint was progression free survival (PFS), which was significantly greater for niraparib compared with placebo in each of the three subpopulations (p<0.001). In the gBRCA mutant cohort, median PFS was 21.0 months in the niraparib arm (n=138) and 5.5 months in the placebo arm (n=65) (HR 0.27; 95% confidence interval [CI], 0.17 to 0.41). The same pattern was seen in the overall non-gBRCA cohort: 9.3 months with niraparib (n=234) versus 3.9 months with placebo (n=116) (HR 0.45; 95% CI, 0.34 to 0.61). Further, this effect was more pronounced in the HRD-positive subgroup of the non-gBRCA cohort: 12.9 months with niraparib (n=106) compared with 3.8 months with placebo (n=56) (HR 0.38; 95% CI, 0.24 to 0.59).

These data were received extremely positively by the crowd in attendance. During the discussion, the strong data in this “BRCA-like” group were considered particularly exciting and could change the landscape of treatment in ovarian cancer. Given the large number of non-gBRCA patients included in the trial as well as the positive results, Tesaro can seek a broad label without the BRCA mutation restriction. Indeed, during the discussion, emphasis was placed not on BRCA, or being “BRCA-like,” but rather on the platinum sensitivity of this patient population. In Europe, niraparib will be seeking a label very similar to Lynparza™ (olaparib, AstraZeneca); in the United States, however, niraparib will have a broad label, distinct from Lynparza, whose FDA-approved indication limits its use to fourth-line in patients with gBRCA mutations.

In platinum-sensitive ovarian cancer patients with gBRCA mutations, PARP inhibitors are ascendant.  As noted above, Lynparza is currently approved in the United States and Europe, albeit with divergent indications. Clovis Oncology’s rucaparib adds another dimension to this space. In a combined analysis of two Phase II studies (Study 10 and ARIEL2, n=106) and using an assay developed by Foundation Medicine, the BRCA (germ line and somatic) mutant subgroup demonstrated a 53.8% objective response rate and 10-month median PFS in patients previously treated with a median of three prior chemotherapies and predominantly platinum-sensitive.4 Previous analysis of just the ARIEL2 study indicated improved efficacy in patients with BRCA (germ line and somatic) mutation and in patients with BRCA-like HRD-positive ovarian cancer, in comparison with non-BRCA-like patients.5

The PARP inhibitors are racing to establish and gain share in this space. Clovis has completed their accelerated approval application with the U.S. FDA for use in BRCA (germ line and somatic) mutant patients who have been treated with two or more prior chemotherapies. This application received a priority review, which could put it on the market by February 2017; they plan to file an MAA in Europe by the end of 2016. Tesaro is further behind, but the robust Phase III NOVA data will likely put it at an advantage once it launches; U.S. and European filings should be complete in the fourth quarter of 2016. While Lynparza is already EMA-approved in patients with gBRCA mutations, niraparib’s Phase III data in “BRCA-like” patients may help eclipse Lynparza’s standing; in the United States, the launch of niraparib may have a more pronounced effect on Lynparza, as it is expected to be approved and utilized in an earlier treatment setting. With so many novel agents demonstrating strong efficacy, the stars are beginning to shine brightly on the ovarian cancer space.


  1. Mirza MR, et al.; “A randomized, double-blind phase 3 trial of maintenance therapy with niraparib vs placebo in patients with platinum-sensitive recurrent ovarian cancer (ENGOT-OV16/NOVA trial);” Annal Oncol, 27 (s1): Abstract LBA3_PR,2016.
  2. Mirza MR, Monk BJ, Herrstedt J, et al.; “Niraparib Maintenance Therapy in PlatinumSensitive, Recurrent Ovarian Cancer;” New Engl J Med, 2016: DOI: 10.1056/NEJMoa1611310.
  3. Kantar Health, CancerMPact® U.S. Treatment Architecture, Ovarian cancer;; accessed October 8, 2016.
  4. Kirsteleit RS, Shapira-Frommer R, Oaknin A, et al.; “Clinical Activity of the Poly(ADP-Ribose) Polymerase (PARP) Inhibitor Rucaparib in Patients with High-Grade Ovarian Carcinoma and a BRCA Mutation: Analysis of Pooled Data from Study 10 (Parts 1, 2a, and 3) and ARIEL2 (Parts 1 and 2);” Annal Oncol, 27 (s1): Abstract 856O, 2016.
  5. Coleman RL, Swisher E, Oza A, et al.; “Refinement of Prespecified Cutoff for Genomic Loss of Heterozygosity (LOH) in ARIEL2 Part 1: A Phase 2 Study of Rucaparib in Patients with High-Grade Ovarian Carcinoma (HGOC);” J Clin Oncol 34, 2016 (suppl; abstr 5540).

October 10, 2016 - 02:10 pm Posted in Featured comments0 Comments

By Liseth  Parra, Ph.D., Analyst, Clinical & Scientific Assessment, Kantar Health and Stephanie Hawthorne, Ph.D., Vice President, Clinical & Scientific Assessment, Kantar Health




A biologics license application (BLA) for Tecentriq® (atezolizumab,  Roche/Chugai) was accepted with priority review by the U.S. Food and Drug Administration (FDA)  in April 2016 for the treatment of patients with PD-L1-positive, locally advanced or metastatic non-small cell lung cancer (NSCLC) patients who have progressed on or after platinum-containing chemotherapy, an indication in which Tecentriq also has Breakthrough Therapy Designation (BTD). This filing for accelerated FDA approval was based on the single-arm Phase II BIRCH trial, in which Tecentriq produced a 17% objective response rate (ORR) in PD-L1-positive second-line NSCLC.1 Supporting data for Tecentriq in second-line NSCLC also come from the randomized Phase II POPLAR study that showed an improved median overall survival (OS) of 12.6 months with Tecentriq compared with 9.7 months with docetaxel in  second-line NSCLC (HR: 0.69, p=0.04).2  Confirmatory data to support its approval can now include the Phase III OAK trial, whose results were newly presented at the 2016 European Society of Medical Oncology (ESMO) Congress.3 A PDUFA regulatory decision for Tecentriq in second-line NSCLC treatment is expected as early as October 19, 2016.

Tecentriq is an engineered monoclonal antibody designed to block the PD-L1 protein, expressed on tumor cells and tumor-infiltrating immune cells (IC), whose main function is to inhibit T-cell immune response. Once this pathway is inactivated by a PD-L1 blocker, such as Tecentriq, the T-cell ability to attack tumor cells is restored, increasing the body’s ability to fight cancer.4 Tecentriq is one of several checkpoint inhibitors in development for NSCLC and is the first and only anti-PD-L1 cancer immunotherapy approved by the FDA to date, obtaining accelerated approval for second-line treatment of locally advanced or metastatic urothelial carcinoma (mUC) in May 2016. Genentech and Roche are aggressively developing Tecentriq in the NSCLC space, with initial commercial launch planned in the second- and third-line settings for patients who overexpress PD-L1 and with eight more Phase III trials ongoing in first-line and the adjuvant setting.

The OAK trial is a randomized, global, multicenter, open-label Phase III study, whose main objective is to evaluate the efficacy and safety of Tecentriq (1,200 mg IV, Q3W) when compared with a historical standard of care treatment, docetaxel (75 mg/m2, Q3W) in patients with locally advanced or metastatic NSCLC previously treated with platinum-containing chemotherapies. The data from OAK presented Sunday at the 2016 ESMO congress are the first Phase III results for a PD-L1 directed antibody. The trial enrolled 1,225 patients with any PD-L1 status with locally advanced or metastatic NSCLC who had one or two prior lines of chemotherapy, including at least one platinum-based. The primary and secondary endpoints for the first 850 enrolled patients were presented. Patients were randomized to receive Tecentriq (n=425) or docetaxel (n=425). Median OS was 13.8 months versus 9.6 months, respectively (HR 0.73, p=0.0003). In addition, the median OS of patients with ≥1% PD-L1 expression in immune cells (IC) or tumor cells (TC) (55%  of enrolled patients) was 15.7 months with Tecentriq versus 10.3 months with docetaxel (HR 0.74, p=0.0102). Comparable clinical significance was found in patients with IC or TC, PD-L1 expression <1%, with a median OS of 12.6 months versus 8.9 months, respectively (HR 0.75, p=0.0205). Importantly, patients with ≥ 50% TC or ≥ 10% IC PD-L1 expression (16% of enrolled patients) treated with Tecentriq had an outstanding median OS of 20.5 months compared with 8.9 months in the docetaxel treatment arm (HR: 0.41, p<0.0001). An OS benefit with Tecentriq was observed regardless of histology, although the magnitude of benefit was more pronounced in patients with non-squamous histology (15.6 versus 11.2 months; HR 0.73, p=0.0015) than in patients with squamous histology (8.9 versus 7.7 months; HR 0.77, p=0.0383). Tecentriq had a significant OS benefit across all subgroups regardless of age, PD-L1 status and smoking status, with the exception of patients harboring active EGFR mutations, who showed no benefit with Tecentriq.

Secondary endpoint results were mixed, with Tecentriq-treated patients attaining a progression-free survival (PFS) per RECIST v1.1 numerically lower than the docetaxel arm (2.8 months versus 4.0 months; HR 0.95, p=0.4928). PFS benefit increased with higher PD-L1 expression, with TC3 or IC3 subgroups presenting a median PFS of 4.2 months in Tecentriq-treated patients compared with 3.3 months in the docetaxel group. Similarly, the ORR for Tecentriq was higher in high PD-L1 expressers, with an ORR of 31% compared with 11% of patients treated with docetaxel.

In summary, the OAK study presented the first Phase III data for a PD-L1 directed antibody in lung cancer. Tecentriq will be a new option for second-line NSCLC treatment, with an adverse event (AE) profile that appears to be similar to that of other immune-checkpoint inhibitors. This is a competitive space, with Opdivo currently dominating the second-line market5 and Keytruda also approved. How will Tecentriq be welcomed given that it is coming to market one year behind its biggest rivals?

A more important question may be what role immune checkpoint inhibitors will play in second-line given the positive results of the KEYNOTE-024 trial for Keytruda in first-line PD-L1 strongly positive patients. Given those data, up to one-third of NSCLC patients (those with PD-L1 tumor proportion score of ≥ 50%) may soon receive Keytruda in the first-line setting; given the lack of data to support multiple lines of immune checkpoint inhibition, it seems likely that any patient receiving first-line Keytruda would not be considered for checkpoint inhibitor therapy in second-line, shrinking the available market considerably. Although Opdivo has a broad label in second-line, irrespective of PD-L1 expression, its negative data in the first-line CheckMate 026 trial could have a trickle-down effect on its role in second-line patients who did not receive Keytruda in first-line; this is where Tecentriq will compete with both Opdivo and Keytruda.

Overall, immuno-oncology continues to generate significant enthusiasm, with several overflow rooms set up for the large number of people who attended Sunday’s Presidential Symposium. The entrance of Tecentriq will expand the competitive set in second-line, while other presentations during this ESMO session look to the future as these immuno-oncology agents move into earlier treatment settings. And this is only the tip of the iceberg, as multiple other checkpoint inhibitors are being studied in various treatment settings in NSCLC. OAK has borne fruit, but there’s still a whole forest that remains yet to bloom.


  1. Besse B, Johnson M, Janne PA, et al.; “Phase II, single-arm trial (BIRCH) of atezolizumab as first-line or subsequent therapy for locally advanced or metastatic PD-L1-selected non-small cell lung cancer (NSCLC);” Eur J Canc, 51(s3): Abstract 16LBA, 2015.
  2. Vansteenkiste J, Fehrenbacher L, Spira AI, Mazieres J, Park K, et al., “Atezolizumab monotherapy vs docetaxel in 2L/3L non-small cell lung cancer: Primary analyses for efficacy, safety and predictive biomarkers from a randomized phase II study (POPLAR),” European Journal of Cancer, 51 (3): S716-S717, 2015.
  3. Barlesi F, “Primary analysis from OAK, a randomized phase III study comparing atezolizumab with docetaxel in 2L/3L NSCLC,” ESMO Congress, Abstract LBA44_PR, Presidential Symposium 2, 2016.
  4. Califano R, Kerr K, Morgan RD, Lo Russo G, Garassino M, Morgillo F, Rossi A., “Immune Checkpoint Blockade: A New Era for Non-Small Cell Lung Cancer.” Current Oncology Reports, 18 (9), 2016.
  5. Kantar Health, CancerMPact® Treatment Architecture U.S. NSCLC, accessed October 9, 2016 from
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