Paul B Chapman

Memorial Sloan-Kettering Cancer Center, New York City, New York, United States

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Publications (144)1527.65 Total impact

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    ABSTRACT: To the Editor: Both ipilimumab(1) (anti-cytotoxic T-lymphocyte-associated antigen 4 monoclonal antibody) and nivolumab(2) (anti-programmed death 1 monoclonal antibody) have been approved by the Food and Drug Administration for the treatment of metastatic melanoma on the basis of increased progression-free and overall survival. A phase 1 trial of a combination of ipilimumab and nivolumab showed that 53% of patients had at least 80% tumor shrinkage.(3) We currently have treated 13 patients with melanoma with this combination as part of an expanded-access program ( number, NCT02186249), and we have observed a remarkable tumor response in 1 patient. The patient is a 49-year-old . . .
    New England Journal of Medicine 04/2015; DOI:10.1056/NEJMc1501894 · 54.42 Impact Factor
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    ABSTRACT: Purpose: Although durable responses can be achieved with tyrosine kinase inhibitors such as imatinib in melanomas harboring KIT mutations, the efficacy of alternative inhibitors after progression to imatinib and the activity of these agents on brain metastases is unknown. Experimental Design: We conducted a phase II study of nilotinib 400 mg BID in two cohorts of patients with melanomas harboring KIT mutations or amplification: A) those refractory or intolerant to a prior KIT inhibitor; and B) those with brain metastases. The primary endpoint was 4-month disease control rate. Secondary endpoints included response rate, time-to-progression and overall survival. A Simon two-stage and a single-stage design was planned to assess for the primary endpoint in Cohorts A and B, respectively. Results: Twenty patients were enrolled and 19 treated (11-Cohort A; 8-Cohort B). Three patients on Cohort A (27%; 95% CI, 8% - 56%) and 1 on Cohort B (12.5%; 90% CI, 0.6% - 47%) achieved the primary endpoint. Two partial responses were observed in Cohort A (18.2%, 90% CI, 3% - 47%); none were observed in Cohort B. The median time-to-progression and overall survival was 3·3 (90% CI, 2.1 - 3.9 months) and 9.1 months (90% CI, 4.3 - 14.2 months), respectively, in all treated patients. Conclusion: Nilotinib may achieve disease control in patients with melanoma harboring KIT alterations and whose disease progressed after imatinib therapy. The efficacy of this agent in KIT altered melanoma with brain metastasis is limited. Copyright © 2015, American Association for Cancer Research.
    Clinical Cancer Research 02/2015; DOI:10.1158/1078-0432.CCR-14-1630 · 8.19 Impact Factor
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    ABSTRACT: A central mechanism of tumour progression and metastasis involves the generation of an immunosuppressive 'macroenvironment' mediated in part through tumour-secreted factors. Here we demonstrate that upregulation of the Inhibitor of Differentiation 1 (Id1), in response to tumour-derived factors, such as TGFβ, is responsible for the switch from dendritic cell (DC) differentiation to myeloid-derived suppressor cell expansion during tumour progression. Genetic inactivation of Id1 largely corrects the myeloid imbalance, whereas Id1 overexpression in the absence of tumour-derived factors re-creates it. Id1 overexpression leads to systemic immunosuppression by downregulation of key molecules involved in DC differentiation and suppression of CD8 T-cell proliferation, thus promoting primary tumour growth and metastatic progression. Furthermore, advanced melanoma patients have increased plasma TGFβ levels and express higher levels of ID1 in myeloid peripheral blood cells. This study reveals a critical role for Id1 in suppressing the anti-tumour immune response during tumour progression and metastasis.
    Nature Communications 01/2015; 6:6840. DOI:10.1038/ncomms7840 · 10.74 Impact Factor
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    ABSTRACT: BACKGROUND The use of BRAF inhibitors may lead to the development of cutaneous toxicities such as rashes, photosensitivity, alopecia, palmoplantar erythrodysesthesia, and proliferative skin lesions, including keratoacanthomas (KAs) and cutaneous squamous cell carcinomas (cuSCCs). The latter are noteworthy for their potential to exhibit malignant features, and they may necessitate invasive treatment. Their prompt identification is of primary importance for directing supportive care efforts and maintaining dose intensity while minimizing the morbidity associated with supportive care interventions. Because such lesions are less familiar to oncologists, this study was designed to characterize their clinico-morphological features, which have not been hitherto described.METHODS The clinical and dermoscopic characteristics and risk factors of new-onset proliferative skin lesions (benign verrucous lesions and KAs/cuSCCs) developing after the initiation of treatment with vemurafenib, dabrafenib, and XL281 were analyzed; the histopathological diagnoses were ascertained.RESULTSThe majority of the lesions were benign verrucous lesions (78%, n = 87), whereas KAs/cuSCCs represented 22% (n = 25). The median times to biopsy for the initial verrucous lesions and KAs/cuSCCs were 4.8 and 10.5 weeks, respectively. The clinico-morphological features significant for KAs/cuSCCs included a larger size (P < .001), a nodular appearance (P < .001), a central keratin plug (P < .001), a central ulceration or crust (P = .04), an adherent scale (P = .02), an erythematous halo (P = .03), and a scaly ring (collarette; P < .001) at the periphery.CONCLUSIONS Our findings represent the first detailed description of the clinico-morphological characteristics that permit distinction between the benign and malignant skin lesions induced by BRAF inhibitors. They are valuable for the recognition of lesions that require intervention and/or a dermatology referral versus those that permit provisional monitoring. Cancer 2014. © 2014 American Cancer Society.
    Cancer 01/2015; 121(1). DOI:10.1002/cncr.28980 · 4.90 Impact Factor
  • Paul B Chapman, David B Solit, Neal Rosen
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    ABSTRACT: In BRAF V600E melanoma patients, RAF inhibitor treatment causes a MEK-inhibitor-sensitive, RAF-inhibitor-resistant adaptive reactivation of ERK signaling. In clinical trials combining MEK and RAF inhibitors, therapeutic efficacy was modestly enhanced, suggesting the utility of inhibiting feedback-reactivated pathways. Strategies for optimally inhibiting ERK signaling should be explored. Copyright © 2014 Elsevier Inc. All rights reserved.
  • Journal der Deutschen Dermatologischen Gesellschaft 08/2014; 12(8). DOI:10.1111/ddg.12327_suppl · 1.40 Impact Factor
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    ABSTRACT: Immunomodulatory antibodies that enhance the immune system to fight cancer are revolutionizing the treatment of patients with an expanding variety of malignancies. There is a unique spectrum of side effects associated with immunomodulatory antibodies, termed immune-related adverse events (irAEs), which include colitis and hepatitis among others. The treatment of refractory or severe irAEs can occasionally require significant immunosuppression, involving steroids or tumor necrosis factor-alpha antagonists, placing these patients at risk for infections. We present the first reported case to our knowledge of an opportunistic infection in a patient treated with an immunomodulatory antibody. As the use of immunomodulatory antibodies expands and more patients develop irAEs that require treatment with immunosuppression, recognition of the potential for opportunistic infections in this emerging patient population will be critical. Prospective trials are needed to define the optimal immunosuppressive management of irAEs and determine whether prophylactic antiviral, antibacterial, or antifungal therapies are beneficial in this unique population.
    06/2014; 2:19. DOI:10.1186/2051-1426-2-19
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    ABSTRACT: Uveal melanoma is characterized by mutations in GNAQ and GNA11, resulting in mitogen-activated protein kinase pathway activation.
    JAMA The Journal of the American Medical Association 06/2014; 311(23):2397-405. DOI:10.1001/jama.2014.6096 · 30.39 Impact Factor
  • Journal der Deutschen Dermatologischen Gesellschaft 06/2014; 12(8). DOI:10.1111/ddg.12327 · 1.40 Impact Factor
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    ABSTRACT: Vemurafenib, a RAF inhibitor, extends survival in patients with BRAFV600-mutant melanoma but activates ERK signaling in RAS-mutant cells. In a patient with a BRAFV600K-mutant melanoma responding to vemurafenib, we observed accelerated progression of a previously unrecognized NRAS-mutant leukemia. We hypothesized that combining vemurafenib with a MEK inhibitor would inhibit ERK activation in the melanoma and prevent ERK activation by vemurafenib in the leukemia and thus suppress both malignancies. We demonstrate that intermittent administration of vemurafenib led to a near-complete remission of the melanoma and the addition of the MEK inhibitor cobimetinib (GDC-0973) caused suppression of vemurafenib-induced leukemic proliferation and ERK activation. Anti-melanoma and anti-leukemia response have been maintained for nearly 20 months as documented by serial measurements of tumor-derived DNA in plasma in addition to conventional radiographic and clinical assessments of response. These data support testing of intermittent ERK pathway inhibition in the therapy of both RAS-mutant leukemia and BRAF-mutant melanoma.
    Cancer Discovery 03/2014; 4(5). DOI:10.1158/2159-8290.CD-13-1038 · 15.93 Impact Factor
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    ABSTRACT: Melanoma is a disease characterized by lesions that activate ERK. Though 70% of cutaneous melanomas harbor activating mutations in the BRAF and NRAS genes, the alterations that drive tumor progression in the remaining 30% are largely undefined. Vemurafenib, a selective inhibitor of RAF kinases, has clinical utility restricted to BRAF mutant tumors. MEK inhibitors, which have shown clinical activity in NRAS-mutant melanoma, may be effective in other ERK pathway-dependent settings. Here, we investigated a panel of melanoma cell lines wild-type for BRAF and NRAS to determine the genetic alteration driving their transformation and their dependence on ERK signaling in order to elucidate a candidate set for MEK inhibitor treatment. A cohort of the BRAF/RAS wild-type cell lines with high levels of RAS-GTP had loss of NF1, a RAS GTPase activating protein. In these cell lines, the MEK inhibitor PD0325901 inhibited ERK phosphorylation, but also relieved feedback inhibition of RAS resulting in induction of pMEK and a rapid rebound in ERK signaling. In contrast, the MEK inhibitor trametinib impaired the adaptive response of cells to ERK inhibition leading to sustained suppression of ERK signaling and significant antitumor effects. Notably, alterations in NF1 frequently co-occurred with RAS and BRAF alterations in melanoma. In the setting of BRAF(V600E), NF1 loss abrogated negative feedback on RAS activation resulting in elevated activation of RAS-GTP and resistance to RAF, but not MEK, inhibitors. We conclude that loss of NF1 is common in cutaneous melanoma and is associated with RAS activation, MEK-dependence and resistance to RAF inhibition.
    Cancer Research 02/2014; 74(8). DOI:10.1158/0008-5472.CAN-13-2625 · 9.28 Impact Factor
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    ABSTRACT: In the BRIM-3 trial, vemurafenib was associated with risk reduction versus dacarbazine of both death and progression in patients with advanced BRAF(V600) mutation-positive melanoma. We present an extended follow-up analysis of the total population and in the BRAF(V600E) and BRAF(V600K) mutation subgroups. Patients older than 18 years, with treatment-naive metastatic melanoma and whose tumour tissue was positive for BRAF(V600) mutations were eligible. Patients also had to have a life expectancy of at least 3 months, an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1, and adequate haematological, hepatic, and renal function. Patients were randomly assigned by interactive voice recognition system to receive either vemurafenib (960 mg orally twice daily) or dacarbazine (1000 mg/m(2) of body surface area intravenously every 3 weeks). Coprimary endpoints were overall survival and progression-free survival, analysed in the intention-to-treat population (n=675), with data censored at crossover. A sensitivity analysis was done. This trial is registered with, NCT01006980. 675 eligible patients were enrolled from 104 centres in 12 countries between Jan 4, 2010, and Dec 16, 2010. 337 patients were randomly assigned to receive vemurafenib and 338 to receive dacarbazine. Median follow-up was 12·5 months (IQR 7·7-16·0) on vemurafenib and 9·5 months (3·1-14·7) on dacarbazine. 83 (25%) of the 338 patients initially randomly assigned to dacarbazine crossed over from dacarbazine to vemurafenib. Median overall survival was significantly longer in the vemurafenib group than in the dacarbazine group (13·6 months [95% CI 12·0-15·2] vs 9·7 months [7·9-12·8]; hazard ratio [HR] 0·70 [95% CI 0·57-0·87]; p=0·0008), as was median progression-free survival (6·9 months [95% CI 6·1-7·0] vs 1·6 months [1·6-2·1]; HR 0·38 [95% CI 0·32-0·46]; p<0·0001). For the 598 (91%) patients with BRAF(V600E) disease, median overall survival in the vemurafenib group was 13·3 months (95% CI 11·9-14·9) compared with 10·0 months (8·0-14·0) in the dacarbazine group (HR 0·75 [95% CI 0·60-0·93]; p=0·0085); median progression-free survival was 6·9 months (95% CI 6·2-7·0) and 1·6 months (1·6-2·1), respectively (HR 0·39 [95% CI 0·33-0·47]; p<0·0001). For the 57 (9%) patients with BRAF(V600K) disease, median overall survival in the vemurafenib group was 14·5 months (95% CI 11·2-not estimable) compared with 7·6 months (6·1-16·6) in the dacarbazine group (HR 0·43 [95% CI 0·21-0·90]; p=0·024); median progression-free survival was 5·9 months (95% CI 4·4-9·0) and 1·7 months (1·4-2·9), respectively (HR 0·30 [95% CI 0·16-0·56]; p<0·0001). The most frequent grade 3-4 events were cutaneous squamous-cell carcinoma (65 [19%] of 337 patients) and keratoacanthomas (34 [10%]), rash (30 [9%]), and abnormal liver function tests (38 [11%]) in the vemurafenib group and neutropenia (26 [9%] of 287 patients) in the dacarbazine group. Eight (2%) patients in the vemurafenib group and seven (2%) in the dacarbazine group had grade 5 events. Inhibition of BRAF with vemurafenib improves survival in patients with the most common BRAF(V600E) mutation and in patients with the less common BRAF(V600K) mutation. F Hoffmann-La Roche-Genentech.
    The Lancet Oncology 02/2014; DOI:10.1016/S1470-2045(14)70012-9 · 24.73 Impact Factor
  • Molecular Cancer Therapeutics 01/2014; 12(11_Supplement):C138-C138. DOI:10.1158/1535-7163.TARG-13-C138 · 6.11 Impact Factor
  • Journal of Clinical Oncology 01/2014; 32(14). DOI:10.1200/JCO.2013.49.3528 · 17.88 Impact Factor
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    ABSTRACT: This open-label, multicenter study was designed to allow access to vemurafenib for patients with metastatic melanoma, bridging the time between end of enrollment in the phase III registration trial (December 2010) and commercial availability following US Food and Drug Administration approval of vemurafenib for the treatment of unresectable or metastatic BRAF-mutated melanoma (August 2011). Eligible patients had metastatic melanoma with a BRAF mutation (detected by the cobas 4800 BRAF V600 Mutation Test). Unlike previous vemurafenib trials, patients with poor performance status (PS) and treated brain metastases were permitted. Enrolled patients received oral vemurafenib 960 mg twice daily. Of 374 patients enrolled at 29 US sites (December 2010 to October 2011), 371 patients received vemurafenib and were followed up for a median of 2.8 months (the study had a prespecified end upon vemurafenib approval and commercial availability). At baseline, most patients (75%) had stage M1c disease, and 19% had an Eastern Cooperative Oncology Group PS of 2 or 3; 72% of patients had received prior systemic therapy for metastatic melanoma, 27% received prior ipilimumab, and 29% radiotherapy for prior brain metastases. Because reassessment data to confirm response were not available for most patients, point estimates of objective response rate (ORR) are reported. Among 241 efficacy-evaluable patients, the ORR was 54% (median time to response, 1.9 months). The ORR in non-central nervous system sites in patients with previously treated brain metastases (n = 68) was 53%. The ORR in prior ipilimumab-treated patients (n = 68) was 52%. For patients with PS of 0 or 1 (n = 210) and 2 or 3 (n = 31), the ORRs were 55%, and 42%, respectively. The safety profile observed was consistent with that reported in previous studies. The number of patients with grade 3 or 4 treatment-related adverse events was higher in patients with PS 2 or 3 than in those with PS 0 or 1 (10% vs. 5%, respectively). Adverse events requiring a dose reduction (at least 1 level) occurred in 11% of patients, and 9 patients (2%) experienced events leading to vemurafenib withdrawal, including 2 with repeated QT interval prolongation. This study confirmed the established rapid and high tumor response rate achievable with vemurafenib in BRAF mutation-positive metastatic melanoma. Several groups not included in previous studies, including patients with previously treated brain metastases, Eastern Cooperative Oncology Group PS 2 to 3, or previous ipilimumab treatment had benefitted from vemurafenib similar to the overall population. No new safety signals were detected.
    The Cancer Journal 01/2014; 20(1):18-24. DOI:10.1097/PPO.0000000000000024 · 3.61 Impact Factor
  • Paul B Chapman
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    ABSTRACT: In recent years the expectation related to treating patients with metastatic melanoma has changed. Three years ago, a diagnosis of metastatic melanoma was bleak; only a small number of patients would benefit from standard treatment and the reason for treatment benefit was often unknown, leaving physicians with limited options to help their patients. Today, just 3 years later, there are proven therapies that allow physicians to expect to shrink tumors and extend the lives of their patients after diagnosis. In this article, Paul B. Chapman, MD, Memorial Sloan Kettering Cancer Center, summarizes the recent advances in the field of metastatic melanoma and looks ahead to topics such as focusing on specificity, shutting down the ERK pathway, intermittent dosing, discovering driver mutations, individualizing checkpoint inhibition, and identifying rejection antigens to identify what should occur next in order to continue to improve outcomes for a larger population of patients with metastatic melanoma. Dr. Chapman's paper reminds us of the exciting progress that has been made while focusing on the work that is left in the field. Dr. Chapman is a physician-scientist who specializes in diagnosing and treating melanoma that has metastasized to other parts of the body. Dr. Chapman led a clinical trial that paved the way, in part, to the approval of vemurafenib-a drug that targets a BRAF mutation that is present in approximately 50% of patients with metastatic melanoma. Dr. Chapman is one of five Memorial Sloan Kettering scientists to be appointed to a melanoma "Dream Team" that focuses on identifying potential therapies for metastatic melanoma patients who do not have the mutated form of the BRAF gene. Dr. Chapman is also a professor of medicine at the Weill Cornell Medical College and is the chair of the Melanoma Research Alliance Medical Advisory Board. In addition to the above, Dr. Chapman is a sought-after mentor for medical oncology fellows and has a current research interest in identifying novel means to more durably block signaling in the MAPK pathway in melanoma cells. Jedd Wolchok, MD, PhD, Scientific Program Committee Chair.
    01/2014; 34:16-9. DOI:10.14694/EdBook_AM.2014.34.16
  • Paul B Chapman, Axel Hauschild, Vernon K Sondak
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    ABSTRACT: An estimated 76,100 patients will be diagnosed with invasive melanoma in the United States in 2014, and 9,710 patients will die from the disease. In almost all cases, the cause of death is related to the development of widespread metastatic disease. Although death rates from most types of cancer have steadily decreased in the United States -a 20% decrease during two decades from a peak of 215.1 deaths per 100,000 population in 1991 to 171.8 in 2010 -death rates from melanoma have steadily increased during the same time, especially among males. The news regarding melanoma is far from all bad. Increases in our understanding of the human immune system have led to the development of new immunotherapeutic drugs such as ipilimumab, which has been shown to improve survival in phase III trials in metastatic melanoma, and anti-programmed death 1 (anti-PD1) antibodies, recently hailed by ASCO as one of the past year's most noteworthy clinical cancer advances. However, no discovery has influenced and, indeed, transformed the management of metastatic melanoma more than the identifıcation of activating mutations in the BRAF gene in the mitogen-activated protein kinase (MAPK) pathway, which occur in about half of cutaneous melanomas and can be targeted with small molecule inhibitors of the BRAF protein, the downstream MEK protein, or both. This article will address how patients with metastatic melanoma are evaluated for their mutation status and how the presence of a targetable mutation influences therapeutic decisions regarding systemic therapy and even surgery.
    01/2014; 34:e412-21. DOI:10.14694/EdBook_AM.2014.34.e412
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    ABSTRACT: Prior studies show that intramuscular injection and particle-mediated epidermal delivery of xenogeneic melanosomal antigens (tyrosinase or Tyr, gp100) induce CD8(+) T cell responses to the syngeneic protein. To further define the optimal vaccination strategy, we conducted a phase I study of in vivo electroporation (EP) of a murine Tyr DNA vaccine (pINGmuTyr) in malignant melanoma patients. Human leukocyte antigen (HLA)-A1, A2, A24 or B35 stage IIb-IV melanoma patients received up to five doses of the mouse tyrosinase DNA vaccine by EP every three weeks at dose levels of 0.2 mg, 0.5 mg, or 1.5 mg per injection. Peripheral blood mononuclear cells (PBMC) were collected, cultured with a peptide pool containing eight HLA class I-restricted Tyr-specific T-cell epitopes, and analyzed by HLA-A*0101-restricted tetramers and intracellular cytokine staining (ICS). Twenty-four patients received ≥1 dose of the pINGmuTyr vaccine; PBMCs from 21 patients who completed all five doses were available for Tyr immune assays. The only common toxicity was grade 1 injection site reaction. Six of 15 patients (40%) in the 1.5 mg dose cohort developed Tyr-reactive CD8(+) T cell responses following stimulation, defined as a ≥3 standard deviation increase in baseline reactivity by tetramer or ICS assays. No Tyr-reactive CD8(+) T cell response was detected in the 0.2 mg and 0.5 mg dose cohort patients. Epitope spreading of CD8(+) T cell response to NY-ESO-1 was observed in one patient with vitiligo. One patient subsequently received ipilimumab and developed an enhanced Tyr-reactive response with polyfunctional cytokine profile. After a median follow-up of 40.9 months, median survival has not been reached. A regimen of five immunizations with pINGmuTyr administered by EP was found to be safe and resulted in Tyr-reactive immune responses in six of 15 patients at 1.5 mg dose cohort. NCT00471133.
    11/2013; 1:20. DOI:10.1186/2051-1426-1-20
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    ABSTRACT: Uveal melanoma exhibits a high incidence of metastases; and, to date, there is no systemic therapy that clearly improves outcomes. The anticytotoxic T-lymphocyte-associated protein 4 (anti-CTLA-4) antibody ipilimumab is a standard of care for metastatic melanoma; however, the clinical activity of CTLA-4 inhibition in patients with metastatic uveal melanoma is poorly defined. To assess ipilimumab in this setting, the authors performed a multicenter, retrospective analysis of 4 hospitals in the United States and Europe. Clinical characteristics, toxicities, and radiographic disease burden, as determined by central, blinded radiology review, were evaluated. Thirty-nine patients with uveal melanoma were identified, including 34 patients who received 3 mg/kg ipilimumab and 5 who received 10 mg/kg ipilimumab. Immune-related response criteria and modified World Health Organization criteria were used to assess the response rate (RR) and the combined response plus stable disease (SD) rate after 12 weeks, after 23 weeks, and overall (median follow-up, 50.4 weeks [12.6 months]). At week 12, the RR was 2.6%, and the response plus SD rate was 46.%; at week 23, the RR was 2.6%, and the response plus SD rate was 28.2%. There was 1 complete response and 1 late partial response (at 100 weeks after initial SD) for an immune-related RR of 5.1%. Immune-related adverse events were observed in 28 patients (71.8%) and included 7 (17.9%) grade 3 and 4 events. Immune-related adverse events were more frequent in patients who received 10 mg/kg ipilimumab than in those who received 3 mg/kg ipilimumab. The median overall survival from the first dose of ipilimumab was 9.6 months (95% confidence interval, 6.3-13.4 months; range, 1.6-41.6 months). Performance status, lactate dehydrogenase level, and an absolute lymphocyte count ≥1000 cells/μL at week 7 were associated significantly with survival. In this multicenter, retrospective analysis of 4 hospitals in the United States and Europe of patients with uveal melanoma, durable responses to ipilimumab and manageable toxicity were observed. Cancer 2013. © 2013 American Cancer Society.
    Cancer 08/2013; DOI:10.1002/cncr.28282 · 4.90 Impact Factor
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    ABSTRACT: Measures of prognosis are typically estimated from the time of diagnosis. However, these estimates become less relevant as the time from diagnosis increases for a patient. Conditional survival measures the probability that a cancer patient will survive some additional number of years, given that the patient has already survived for a certain number of years. In the current study, the authors analyzed data regarding patients with stage III melanoma to demonstrate that survival estimates from the time of diagnosis underestimate long-term survival as the patient is followed over time. The probability of surviving to year 5 for patients at the time of presentation compared with patients who had already survived for 4 years increased from 72% to 95%, 48% to 90%, and 29% to 86%, respectively, for patients with substage IIIA, IIIB, and IIIC disease. Considering the major role played by survival estimates during follow-up in patient counseling and the development of survivorship programs, the authors strongly recommend the routine use of conditional survival estimates. Cancer 2013. © 2013 American Cancer Society.
    Cancer 07/2013; 119(20). DOI:10.1002/cncr.28273 · 4.90 Impact Factor

Publication Stats

10k Citations
1,527.65 Total Impact Points


  • 1988–2015
    • Memorial Sloan-Kettering Cancer Center
      • Department of Medicine
      New York City, New York, United States
  • 2014
    • Weill Cornell Medical College
      New York, New York, United States
  • 1993–2014
    • Cornell University
      • Department of Medicine
      Итак, New York, United States
  • 2011
    • International Prevention Research Institute
      Lyons, Rhône-Alpes, France
  • 2010
    • Yale University
      New Haven, Connecticut, United States