Fred Millard
· M.D.University of California, San Diego · Hematology and Medical Oncology
Active 1998–2025
About
Frederick Millard is a Clinical Professor of Medicine at UC San Diego School of Medicine, located at 9500 Gilman Drive, La Jolla, CA. Since 2002, he has collaborated with the UC San Diego Division of Urology to establish the first dedicated genitourinary malignancies clinic in San Diego County, focusing on the care of patients with prostate, testicular, kidney, bladder cancers, and other urinary tract cancers. His work involves a multidisciplinary team including surgeons, medical oncologists, radiation oncologists, nurses, basic scientists, clinical research associates, and other personnel, with a biweekly tumor board and a menu of clinical trials investigating new treatment approaches. His research includes studies on cellular immunotherapy, immune checkpoint inhibitors, targeted therapies, and collaborations on defining the natural history and treatment of brain metastases in germ cell tumor patients. Dr. Millard's educational background includes an MD from Thomas Jefferson University Hospital, a residency in Internal Medicine at Naval Medical Center San Diego, and a fellowship in Hematology/Oncology at Naval Medical Center San Diego and Scripps Clinic.
Research topics
- Biology
- History
- Genetics
- Medicine
- Classics
Selected publications
International Journal of Molecular Sciences · 2025-09-15 · 1 citations
articleOpen accessMolecular profiling of testicular germ cell tumors (TGCTs) provides critical insights into personalized treatment approaches, particularly for patients with recurrent or treatment-resistant disease. In this study, we retrospectively analyzed clinicopathological and targeted genomic sequencing data from 27 TGCT patients, including 7 seminomas, 19 non-seminomas, and 1 prepubertal type teratoma, across stage I (48%), stage II (41%), and stage III (11%). Tumor samples were obtained from 27 orchiectomies, with additional pathological specimens collected from 16 of these patients during retroperitoneal lymph node dissections (RPLNDs); these included 8 chemotherapy-naïve and 8 post-chemotherapy cases. The median tumor mutational burden (TMB) was 0.5 mutations/Mb, consistent with the low mutation rate typically observed in TGCTs. Somatic mutations and copy number gain alterations were detected in 56% (15/27) of patients, primarily in KRAS (25.9%), KIT (11.1%), and PIK3CB (7.4%). PD-L1 positive immunoreactivity by immunohistochemistry was observed in 75% of tumors (60% in stage I, 100% in stage III) analyzed (n = 8), suggesting potential immune checkpoint inhibitor applicability in advanced disease. Microsatellite instability (MSI) status was identified in 23 tumors; all were classified as MSI-low, supporting the rarity of MSI-driven tumorigenesis in TGCTs. Actionable gene alterations linked to FDA-approved therapies, interventional therapies, and clinical trials in TGCTs and other cancers (lung, skin, colon, liver, stomach, and breast) were present in 59.3% (16/27) of patients, indicating potential therapeutic repurposing. Additionally, germline variants of uncertain clinical significance in known cancer actionable genes, including MSH2, MSH6, RB1, and BRCA2, were found in 9 patients, warranting further investigation regarding their clinical relevance and susceptibility risk. Our findings highlight that a substantial proportion of TGCT patients harbor potentially actionable molecular alterations across all disease stages.
The Journal of Urology · 2023
- Medicine
- Classics
- History
You have accessJournal of UrologyCME1 Apr 2023MP33-19 MOLECULAR CHARACTERISTICS AND ACTIONABLE TARGETS OF TESTICULAR GERM CELL TUMORS IN REAL-WORLD CONDITIONS Rafael Morales-Grimany, Cesar Delgado, Fady Baky, Armon Amini, Thomas Gerald, Rohit R Badia, Jacob Taylor, Luke L Wang, Juan Javier-Desloges, Vitaly Margulis, Solomon L. Woldu, Amir Salmasi, Fred Millard, Rana R. Mckay, and Aditya Bagrodia Rafael Morales-GrimanyRafael Morales-Grimany More articles by this author , Cesar DelgadoCesar Delgado More articles by this author , Fady BakyFady Baky More articles by this author , Armon AminiArmon Amini More articles by this author , Thomas GeraldThomas Gerald More articles by this author , Rohit R BadiaRohit R Badia More articles by this author , Jacob TaylorJacob Taylor More articles by this author , Luke L WangLuke L Wang More articles by this author , Juan Javier-DeslogesJuan Javier-Desloges More articles by this author , Vitaly MargulisVitaly Margulis More articles by this author , Solomon L. WolduSolomon L. Woldu More articles by this author , Amir SalmasiAmir Salmasi More articles by this author , Fred MillardFred Millard More articles by this author , Rana R. MckayRana R. Mckay More articles by this author , and Aditya BagrodiaAditya Bagrodia More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000003266.19AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Molecular features of testicular germ cell tumors (GCT) in various clinical states (pre- vs post-chemotherapy, localized versus metastatic) may inform treatment options for patients with recurrence after definitive therapy. In his study, we describe molecular features and potential therapeutic targets in a cohort of patients with testicular GCT. METHODS: We retrospectively examined clinicopathologic and next-generation sequencing (NGS) data from 27 patients with GCT. Tumors were sequenced using the TempusxT solid tumor assay, which includes DNA sequencing of 595-648 genes at 500x coverage and RNA sequencing for all human coding genes. Tumor mutational burden (TMB) was measured for all tumors and PD-L1 levels were assessed qualitatively by 22C3 pharmDx immunohistochemistry assay in 8 patients. All genetic variants detected were quantified and analyzed to identify potentially actionable targets. RESULTS: We identified 13 (48%) stage I GCT, 11 (41%) stage II, and 3 (11%) stage III. There were 7 seminomas and 20 nonseminomas. 12 tumor specimen resections were obtained from orchiectomy, and 15 from retroperitoneal lymph node dissection (RPLND), of which, 8 were chemotherapy-naïve and 7 were post-chemotherapy. Chemo-naïve RPLND histology showed a combination of teratoma, seminoma, and mixed GCT, while post-chemo histology revealed 6 teratomas and 9 benign pathologies. The median TMB for the cohort was 0.75 mutations/megabase. Somatic mutations were identified in 55% of patients and most commonly within: KRAS (25.9%), KIT (11.1%), and PIK3CB (7.4%). PD-L1 expression was observed in 75% of the tumors measured (60% positivity at stage I and 100% positivity at stage III). Microsatellite stability was stable in 18 tumors tested. DNA alterations- [single base pair substitutions, insertions, and deletions]- in KRAS (GTPase) proto-oncogenes were detected in 7 tumors and tyrosine kinase receptor gene variants (KIT, P1K3CB) were found at similar frequencies across disease stages. Whole transcriptome NGS RNA expression assays were performed on 21 untreated specimens revealing overexpression of MTOR (33%), MAPK1(14%), and MET (8.0%). Actionable targets with FDA-approved therapies in other organ tissues were detected in 11 patients (40.7%). Incidental germline mutations, including MSH6, RB1, and MSH2, were identified in 9 patients though all were variants of unknown significance. CONCLUSIONS: In our study, a significant proportion of patients had potentially actionable molecular targets across the disease spectrum. The identified genetic alterations provide a genomic landscape for risk stratification, future therapies, and molecularly informed treatment paradigms for GCT patients. Source of Funding: Cancer Prevention and Research Institute © 2023 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 209Issue Supplement 4April 2023Page: e458 Advertisement Copyright & Permissions© 2023 by American Urological Association Education and Research, Inc.MetricsAuthor Information Rafael Morales-Grimany More articles by this author Cesar Delgado More articles by this author Fady Baky More articles by this author Armon Amini More articles by this author Thomas Gerald More articles by this author Rohit R Badia More articles by this author Jacob Taylor More articles by this author Luke L Wang More articles by this author Juan Javier-Desloges More articles by this author Vitaly Margulis More articles by this author Solomon L. Woldu More articles by this author Amir Salmasi More articles by this author Fred Millard More articles by this author Rana R. Mckay More articles by this author Aditya Bagrodia More articles by this author Expand All Advertisement PDF downloadLoading ...
UNC Libraries · 2020-11-04
articleOpen accessSenior authorWe sought to characterize the pharmacokinetics (PK) and determine a tolerable dose of oral sorafenib in patients with hepatic or renal dysfunction.
Systemic Treatment of Bone Disease in Metastatic Urinary Malignancies
European Urology Focus · 2019-06-27 · 4 citations
reviewThe Journal of Urology · 2018-04-01 · 1 citations
articleOpen accessbetween indolent and aggressive PCa can be inaccurate due to PCa heterogeneity and multi-focality. To compensate, many centres now take upwards of 20 biopsies of the prostate in one sitting, and monitor men with further biopsies to ensure that the disease is not progressing. There is therefore a need for a non-invasive biomarker than can monitor tumour heterogeneity and aggression. Circulating-tumour DNA (ctDNA) represents an exciting opportunity to monitor cancer status non-invasively. We developed a method for analysis of multiple genomic regions whilst retaining sensitivity for detection of individual mutant molecules, using multiplex replicate dilution sequencing, or MRD-Seq.
Cancer Chemotherapy and Pharmacology · 2014-04-09 · 1 citations
articleOpen accessThe Journal of Urology · 2014-03-28
articleYou have accessJournal of UrologyKidney Cancer: Advanced1 Apr 2014MP57-14 CHANGE IN PLATELET COUNT AS A PROGNOSTIC INDICATOR FOR RESPONSE TO NEOADJUVANT TYROSINE KINASE INHIBITOR THERAPY IN METASTATIC RENAL CELL CARCINOMA Hak Lee, Nishant Patel, Ryan Kopp, Michael Liss, Reza Mehrazin, Ramzi Jabaji, Song Wang, Fuad Elkoury, Jason Woo, Kerrin Palazzi, Anthony Patterson, Christopher Kane, Fred Millard, and Ithaar Derweesh Hak LeeHak Lee More articles by this author , Nishant PatelNishant Patel More articles by this author , Ryan KoppRyan Kopp More articles by this author , Michael LissMichael Liss More articles by this author , Reza MehrazinReza Mehrazin More articles by this author , Ramzi JabajiRamzi Jabaji More articles by this author , Song WangSong Wang More articles by this author , Fuad ElkouryFuad Elkoury More articles by this author , Jason WooJason Woo More articles by this author , Kerrin PalazziKerrin Palazzi More articles by this author , Anthony PattersonAnthony Patterson More articles by this author , Christopher KaneChristopher Kane More articles by this author , Fred MillardFred Millard More articles by this author , and Ithaar DerweeshIthaar Derweesh More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.02.1789AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail Introduction and Objectives Biomarkers may be useful as prognostic indicators prior to and during systemic therapy. We evaluated change in platelet count (ΔPlt) as a biomarker for response to neoadjuvant tyrosine kinase inhibitor (TKI) therapy for metastatic renal cell carcinoma (mRCC). Methods Multi-center retrospective study of mRCC patients undergoing neoadjvant TKI therapy from 5/2005-8/2013. ΔPlt was defined as post-treatment Plt after first cycle minus pre-treatment Plt. Primary outcome was response of disease to TKI defined by RECIST criteria for partial response (PR), stable disease (SD), and progressive disease (PD). Demographic and clinical characteristics were analyzed between subgroups with stable/increased (+ΔPlt) and decreased (-ΔPlt) counts. Cox proportional hazards model evaluated factors associated with changes in tumor response. Kaplan-Meier analysis estimated overall survival (OS) and compared Plt groups with log-rank test. Sensitivity, specificity, negative predictive value (NPV), and positive predictive value (PPV) were calculated for ΔPlt and disease response PR/SD. Results A total of 69 patients treated with neoadjuvant TKI therapy were analyzed for ΔPlt. Overall, 15 patients (22%) were noted to have +ΔPlt and 54 (78%) had –ΔPlt after neoadjuvant TKI therapy. There were no other differences in clinical or demographic variables between these two groups (comorbidities, ECOG, tumor size, number of metastases, stage, grade and number of TKI cycles). Patients with +ΔPlt count had a lower post TKI treatment creatinine (1.0 vs. 1.3, p=0.041). PD was more common among +ΔPlt 86.7% vs. –ΔPlt 33.3%, (p=0.001), and SD/PR was more common in –ΔPlt 66.7% vs. +ΔPlt 13.3%, (p=0.001). On MVA, -ΔPlt below baseline was a significant predictor of SD/PR (OR 6.96, p=0.028). A Kaplan Meier analysis (Figure) demonstrated a higher overall survival in -ΔPlt versus +ΔPlt (p=0.009), with median survival 13.8 of and 5.7 months respectively. -ΔPlt had sensitivity of 94.7%, specificity of 41.9%, PPV of 66.7% and NPV of 86.7% for PR/SD after neoadjuvant TKI therapy. Conclusions Patients with -ΔPlt were more likely to respond to TKI therapy and had longer median overall survival. Further investigation is requisite to determine the utility of ΔPlt as a biomarker for RCC response to TKI. © 2014FiguresReferencesRelatedDetails Volume 191Issue 4SApril 2014Page: e647 Advertisement Copyright & Permissions© 2014MetricsAuthor Information Hak Lee More articles by this author Nishant Patel More articles by this author Ryan Kopp More articles by this author Michael Liss More articles by this author Reza Mehrazin More articles by this author Ramzi Jabaji More articles by this author Song Wang More articles by this author Fuad Elkoury More articles by this author Jason Woo More articles by this author Kerrin Palazzi More articles by this author Anthony Patterson More articles by this author Christopher Kane More articles by this author Fred Millard More articles by this author Ithaar Derweesh More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...
366 BIOPSY-DETECTED GLEASON PATTERN 5 PREDICTS RECURRENCE IN MEN WITH HIGH-RISK PROSTATE CANCER
The Journal of Urology · 2013-03-27
articleYou have accessJournal of UrologyProstate Cancer: Staging (II)1 Apr 2013366 BIOPSY-DETECTED GLEASON PATTERN 5 PREDICTS RECURRENCE IN MEN WITH HIGH-RISK PROSTATE CANCER Sean Stroup, Daniel Moreira, Leah Gerber, Stephen Freedland, Fred Millard, Martha Terris, William Aronson, Joseph Presti, Christopher Amling, and Christopher Kane Sean StroupSean Stroup San Diego, CA More articles by this author , Daniel MoreiraDaniel Moreira New Hyde Park, NY More articles by this author , Leah GerberLeah Gerber Durham, NC More articles by this author , Stephen FreedlandStephen Freedland Durham, NC More articles by this author , Fred MillardFred Millard La Jolla, CA More articles by this author , Martha TerrisMartha Terris Augusta, GA More articles by this author , William AronsonWilliam Aronson Los Angeles, CA More articles by this author , Joseph PrestiJoseph Presti Palo Alto, CA More articles by this author , Christopher AmlingChristopher Amling Portland, OR More articles by this author , and Christopher KaneChristopher Kane La Jolla, CA More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.1754AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES We sought to evaluate the relative risk of biochemical recurrence, bone metastases, and risk of death from prostate cancer contributed by biopsy Gleason pattern 5 among high-risk men with Gleason 8-10 disease in the Shared Equal Access Regional Cancer Hospital (SEARCH) cohort. METHODS Men with biopsy Gleason sum 8-10 prostate cancer treated with radical prostatectomy were evaluated. The cohort was divided: Gleason 4+4, and those with any pattern 5 (i.e., Gleason 4+5, 5+3, 5+4, and 5+5; men with Gleason 3+5 were not included). Biochemical recurrence was defined as PSA >0.2ng/mL, 2 values at 0.2ng/mL, or secondary treatment for an elevated PSA. Predictors of PSA recurrence, development of bone metastases, prostate cancer-specific survival, and overall survival were analyzed using Kaplan-Meier, log-rank test and Cox proportional hazards model. RESULTS Of 3499 men in the SEARCH database, 255 (7%) met criteria for inclusion. Of these, 99 (39%) had Gleason 4+4, and 156 (61%) had Gleason pattern 5 on biopsy. On univariable analysis, relative to Gleason 4+4, men with any Gleason pattern 5 had a higher rate of biochemical recurrence (P<0.001), development of bone metastases (P<0.001), prostate cancer-specific mortality (P=0.009), and a trend towards worse overall survival (P=0.083, Figure). On multivariable analysis, men with Gleason pattern 5 had a higher rate of biochemical recurrence (HR=1.75; 95%CI=1.17-2.59; P=0.006) and development of bone metastases (HR=4.64; 95%CI=1.48–14.60; P=0.009), and similar cancer-specific (HR=2.11; 95%CI=0.59–7.53; P=0.247) and overall survival (HR=1.51; 95%CI=0.88–2.60; P=0.134). CONCLUSIONS Subclassification of high risk prostate cancer by biopsy Gleason grading (4+4 vs. presence of any Gleason pattern 5) can identify men at highest risk of prostate cancer progression and mortality. Presence of any Gleason pattern 5 cancer on biopsy portends a poor prognosis and negatively impacts survival. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e148 Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information Sean Stroup San Diego, CA More articles by this author Daniel Moreira New Hyde Park, NY More articles by this author Leah Gerber Durham, NC More articles by this author Stephen Freedland Durham, NC More articles by this author Fred Millard La Jolla, CA More articles by this author Martha Terris Augusta, GA More articles by this author William Aronson Los Angeles, CA More articles by this author Joseph Presti Palo Alto, CA More articles by this author Christopher Amling Portland, OR More articles by this author Christopher Kane La Jolla, CA More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...
The Journal of Urology · 2013-03-27
articleYou have accessJournal of UrologyProstate Cancer: Localized (I)1 Apr 2013357 RADICAL PROSTATECTOMY AND THE EFFECT OF CLOSE SURGICAL MARGINS: ANALYSIS FROM THE SEARCH DATABASE Sean Stroup, Daniel Moreira, Stephen Freedland, Fred Millard, Martha Terris, William Aronson, Joseph Presti, Christopher Amling, and Christopher Kane Sean StroupSean Stroup San Diego, CA More articles by this author , Daniel MoreiraDaniel Moreira New Hyde Park, NY More articles by this author , Stephen FreedlandStephen Freedland Durham, NC More articles by this author , Fred MillardFred Millard La Jolla, CA More articles by this author , Martha TerrisMartha Terris Augusta, GA More articles by this author , William AronsonWilliam Aronson Los Angeles, CA More articles by this author , Joseph PrestiJoseph Presti Palo Alto, CA More articles by this author , Christopher AmlingChristopher Amling Portland, OR More articles by this author , and Christopher KaneChristopher Kane La Jolla, CA More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.1744AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Positive surgical margins after radical prostatectomy are a significant predictor for biochemical failure, disease progression, and cancer mortality. Close surgical margins however represent a diagnostic challenge for surgeons. We sought to evaluate the biochemical recurrence patterns among men with radical prostatectomy specimens having negative, positive, and close surgical margins from the Shared Equal Access Regional Cancer Hospital (SEARCH) cohort. METHODS Men undergoing radical prostatectomy between 1988 and 2009 with known final pathologic margin status were evaluated. The cohort was divided into 3 groups based on margin status; negative, positive, and close. Close margins were defined by distance of tumor ≤1mm from the surgical margin or by pathologic description from reports. Biochemical recurrence was defined as PSA >0.2ng/ml, 2 values at 0.2ng/ml, or secondary treatment for an elevated PSA. Predictors of PSA recurrence and prostate cancer specific death were analyzed using Cox-proportional Hazard models. RESULTS Of 3499 men in the SEARCH database, 2468 (70%) men met criteria for inclusion in the analysis. Of these, 1188 (48%) had negative margins, 1058 (43%) had positive margins, and 222 (9%) had close margins. On multivariate analysis, relative to negative margins, men with close margins had a higher risk of biochemical recurrence (HR=1.51, 95%CI=1.18-1.92, P=0.001) and a decreased risk of biochemical recurrence when compared to those men with positive margins (HR=0.74, 95%CI=0.59-0.94, P=0.013). CONCLUSIONS Management of men with close surgical margins is a diagnostic challenge, with a disease course that is not entirely benign. Evaluation of other risk factors in these patients, including Gleason score, seminal vesicle involvement, perineural invasion, and tumor burden may provide further insight for patient management. Ultimately these factors will help better select patients who may benefit from adjuvant therapies. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e144-e145 Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information Sean Stroup San Diego, CA More articles by this author Daniel Moreira New Hyde Park, NY More articles by this author Stephen Freedland Durham, NC More articles by this author Fred Millard La Jolla, CA More articles by this author Martha Terris Augusta, GA More articles by this author William Aronson Los Angeles, CA More articles by this author Joseph Presti Palo Alto, CA More articles by this author Christopher Amling Portland, OR More articles by this author Christopher Kane La Jolla, CA More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...
The Journal of Urology · 2011-04-01 · 1 citations
articleYou have accessJournal of UrologyKidney Cancer: Advanced1 Apr 20111776 DOES TIMING OF CYTOREDUCTIVE NEPHRECTOMY IMPACT PATIENT SURVIVAL WITH METASTATIC RENAL CELL CARCINOMA IN THE TYROSINE KINASE INHIBITOR ERA? Sean Stroup, Omer Raheem, Ryan Kopp, Kerrin Palazzi-Churas, Reza Mehrazin, Fred Millard, Anthony Patterson, and Ithaar Derweesh Sean StroupSean Stroup San Diego, CA More articles by this author , Omer RaheemOmer Raheem San Diego, CA More articles by this author , Ryan KoppRyan Kopp San Diego, CA More articles by this author , Kerrin Palazzi-ChurasKerrin Palazzi-Churas San Diego, CA More articles by this author , Reza MehrazinReza Mehrazin Memphis, TN More articles by this author , Fred MillardFred Millard San Diego, CA More articles by this author , Anthony PattersonAnthony Patterson Memphis, TN More articles by this author , and Ithaar DerweeshIthaar Derweesh San Diego, CA More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2011.02.2104AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Metastatic renal cell carcinoma (mRCC) has been associated with a poor prognosis. While multimodal treatment with cytoreductive nephrectomy (CN) was established in the immunotherapy era, the role of CN in the setting of targeted therapy has been questioned. We sought to compare our experience of mRCC patients undergoing CN followed by adjuvant tyrosine kinase inhibitor (TKI) therapy vs. those undergoing primary TKI therapy prior to planned CN. METHODS We performed a retrospective, multi-institutional analysis of patients with mRCC from 5/2005 to 8/2009. The cohort was divided between those undergoing CN with adjuvant TKI therapy (Group 1) vs. those undergoing primary TKI therapy followed by planned CN (Group 2). Patient demographics, clinical variables, and oncological outcomes were compared. Disease response to therapy was determined using Response Evaluation Criteria Solid Tumors (RECIST) v.1.1. Patients in Group 2 who did not respond to TKI therapy (i.e, disease progression) were not offered CN, and were instead treated with salvage systemic therapy. Primary outcome measures were disease-specific (DSS) and overall survival (OS). RESULTS Of 35 patients with mRCC, 17 in Group 1 underwent primary CN and adjuvant TKI therapy, while 18 in Group 2 underwent neoadjuvant TKI therapy prior to intended CN. Patient demographic and tumor characteristics were similar between Group 1 and Group 2, including; age (years): 57 vs. 55, p=0.554, BMI (kg/m2): 29 vs. 28, p=0.521, ECOG status 0–1: 82% vs. 67% p=0.443, mean tumor size (cm): 9.2±2.5 vs. 10.4±4.4, p=0.378, and median length of follow-up (mo): 29.9 vs. 25.4, p=0.219)]. On univariate analysis, DSS and OS were no different among groups, p=0.721 and p=0.579. In Group 2, 11 had a favorable response and 7 progressed despite therapy. Response to primary therapy was highly predictive of DSS, with 1/7 (14.3%) non-responders by RECIST surviving vs. 6/7 (90.9%) of responders surviving, p<0.001. DSS was significantly improved among patients who underwent primary TKI followed by nephrectomy vs. those undergoing primary CN followed by adjuvant TKI (p=0.028) vs. primary TKI non responders prior to planned nephrectomy (p<0.001 for all) (Fig 1). CONCLUSIONS Non-responders to primary TKI therapy have a particularly poor prognosis. Responders to TKI therapy who underwent CN had better DSS than patients who underwent primary CN followed by TKI therapy. Further investigation is required to assess the role, timing, and sequencing of targeted therapy and CN in the treatment of metastatic RCC. © 2011 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 185Issue 4SApril 2011Page: e713 Peer Review Report Advertisement Copyright & Permissions© 2011 by American Urological Association Education and Research, Inc.MetricsAuthor Information Sean Stroup San Diego, CA More articles by this author Omer Raheem San Diego, CA More articles by this author Ryan Kopp San Diego, CA More articles by this author Kerrin Palazzi-Churas San Diego, CA More articles by this author Reza Mehrazin Memphis, TN More articles by this author Fred Millard San Diego, CA More articles by this author Anthony Patterson Memphis, TN More articles by this author Ithaar Derweesh San Diego, CA More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...
Frequent coauthors
- 50 shared
Richard C. Frank
Norwalk Hospital
- 50 shared
Daryl J. Murry
University of Nebraska Medical Center
- 50 shared
Kouros Owzar
Duke University
- 50 shared
Marwan Fakih
City Of Hope National Medical Center
- 50 shared
Apurva A. Desai
- 50 shared
Miguel A. Villalona‐Calero
- 50 shared
Antonius A. Miller
- 50 shared
Martin J. Edelman
Realistic Education in Action Coalition to Foster Health
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