tbuckley/cabot-search huggingface dataset:
Proteomic Signature Predicting Achievement of Very Good Partial Response In Patients with Multiple Myeloma Based On Complementary Label-Free and iTRAQ Quantitative Proteome Analysis
Authors: Dominik Dytfeld, Malathi Kandarpa, John R Strahler, Dattatreya Mellacheruvu, Suchitra Subramani, Stephanie J Kraftson, Lambert Ngoka, Alexey Nesvizhskii, Arun Sreekumar, Andrzej J Jakubowiak
Journal: Blood (2010)
Hypercvad Induction Chemotherapy Is Associated with Higher Rates of Stem Cell Mobilization Failure in Mantle Cell Lymphoma ( MCL)
Authors: Amandeep Salhotra, Shan Yuan, Joycelynne Palmer, Ibrahim Aldoss, Ni-Chun Tsai, Tanya Paris, Stephen J. Forman, Robert W Chen
Journal: Blood (2014)
Development of a Diagnostic Support System for Hematological Disorders Using a Self-Organizing Map.
Authors: Yohko Kawai, Nobuko Shimizu, Minoru Okamoto, Takayuki Mitsuhashi, Naoki Minamide, Hisako Kataguru, Tadashi Murase, Naoshiro Minamiide, Takeyoshi Fujihara, Toshio Kawaguchi, Kiyoaki Watanabe
Journal: Blood (2004)
Treatment of metastatic renal cell carcinoma with low-dose interleukin-2
Authors: Yuta Takezawa, Kouji Izumi, Takahiro Nohara, Kazutaka Narimoto, Satoru Ueno, Yoshihumi Kadono, Yasuhide Kitagawa, Hiroyuki Konaka, Atsushi Mizokami, Mikio Namiki
Journal: Annals of Oncology (2015)
230. A Novel Gammaretroviral Shuttle Vector Insertional Mutagenesis Screen To Identify Breast Cancer Metastasis Genes
Authors: Victor M. Bii, Dustin T. Rae, Grant T. Trobridge
Journal: Molecular Therapy (2015)

Retroviral insertional mutagenesis screens have been used to efficiently identify genes involved in a wide variety of cancers. Identifying causal driver genes in malignant disease is crucial to develop improved targeted therapies. Here, we have utilized a replication-incompetent gammaretroviral vector to perform a mutagenesis screen to identify genes involved in breast cancer metastasis progression. MDA-MB-231 cells that were mutagenized with a gammaretroviral vector were xenotransplanted into the mammary fat pad of immunodeficient mice, and the primary tumors and metastases allowed to develop. Metastatic tumors were collected and analyzed for proviral integration sites using a shuttle vector rescue approach that allows for rapid rescue of plasmids in E. coli that contain long terminal repeat-chromosomal junctions. In our approach, clones with vector proviruses that dysregulate nearby metastatic driver genes have a selective advantage to form metastatic tumors. The vector provirus acts as a molecular tag to identify candidate dysregulated metastasis driver genes. Using this approach, we identified several candidate breast cancer metastasis genes including WWTR1 (TAZ), a known and recently validated breast cancer metastasis gene. Identifying genes that drive the metastatic process can identify targets for improved therapy.
Self-Enforcing Feedback Activation Between BCL6 and Tonic Pre-B Cell Receptor Signaling in Acute Lymphoblastic Leukemia
Authors: Huimin Geng, Christian Hurtz, Dirk Baumjohann, Zhengshan Chen, Wei-Yi Chen, Erica Ballabio, Gang Xiao, Jae-Woong Lee, Anne Deucher, Zhongxia Qi, Chuanxin Huang, Rahul Nahar, Soo-mi Kweon, Seyedmehdi Shojaee, Lai N Chan, Jingwei Yu, Jeffrey W. Tyner, Bill H Chang, Steven M. Kornblau, Janetta Jacoba Bijl, B. Hilda Ye, Elisabeth Paietta, Ari Melnick, Robert Roeder, Stephen Hunger, Mignon Loh, Thomas Milne, Markus Muschen
Journal: Blood (2014)
Cardiotoxicity of aromatase inhibitors and tamoxifen in postmenopausal women with breast cancer: a systematic review and meta-analysis of randomized controlled trials
Authors: F. Khosrow-Khavar, K.B. Filion, S. Al-Qurashi, N. Torabi, N. Bouganim, S. Suissa, L. Azoulay
Journal: Annals of Oncology (2016)
Patient-reported outcomes after treatment for cancers of the pancreas and biliary tract.
Authors: James M. Metz, Carolyn Vachani, Margaret K. Hampshire, Christine E. Hill-Kayser
Journal: Journal of Clinical Oncology (2015)

375 Background: Pancreas and biliary (PBT) cancers are generally associated with poor overall prognosis, despite aggressive, multimodality therapy. The population of cancer survivors after these diagnoses may be largely ignored, despite risk of late effects. This Internet-based study seeks to evaluate patient-reported outcomes and survivorship care patterns after treatment of PBT cancers. Methods: Patient-reported data were gathered via a convenience sample frame from PBT survivors voluntarily utilizing a publically available Internet-based tool for creation of survivorship care plans. Available through the OncoLinkwebsite, the tool asks survivors to enter data regarding diagnosis, demographics, and treatments, and provides customized guidelines for future care. During use of the tool, PBT survivors are queried regarding late effects associated with specific treatments. Results: 134 PBT survivors utilized the tool from 2010-2014, 67% with pancreas cancer, 20% biliary, and 12% liver. Of the entire group, 59% were female and 81% Caucasian. Median diagnosis age was 59 and median current age 61. Average time since diagnosis was 2 years (range &lt;1-8). Most reported having had multimodality therapy - 71% surgery, 78% chemotherapy, and 46% radiation. Most patients (70%) reported not receiving continued care from an oncologist, and &gt;90% had never received previous survivorship information. Of 35 patients queried, 6 had metastatic disease and 7 had recurrent disease. When the entire group was queried regarding possible side effects of treatment, 44% reported persistent neuropathy, 24% chronic diarrhea, 21% bowel stricture or obstruction, and 15% chronic skin changes in the radiation portal. Conclusions: Although the prognosis after PBT cancers remains relatively poor, a population of long-term survivors exists. Survivors using this tool have generally not received survivorship information and most are no longer followed by an oncologist despite having received multimodality treatment. Neuropathy and gastrointestinal side effects appear to be the most bothersome to this group. This tool represents a potential way to provide information to underrepresented survivorship groups such as PBT survivors in the future.
Switching to Nilotinib Is Associated with Continued Deeper Molecular Responses in CML-CP Patients with Minimal Residual Disease After ≥ 2 Years On Imatinib: Enestcmr 2-Year Follow-up Results
Authors: Timothy P. Hughes, Jeffrey H. Lipton, Nelson Spector, Brian Leber, Ricardo Pasquini, Nelma Clementino, Anthony P. Schwarer, Gabriel Etienne, Agnès Guerci-Bresler, Susan Branford, Das Purkayastha, LaTonya Collins, Tomasz Szczudlo, Francisco Cervantes
Journal: Blood (2012)
Abstract 3974: A preclinical study for miR181b as therapeutic in Eu-TCL1FL-tg mouse model for CLL
Authors: Antonella Bresin, Elisa Callegari, Lucilla D'Abundo, Caterina Cattani, Cristian Bassi, Barbara Zagatti, Maria Grazia Narducci, Elisabetta Caprini, Yuri Pekarsky, Carlo Maria Croce, Silvia Sabbioni, Massimo Negrini, Giandomenico Russo
Journal: Cancer Research (2015)

Abstract Chronic lymphocytic leukemia (CLL) is a malignancy of B cells with immunophenotype of memory cells. Downstream pathways to BCR, like NFkB, AKT and ERK, and anti-apoptotic proteins such as Bcl2 and Mcl1, are thought to contribute to expansion and survival of the malignant cells. CLL patients show different clinical course: tumor clones having no V-gene mutations, many CD38+ or ZAP-70+ B cells, chromosome 11q deletion and high expression of TCL1, had an aggressive, usually fatal course, whereas patients with mutated clones, few CD38+ or ZAP-70+ B cells and low TCL1 expression, had an indolent course. Recent studies identified a microRNA signature associated with prognosis and progression in B-CLL. Particularly, miR181b is down-regulated in aggressive forms of CLL and its expression is inversely correlated to Tcl1 levels. An increasing number of studies are considering microRNAs as potentially useful therapeutic agents. Given that MCL-1, BCL-2 and TCL1 are proved targets for miR181b, that Akt activation is enhanced by Tcl1 and a crosstalk between Akt and ERK or NFkB exists, we performed a preclinical evaluation of miR181b therapeutic efficacy in a mouse model of CLL, the Eu-TCL1 transgenic mouse, previously generated by us. In vitro enforced expression of miR-181b mimics induced a significant apoptotic effect in human B-cell line EHEB, as well as in mouse Eμ-TCL1 leukemic splenocytes. Molecular analyses revealed that miR-181b not only affected the expression of Tcl1, Bcl2 and Mcl1 anti-apoptotic proteins, but also increased the expression level of the NFkB inhibitor protein IkB-alpha and reduced the phosphorylation levels of Akt and Erk1/2. Notably, an anti-TCL1 siRNA could similarly down-modulate Tcl1 but exhibited a reduced or absent activity on other relevant proteins, as well as a reduced effect on cell apoptosis and viability. In vivo studies indicated a significant capability of miR-181b in reducing leukemic cells expansion and increasing survival of treated mice. These data indicate that miR-181b exerts a broad range of actions, affecting proliferative, survival and apoptotic pathways, both in mice and human, and can potentially be employed to reduce expansion of B-CLL leukemic cells. Citation Format: Antonella Bresin, Elisa Callegari, Lucilla D'Abundo, Caterina Cattani, Cristian Bassi, Barbara Zagatti, Maria Grazia Narducci, Elisabetta Caprini, Yuri Pekarsky, Carlo Maria Croce, Silvia Sabbioni, Massimo Negrini, Giandomenico Russo. A preclinical study for miR181b as therapeutic in Eu-TCL1FL-tg mouse model for CLL. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3974. doi:10.1158/1538-7445.AM2015-3974
Abstract LB-054: Normal stem cell divisions, cancer incidence, and driver gene mutations
Authors: Cristian Tomasetti, Bert Vogelstein
Journal: Cancer Research (2015)

Abstract Cancer arises through the sequential accumulation of mutations in oncogenes and tumor suppressor genes. We show that the incidence of many cancers is strongly correlated (0.80; P &amp;lt; 1.8 × 10-6) with the lifetime number of divisions of the normal stem cells maintaining that tissue's homeostasis. These results suggest that only ∼35% of the variation in cancer incidence among tissues is attributable to environmental factors or inherited predispositions. Moreover, we derive an approach to assess the evidence for environmental and inherited factors that contribute to a given cancer type vs. other cancer types. The slope of the correlation noted above suggests that the number of driver gene mutations required to develop cancer must be smaller than what was previously estimated. We describe a novel approach to derive this estimate that combines conventional epidemiologic studies with genome-wide sequencing data. In two well-documented cancer types (lung and colon adenocarcinomas), we find that no more than three sequential mutations are needed. Finally, we explore the role of chance and aging in acquiring the driver gene mutations required to develop cancer. We provide novel experimental evidence, in both mice and humans, of an unexpected relationship between the dynamics of division rates in normal tissues and age-specific cancer incidence. These data and analyses provide a firm basis for understanding the role of random, replicative mutations during stem cell division in cancer incidence. Citation Format: Cristian Tomasetti, Bert Vogelstein. Normal stem cell divisions, cancer incidence, and driver gene mutations. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-054. doi:10.1158/1538-7445.AM2015-LB-054
Effect of the Pan-PIM Kinase Inhibitor, AZD1208, Alone and in Combination with Bortezomib in Multiple Myeloma
Authors: Loredana Santo, Janani Ramachandran, Diana D Cirstea, Homare Eda, Neeharika Nemani, Teru Hideshima, Chauhan Dharminder, Dennis Huszar, Kenneth C. Anderson, Noopur Raje
Journal: Blood (2014)
Abstract P3-13-09: Personalized therapy in breast cancer: Brazilian experience
Authors: Raphael Brandao Moreira, Matheus Bongers Alessandretti, Antonio Carlos Buzaid, Marcelo Rocha Cruz
Journal: Cancer Research (2015)

Abstract INTRODUCTION Cancer biology is characterised by genomic alterations. There is an ongoing revolution in cancer research due to the emergence of novel technologies based on next generation sequencing (NGS). OBJECTIVES To identify abnormalities in individual patients with the aim of providing targeted therapy matched to individuals genomic alterations. METHODS From April 2013, to February 2014, we included patients who had metastatic breast cancer with lesion accessible for biopsy. The tumor tissue stored in paraffin was evaluated by the method of next-generation sequencing (NGS) where 236 cancer-related genes were sequenced. ResultsPatientsTarget TherapyObjective ResponseMutations1EverolimusNOERBB2, PIK3CA2EverolimusYesPI3KCA, FGFR, AKT3EverolimusYesPI3KCA, FGFR4EverolimusYesAKT1, PI3KCA5EverolimusYesAKT16EverolimusYesAKT1, FGFR7EverolimusYesAKT1. FGFR8EverolimusNoERBB2, PI3KTable1 Mutations PrevalenceMutationPrevalenceTP5383,30%PIK3CA60,60%FGFR33%CCND125%PTEN25%BRCA216%AKT50%Table2 RESULTS Fourteen patients were included and NGS was feasible. An actionable genomic alteration was identified in 12 (85,7%) patients, most frequently in TP53 (10 [83,3%], PIK3CA (8 [66,6%]), AKT (5 [50%]), FGFR1 (4 [33%]), CCND1 (3 [25%]), PTEN (3[25%]) and BRCA2 (2[16%]). Therapy could be personalized in 12 of 14 patients. Of the 8 patients who received targeted therapy, 5 presented objective response. CONCLUSION . NGS was able to find genomic alterations in the majority of breast cancer tissues; . Most patients did not have "actionable" mutations for which a specific therapy could be offered; . We are just at the dawn of exploring this strategy and NGS can effectively contribute for increasing the understanding of the disease. REFERENCES 1. Jeffrey. Ross, Massimo Cristofanilli et al, JClin Oncol 3, 2013 (suppl; abster 1009). Citation Format: Raphael Brandao Moreira, Matheus Bongers Alessandretti, Antonio Carlos Buzaid, Marcelo Rocha Cruz. Personalized therapy in breast cancer: Brazilian experience [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P3-13-09.
Motexafin Gadolinium, a Redox Mediator, Induces Apoptosis in Chronic Lymphocytic Leukemia B Cells and Is Additive or Synergistic with Fludarabine.
Authors: Louie Naumovski, Nancy D. Bone, Mint Sirisawad, Richard Miller, Diane F. Jelinek, Renee C. Tschumper, Neil E. Kay
Journal: Blood (2004)
Copy Number Variants Underlying Inherited Bone Marrow Failure Syndromes
Authors: Nicolas Waespe, Santhosh Dhanraj, Manju Wahala, Tom Enbar, Bozana Zlateska, Hongbing Li, Robert J. Klaassen, Conrad Fernandez, Rochelle Yanofsky, John K. Wu, Yves D. Pastore, Mariana Silva, Jeffrey H. Lipton, Josee Brossard, Bruno Michon, Sharon Abish, MacGregor Steele, Roona Sinha, Mark J. Belletrutti, Vicky R. Breakey, Lawrence Jardine, Lisa Goodyear, Liat Kofler, Ibrahim A. Ghemlas, Michaela Cada, Lillian Sung, Mary Shago, Stephen W. Scherer, Yigal Dror
Journal: Blood (2015)
Prognostic Factors of Survival in Dermatofibrosarcoma Protuberans—Reply
Authors: Maressa C. Criscito, Kathryn J. Martires, Jennifer A. Stein
Journal: JAMA Dermatology (2016)

In Reply We appreciate the interest of Chidambaram and Goh in our study, in which we demonstrate age, sex, and tumor size as important predictors of survival in patients with dermatofibrosarcoma protuberans (DFSP).1
Efficacy and safety of clonazepam (CZ) for sensory neurotoxicity (sNT) with paclitaxel (PTX)
Authors: K. Matsumoto, N. Katsumata, K. Yonemori, T. Kouno, C. Shimizu, M. Andoh, Y. Fujiwara
Journal: Journal of Clinical Oncology (2005)

8174 Background: Neurotoxicity(NT) is dose-limiting toxicity in high proportion of patients (pts) with various solid tumors treated by PTX. There is no standard prevention or treatment for NT caused by PTX. CZ is an anti-convulsion agent, which is also used as treatment for neuropathic pain. We have experienced some successful treatment of PTX-induced sNT by CZ. So we examined this drug for the treatment of sNT caused by PTX. Method: We conducted a retrospective chart review from 1999 to 2004. Eligible pts must have received PTX (if it’s given in every 3 weeks regimen, up to 6 cycles, or if in weekly regimen, up to 18 cycles) for their malignancy, then developed sNT, and prescribed CZ. CZ was orally given twice a day (1mg/day). Improvement rate for sNT was primarily evaluated. sNT was evaluated according to NCI-CTC(ver.2). Improvement was defined as decreasing grade of sNT(“grade improvement”) or subjective improvement of symptom without decreasing grade of sNT(“symptom improvement”), at a next visit. Result: 43 pts were eligible. Pts received PTX every 3 weeks (31 pts) or weekly (12 pts). 21 pts had Grade 1, 11 had Grade 2, and 3 had Grade 3 sNT at the time of CZ prescription. 10 of 43(23%; 95% confidential interval= 11–36) pts decreased their grade of sNT(“grade improvement”). Another 10 of 43(23%) pts experienced their subjective symptoms without decreasing sNT grade (“symptom improvement”). Totally, 20 of 43(47%; 95% confidential interval= 31–61) pts experienced their sNT improvement by CZ. Among them, 12 pts were responded to CZ during the chemotherapy and they could complete remaining cycles (1–5 cycles). 4 of pts ceased their planned chemotherapy due to sNT. Toxicity of CZ was observed in 4 pts (2 somnolence grade 3, 1 dizziness grade 2, 1 delusion garde 3). All toxicities disappeared soon after quitting CZ. Conclusion: CZ is potentially effective treatment of sNT caused by PTX. Prospective evaluation of this drug is warranted. No significant financial relationships to disclose.
A Phase I Study of GA101 (RO5072759) Monotherapy Followed by Maintenance in Patients with Multiply Relapsed/Refractory CD20+ Malignant Disease.
Authors: Laurie H. Sehn, Sarit E. Assouline, Douglas A. Stewart, Joy Mangel, Pavel Pisa, Jaimal Kothari, Michael Crump
Journal: Blood (2009)
Trimethoprim–Sulfamethoxazole (Co-Trimoxazole) for the Prevention of Relapses of Wegener's Granulomatosis
Authors: Coen A. Stegeman, Jan Willem Cohen Tervaert, Paul E. de Jong, Cees G.M. Kallenberg
Journal: New England Journal of Medicine (1996)

Respiratory tract infections may trigger relapses in patients with Wegener's granu-lomatosis in remission. Uncontrolled data have suggested that treatment with trimethoprim–sulfamethoxazole (co-trimoxazole) may be beneficial.
Abstract 2023: MYC amplification and overexpression in metastatic anaplastic thyroid cancer dictates response to therapy
Authors: Emrullah Yilmaz, Marika A. Russo, Arturo Orlacchio, Toni Forde, Antonio Di Cristofano
Journal: Cancer Research (2015)

Abstract Anaplastic thyroid cancer (ATC) is a very aggressive and lethal cancer with few months of survival from diagnosis. Although less than 2% of all thyroid carcinomas are ATC, it accounts for up to 40% of thyroid carcinoma deaths. TRP53 inactivating mutations and PI3K activation through loss of PTEN, or PIK3CA mutations and amplification are common in ATC. In fact, targeted deletion of Pten and Trp53 in the mouse thyroid results in ATC development. Using this mouse model, we found that Myc is amplified in 38% (11/29) of [Pten,Trp53]thyr-/− ATCs with distant metastasis, but only in 10% (3/30) non-metastatic ATCs. Conversely Myc was not amplified in any of 15 metastatic follicular thyroid carcinomas developed by Ptenthyr-/− mice. Analysis of human ATCs showed Myc amplification in 17% (3/18) tumors and protein overexpression in 25% of samples in a tissue microarray. Myc amplification has been shown to be associated with resistance to PI3K targeted therapies in different tumor types. We evaluated the role of Myc in ATC growth and response to therapy using cell lines derived from our [Pten,p53]thyr-/− mouse model. Myc-amplified cell lines grew faster than cell lines from tumors without Myc amplification both in full medium and under serum deprivation. Myc knockdown resulted in a dramatic decrease in growth rate, especially under serum starvations, suggesting that tumors with Myc amplification are less dependent on growth factors present in the serum. Myc knockdown in Myc-amplified cells completely impaired tumor formation in syngeneic mice. To evaluate the effect of Myc amplification on drug sensitivity, we screened a panel of drugs on cultured cells. Myc knockdown sensitized ATC cells to PLK1 inhibition with BI6727, PI3K inhibition with BKM120, as well as to doxorubicin and etoposide. Conversely, Myc-amplified cells were more sensitive to carboplatin. Our results show that Myc amplification is a biomarker for more aggressive and resistant ATCs and that MYC-targeting strategies could be employed to sensitize these tumors to conventional and targeted therapy. Citation Format: Emrullah Yilmaz, Marika A. Russo, Arturo Orlacchio, Toni Forde, Antonio Di Cristofano. MYC amplification and overexpression in metastatic anaplastic thyroid cancer dictates response to therapy. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2023. doi:10.1158/1538-7445.AM2015-2023
Impact of sarcopenia (Sp) on early dose-limiting toxicity (DLT) and acute vascular toxicity in patients (pts) with metastatic renal cell carcinoma (mRCC) receiving sunitinib (SUT).
Authors: O. Huillard, O. Mir, N. Barry Delongchamps, B. Blanchet, B. Knebelmann, P. Boudou-Rouquette, R. Coriat, B. Debre, J. Durand, T. Flam, M. Peyromaure, M. Zerbib, S. Ropert, F. Goldwasser
Journal: Journal of Clinical Oncology (2011)

e15094 Background: mRCC pts with severe muscle wasting (Sp) are at increased risk of DLT during anti-VEGF therapy with sorafenib (Antoun et al., Ann Oncol 2010). We hypothesized that Sp could also predict SUT-induced toxicity. Methods: mRCC outpatients received SUT 50 mg OD (4/6 weeks) or 37.5 mg OD, from June 2006 to December 2010. From July 2008, SUT plasma levels were routinely monitored every 15 days. Skeletal muscle cross-sectional area at the third lumbar vertebra was measured by CT-scan, and Sp was defined using standardized thresholds. Blood pressure was monitored twice daily at home, and other toxicities were assessed every 15 days. The primary evaluation criterion was DLT during the first month. Secondary criteria were SUT AUC on day 28, acute vascular toxicities (thrombotic microangiopathy, TMA and reversible posterior leukoencephalopathy syndrome, RPLS) during treatment, and progression-free survival (PFS). Results: 45 pts (71.1% males, median age: 60.3 years, range 29-83) were eligible for CT-scan, toxicity and PFS analyses. Pharmacokinetic data were available for 16 pts. A total of 287 cycles (median/pt: 6, range 1-22) were given, for a median follow-up of 14.4 months (range: 1.5-51.3). During the first month, grade 3 hypertension (not dose-limiting) occurred in 11 pts (24.4%), and DLT occurred in 8 pts (17.8%), including grade 3 fatigue (3 pts, 6.7%), TMA and RPLS (2 pts each, 4.4%), grade 3 hand-foot syndrome and pulmonary embolism (1 pt each, 2.2%). 22 pts (48.9%) had Sp at baseline. Pts with Sp experienced significantly more DLTs during the first month of treatment (7/22 vs. 1/23, p = 0.02). SUT AUC on day 28 (median: 1599 vs. 1228 ng.h/ml, p = 0.12) and PFS (median: 8.0 vs. 8.5 months, p = 0.29) did not differ between pts with or without Sp. Of 7 pts who experienced TMA or RPLS during the whole treatment period, 6 (86%) had Sp at baseline. Conclusions: mRCC pts with Sp receiving SUT are at higher risk of early DLT, and experience more frequently acute vascular toxicities (TMA and RPLS). Sp appears to be a marker of tissular vulnerability that deserves further validation on larger cohorts of pts receiving anti-VEGF agents.