tbuckley/cabot-search huggingface dataset:
A phase I dose finding study of the 3-day administration of BIBW 2992, an irreversible dual EGFR/HER-2 inhibitor, in combination with three-weekly docetaxel in patients with advanced solid tumors
Authors: A. H. Awada, H. Dumez, P. Wolter, A. Hendlisz, T. Besse-Hammer, M. Piccart, M. Uttenreuther-Fischer, P. Stopfer, M. Taton, P. Schöffski
Journal: Journal of Clinical Oncology (2009)

3556 Background: BIBW 2992 (Tovok) is a potent, irreversible, new generation TKI, an inhibitor of EGFR and HER-2 (IC 50 0.5 and 14 nM, respectively). A Phase I dose finding study of BIBW 2992 with docetaxel is reported. Methods: Patients (pts) had advanced solid malignancies and received docetaxel 75 mg/m 2 i.v. on Day 1 and oral BIBW 2992 once daily on Days 2–4, in 3-week cycles. The BIBW 2992 dose was doubled in successive cohorts of 3–6 pts until ≥Grade 2 CTC, after which dose escalation occurred in increments of ≤50%. The MTD cohort expanded to 12 pts. PK profiles were taken on Days 1 and 2 of treatment cycles 1 and 2. Results: 40 evaluable pts (17 male) were treated at the following doses of BIBW 2992: 10 mg (6), 20mg (3), 40 mg (6), 60 mg (4), 90 mg (13), 120 mg (5) and 160 mg (3). Common adverse events (AEs) (% of patients) were fatigue (62.5%), diarrhea (57.5%), anorexia and stomatitis (52.5%), alopecia (50%), rash (42.5%), nausea and pyrexia (40%), vomiting (35%), general physical health deterioration (32.5%), and peripheral sensory neuropathy (30%). Two DLTs occurred: one pt had Grade 4 neutropenia (a DLT if complicated or lasting &gt;5 or 7 days) and one had Grade 3 nausea, vomiting and diarrhea (BIBW 2992 120 mg). Both fully recovered upon treatment interruption/dose reduction (docetaxel 60 mg/m 2 /BIBW 2992 90 mg). The MTD was 90 mg BIBW 2992 with docetaxel 75 mg/m 2 . Four pts (breast cancer [2], thymoma [1], oesophageal carcinoma [1]) had a PR. One breast cancer pt had a confirmed CR. Two of these pts had prior taxane treatment. Ten pts had SD and received treatment for ≥6 courses with 4 receiving treatment for ≥9 courses. There was no deviation from dose-linearity of BIBW 2992 and docetaxel. Docetaxel (75 mg/m 2 ) plasma concentration-time profiles, C max and AUC 0- ∞ before and after BIBW 2992 dosing were comparable. Conclusions: BIBW 2992 90mg administered for 3 days after docetaxel 75 mg/m 2 is well tolerated and is the recommended dose for further trials. Objective responses or durable SD (≥6 months) were seen in 15 (39%) pts. No PK interaction was observed between BIBW 2992 and docetaxel. [Table: see text]
Detection of RAS, KIT and FLT3 Gene Mutations in t(8;21)-Positive Acute Myeloid Leukemia (AML): Evaluation of the Clinical Relevance.
Authors: Juan Du, Richard F. Schlenk, Andrea Corbacioglu, Marianne Habdank, Claudia Scholl, Stefan Frohling, Lars Bullinger, Arnold Ganser, Hartmut Dohner, Konstanze Dohner
Journal: Blood (2006)
Therapeutic Sensitivity of CD20- Waldenströms Macroglobulinemia Cells Is Determined By Underlying Genomic and Epigenetic Events
Authors: Aneel Paulus, Sharoon Akhtar, Hyejin Yoon, Xue Wang, Maja Blake-Kuranz, Paul K. Wallace, Sikander Ailawadhi, Stephen M. Ansell, Anne J. Novak, Morie A Gertz, Robert A Kyle, Peter Martin, Morton Coleman, Jungsu Kim, Asher Chanan-Khan, Kasyapa S. Chitta
Journal: Blood (2014)
Bortezomib-Induced Apoptosis in Cutaneous T-Cell Lymphoma and Adult T-Cell Leukemia/Lymphoma Cells Partially Depends on up-Regulation of Noxa, Functional Repression of Mcl-1, and Down-Regulation of C-Flip and XIAP.
Authors: Masaki Ri, Shinsuke Iida, Takashi Ishida, Asahi Ito, Hiroki Yano, Atsushi Inagaki, Jianmin Ding, Fumiko Mori, Shigeru Kusumoto, Hirokazu Komatsu, Atae Utsunomiya, Ryuzo Ueda
Journal: Blood (2008)
ACTR-45. A PHASE IB STUDY EVALUATING THE C-MET INHIBITOR INC280 IN COMBINATION WITH BEVACIZUMAB IN GLIOBLASTOMA MULTIFORME (GBM) PATIENTS
Authors: Kent Shih, Gerald Falchook, Kevin Becker, James Battiste, Michael Pearlman, Mythili Shastry, Howard Burris
Journal: Neuro-Oncology (2016)

BACKGROUND:The HGF/c-MET pathway is deregulated in cancer affecting tumor cell proliferation, invasion, metastasis and angiogenesis. INC280 is an oral small molecule inhibitor of c-Met. Bevacizumab produces responses in patients with recurrent glioblastoma (rGBM); however this has not translated into a survival benefit. One reason may be the complex interaction of HGF/c-Met with VEGF and its receptors and their role in glioblastoma. This phase Ib study is evaluating INC280+ bevacizumab in patients with rGBM.
Phase 2 study of dalantercept in recurrent or metastatic squamous cell carcinoma of the head and neck.
Authors: Antonio Jimeno, Marshall R. Posner, Jared Weiss, Lori J. Wirth, Nabil F. Saba, Roger B. Cohen, Elizabeta C. Popa, Athanassios Argiris, Kenneth F. Grossmann, Ammar Sukari, Chris Korth, Dawn Wilson, Ty McClure, Marat Alimzhanov, Scott Pearsall, Kenneth M. Attie, Matthew L. Sherman, Shuchi Sumant Pandya
Journal: Journal of Clinical Oncology (2014)

6045 Background: Limited treatments exist for patients with recurrent or metastatic squamous cell carcinoma of the head and neck (RM-SCCHN) after platinum therapy. Activin receptor-like kinase 1 (ALK1) is a member of the TGF-β superfamily involved in blood vessel maturation that is selectively expressed on activated endothelial cells. ALK1 binds to ligands bone morphogenetic protein (BMP) 9 and 10 and results in phosphorylation of Smad 1/5/8. Dalantercept (Dal) is an ALK1 receptor fusion protein and acts as a ligand trap. In Phase 1 testing Dal had clinical activity in pts with RM-SCCHN. This study sought to determine the activity of Dal monotherapy in pts with RM-SCCHN. Methods: 46 pts were enrolled and received Dal at 80 mg (n=2), 0.6 mg/kg (n=13) or 1.2 mg/kg (n=31) SC Q3W. Serum, archived, and optional biopsies were collected for pharmacodynamic (PD) studies. The primary endpoint was response rate per RECIST 1.1 and secondary endpoints included progression free survival (PFS) and overall survival (OS). Key eligibility: RM-SCCHN of mucosal origin, ≥1 one prior platinum regimen, ECOG ≤1, and no prior anti-angiogenic tx. Results: 41 pts were evaluable (1 at 80 mg, 13 at 0.6 mg/kg, 27 at 1.2 mg/kg). The median age was 60.5 yr, 85%M/15%F, ECOG: 0 (35%)/1(65%), HPV+ 41%, HPV- 33%, HPV unk 26%. Median number of prior tx was 4. 1 pt at 1.2 mg/kg (3.7%) achieved a PR and was on study for 9 mos. 23% (n=3) at 0.6 mg/kg and 37% (n=10) at 1.2 mg/kg had SD ≥ 3 cycles. Of those pts with SD or better (n=16), 62% were known to be HPV+. 17% (2 at 0.6 mg/kg and 5 at 1.2 mg/kg) pts. had SD for ≥ 6 cycles (4.5 mos.). The median OS (n=46) was 6.3 mos. (95% CI: 5.8-10.5) and 5 pts survived beyond 1 year. Common drug-related AEs were anemia, fatigue, peripheral edema, headache, hyponatremia, and pleural effusion. The frequency of grade ≥ 3 related AEs was 13% and the most common were hyponatremia (n=3) and pleural effusion (n=2). There were no thromboembolic or significant bleeding events. Conclusions: Dal is a novel anti-angiogenic agent that inhibits ALK1 signaling. In this heavily pre-treated RM-SCCHN population, Dal monotherapy demonstrated modest dose dependent activity and a favorable safety profile. Detailed safety, efficacy, and correlative PD data will be presented. Clinical trial information: NCT01458392.
NCI #8412: A randomized phase II trial of AZD6244 alone and AZD6244 plus temsirolimus for soft-tissue sarcomas.
Authors: Zeynep Eroglu, Hussein Abdul-Hassan Tawbi, James Hu, Min Guan, Paul Henry Frankel, Nora Ruel, Sharon Wilczynski, Scott Christensen, David R. Gandara, Warren Allen Chow
Journal: Journal of Clinical Oncology (2014)

10526 Background: Outcomes for advanced soft-tissue sarcomas (STS) are poor given their relative insensitivity to chemotherapy. AZD6244 (AZD) is a MEK1/2 inhibitor that suppresses STS proliferation in vitro. mTOR inhibitors (mTORi) possess modest activity against STS, and resistance rapidly develops via MAPK pathway feedback activation. The combination of AZD and the mTOR inhibitor temsirolimus (Tem) synergistically inhibits STS cell line growth. Therefore, a randomized, phase II trial of AZD vs. AZD plus Tem in advanced STS was conducted. Methods: Adults with advanced STS who received ≤2 prior chemotherapeutics were eligible; pediatric-type sarcomas and brain metastases were excluded. 69 subjects were randomized to AZD 75 mg PO bid (n=34) and allowed to crossover upon progression, or to AZD 50 mg PO bid plus Tem 20 mg IV weekly (n=35), with 28 day cycles. Primary endpoint was progression-free survival (PFS). Secondary objectives were to compare: response rate, 4-month PFS rates, and toxicities; and changes in ERK-phosphorylation in stimulated PBMCs pre- and post-treatment. Results: While there was no difference in PFS between the single agent vs. combination arm for the overall cohort (median 1.9 vs. 2.1 months), an improved median PFS was observed in the combination arm (N=11) over single agent (N=10) in the pre-specified leiomyosarcoma stratum (median 3.7 vs. 1.8 months; p=0.01). 4-month PFS rate was 24% for both arms in the overall cohort, but 50% (95% CI 0.19-0.81) with the combination vs. 0% with AZD alone in the leiomyosarcoma cohort. One PR and 4 SD were seen with the combination arm in leiomyosarcoma patients, and 2 SD in AZD alone. 18 of 34 AZD6244 patients crossed over, with 5 patients receiving ≥ 6 cycles after crossover. Most common grade 3/4 adverse events in the combination arm were mucositis (29%), lymphopenia (26%), neutropenia and anemia (20% each); hypertension (12%) was observed with AZD alone. Correlative studies showed that AZD significantly inhibited ERK phosphorylation. Conclusions: The combination of AZD and Tem appears to be an active regimen in the leiomyosarcoma subset. Emerging preclinical data revealing activation of the mTOR pathway in leiomyosarcoma development may explain this result. Clinical trial information: NCT01206140.
The International Prognostic Scoring System for Waldestrom’s Macroglobulinemia (ISSWM) Is Applicable in Patients Treated with Rituximab-Based Regimens.
Authors: Meletios Athanasios Dimopoulos, Efstathios Kastritis, Dimitra Gika, Sossana Delimpassi, Konstantinos Zervas, Argiris Simeonidis, Evangelos Eleftherakis-Papaiakovou, Nicolaos Anagnostopoulos, Evridiki Michali, Marie Christine Kyrtsonis, Evangelos Terpos, Gerassimos Pangalis
Journal: Blood (2007)
Substance use, psychological distress, and quality of life (QOL) in adolescent and young adult (AYA) cancer patients with hematologic malignancies in early survivorship.
Authors: Fay J. Hlubocky, Lori S. Muffly, Jocelyn GOmez, Kate Breitenbach, Mary Lappe, Wendy Stock, Christopher Daugherty
Journal: Journal of Clinical Oncology (2016)

219 Background: Prior research identifies both the physical and psychological effects of cancer treatments as significant predictors of substance use among AYA. However, the prevalence of substance use and its effect on QOL and psychological well-being of AYA hematologic survivors has not been described. Methods: AYA patients (15-40 years at diagnosis) of acute leukemia, aggressive non-Hodgkin lymphoma, Hodgkin lymphoma undergoing curative intent therapy (on-treatment cohort) or 2 year completion of therapy and in remission (early survivor cohort) completed following measures: depression (CES-D), state anxiety (STAI-S), PTSD (PCL-C), QOL (FACIT-G). Semi-structured interviews evaluated substance use. Results: 62 AYA (26 on-treatment, 36 early survivors) were interviewed. For total population: median age at dx 26y (15-40); 64% male; 59% Ca; 79% college/post educ; 41% income &lt;$75,000y; 52% and 48% lymphoma/ leukemia dx, respectively. Overall, 52% AYA reported the current use of a substance (ex. alcohol, nicotine, illicit drug). Of these, 49% AYA reported alcohol use; 20% reported nicotine use; 31% reported illicit drug use (ex. marijuana). AYA who used alcohol had poorer QOL (79±15 v 84±18,p=.02). AYA who used nicotine had higher STAI-S anxiety (44±13 v33±10, p=.01) and CES-D depression (30±16 v 15±8,p&lt;.00). Nicotine use was associated with severe illness-related PTSD symptoms (57±26 v 28±10, p&lt;.00). Also, AYA with illicit drugs use had greater CES-D (20±13 v 11±9, p=.03) and moderate PTSD (41±18 v 29±12, p=.01). On-treatment AYA were more likely to deny current use of illicit drugs (58% v 41%, p=.02) than early survivors. Conclusions: AYAs with hematologic malignancies report substance use negatively impacting QOL thus warranting the need for future age-specific psychological interventions.
Activity of Hypomethylating Agents in the Treatment of Therapy-Related Myelodysplastic Syndrome
Authors: Ana Alfonso Pierola, Guillermo Montalban-Bravo, Koichi Takahashi, Feng Wang, Song Xingzhi, Elias J. Jabbour, Tapan M. Kadia, Farhad Ravandi, Jorge E. Cortes, Courtney D. DiNardo, Naval G. Daver, Gautam Borthakur, Naveen Pemmaraju, Marina Konopleva, Carlos E Bueso-Ramos, Keyur Patel, Andrew Futreal, Sherry Pierce, Hagop M. Kantarjian, Guillermo Garcia-Manero
Journal: Blood (2016)
Symptomatic skeletal events (SSEs) versus skeletal-related events (SREs) in patients with advanced cancer and bone metastases treated with denosumab or zoledronic acid
Authors: R. von Moos, L.A.M. Costa, G. Scagliotti, H. Sleeboom, F. Goldwasser, V. Hirsh, A. Spencer, H.-S. Radcliffe, D. Niepel, D.H. Henry
Journal: Annals of Oncology (2016)
B Cell Lymphomas Escape Bone Morphogenetic Protein (BMP) Induced Growth Inhibition: Downregulation of BMP Receptors and Upregulation of Inhibitory Smads.
Authors: Kanutte Huse, Maren Bakkebo, Morten Oksvold, Erlend B. Smeland, June H. Myklebust
Journal: Blood (2007)
Randomized Comparison of Cladribine Plus Cyclophosphamide with Fludarabine Plus Cyclophosphamde in Untreated Patients with Chronic Lymphocytic Leukemia: Report of the Polish Adult Leukemia Group (PALG-CLL3).
Authors: Tadeusz Robak, Jerzy Z Blonski, Krzysztof Jamroziak, Joanna Gora-Tybor, Beata Stella-Holowiecka, Lech Konopka, Bernadeta Ceglarek, Krzysztof Warzocha, Ilona Seferynska, Janusz Kloczko, Jaroslaw Piszcz, Malgorzata Calbecka, Aleksandra Kostyra, Jadwiga Dwilewicz-Trojaczek, Elzbieta Wiater, Anna Dmoszynska, Malgorzata Kowal, Krystyna Zawilska, Alina Grzywacz, Andrzej Hellmann, Andrzej Mital, Andrzej Zdunczyk, Jacek Dybowicz, Kazimierz Kuliczkowski, Stanislaw Potoczek, Aleksander Skotnicki, Maria Nowakowska-Domagala, Krzysztof Lewandowski, Kazimierz Sulek
Journal: Blood (2008)
IMMU-48. EVALUATING THE IN-VITRO EFFECTS OF TUMOR TREATING FIELDS ON T-CELL RESPONSES
Authors: Gil Diamant, Zvi Ram, Ilan Volovitz
Journal: Neuro-Oncology (2017)

Tumor Treating Fields (TTFields) are low-intensity electrical fields that target proliferating cells by hindering mitotic spindle formation and charged organelle translocation. TTFields were approved for treatment of recurrent and newly diagnosed Glioblastoma. Immunotherapeutic approaches for treatment of GBM are considered promising with multiple strategies evaluated in the clinic. Combining TTFields with immunotherapy is a rational approach as they possess different mechanisms of action (MOA). However, TTFields may interfere with the cellular functions required for effective T cell responses. To evaluate the compatibility between pivotal antitumoral T cell functions and TTFields. Healthy-donor peripheral blood mononuclear cells or viably-dissociated human Glioblastoma samples were cultured under normal or TTFields conditions, with or without activation by PHA (superantigen). Multicolor flow cytometry (FCM) was used to monitor select markers pivotal for an effective antitumoral T-cell response: proliferation (CFSE), cytokine secretion (IFNγ), cytotoxic degranulation (CD107a) and activation/ exhaustion (PD1). Cellular viability was assessed by an FCM viability dye. CAR T cells and their cognate tumor cell targets were used to directly evaluate cytotoxicity under normal and TTFields conditions. TTFields did not alter T cell activation rates for all evaluated functions with the exception of reduced proliferation - in line with its MOA. Polyfunctionality analysis of T-cells demonstrated that under TTFields, the activated non-proliferating T cells retained polyfunctional capabilities. TTFields substantially reduced the viability of activated proliferating T cells, moderately affected activated non-proliferating T cells and had almost no effect on the viability of non-activated cells. In the cytotoxicity assays, T cells under TTFields exhibited identical killing curves as their controls. Most pivotal T-cell functions, except for proliferation, were unhindered by TTFields. Our data suggests that integration of TTFields with immunotherapeutic approaches may potentially be a beneficial strategy to explore for treatment of brain tumors.
Effect of Dermatophagoides Pteronissinus Immunotherapy on T Regulatory Cell Subpopulation.
Authors: Miguel Gonzalez, Maria Francisca Palomares, Inmaculada DoÑa, Maria J. Torres, Francisca Gomez, Maria Jose Rodriguez, Ana Molina, Paloma Campo, Carmen Rondon Segovia, Cristobalina Mayorga
Journal: Journal of Allergy and Clinical Immunology (2017)
A clinical and biological profile to predict risk of development of hypertension in patients with non-clear cell renal cell carcinoma treated with sunitinib.
Authors: N. A. Ilias-Khan, A. Y. Khakoo, N. M. Tannir
Journal: Journal of Clinical Oncology (2010)

4601 Background: Hypertension (HTN) due to sunitinib is a common toxicity that has been linked to the development of severe adverse cardiovascular events. Intriguingly, recent observations also suggest a correlation between treatment related HTN and treatment response to anti-angiogenic therapies, including sunitinib. Risk predictors for the development of HTN have not been established. Methods: This is a single-arm phase II trial with a two-stage design to evaluate sunitinib (50 mg daily, 4/2 schedule) in non clear cell RCC (nccRCC). Eligibility criteria included PS 0-2, measurable disease, and a maximum of 2 prior regimens. Monitoring of cardiovascular events included coronary artery disease (CAD) risk-factor assessment and prospective monitoring of blood pressure and cardiac function. In addition, a panel of circulating angiogenic factors was measured prior to therapy and after the first cycle of therapy. Results: 46 pts (65% male, 26% >65 years of age) received an average of 2.6 cycles of sunitinib therapy for nccRCC from March 2007 to December 2009. There were 28 deaths (61%) which were due to progression of disease. 33% of pts developed Grade 2 or higher treatment-related HTN. 0/12 patients without established risk factors for CAD developed treatment related HTN, while 74% (13/17) of pts with two or more CAD risk factors developed treatment-related hypertension. Treatment with sunitinib was associated with a marked reduction in circulating VEGFR-2 levels after one cycle of treatment (p < 1 × 10-10). Intriguingly, baseline levels of soluble VGEFR-2 were two-fold lower in pts who developed treatment-related HTN (p < 0.05). An association between objective response rate and the development of HTN is being explored. Conclusions: HTN associated with sunitinib was observed at a much higher frequency in patients with underlying CAD risk factors. Soluble VEGFR-2 was significantly reduced after treatment in all patients, and was reduced at baseline in pts who developed treatment related HTN. Our observations suggest a complex and potentially important biological interaction between the host vasculature, tumor, and response to sunitinib therapy. No significant financial relationships to disclose.
P06.07 Fibroblast activation protein alpha is expressed by transformed and stromal cells and is associated with mesenchymal features in glioblastoma
Authors: P. Busek, E. Balaziova, I. Matrasova, M. Hilser, R. Tomas, M. Syrucek, Z. Zemanova, E. Krepela, A. Sedo
Journal: Neuro-Oncology (2016)
GENT-51. EPIGENETIC PROFILING REVEALS A UNIQUE HISTONE CODE IN CHORDOMA
Authors: Nelson Moussazadeh, Yupeng Zheng, Joshua Sommer, Ilya Laufer, Mark H. Bilsky, Neil Kelleher, Cameron Brennan
Journal: Neuro-Oncology (2016)

Pathognomonic genetic “driver” lesions to explain the brachyury transcriptional program have not been described in chordoma. Herein we characterize the epigenetic histone, methyl-genomic and somatic chromatin-modifying genotypic (CMG) landscape of chordoma. Six chordomas with matched germline tissue representing a spectrum of location (sacral, clival, mobile spine), histopathology (classical and dedifferentiated) and stage (primary and post-irradiation recurrences) underwent mass spectrometric histone profiling. Genotype was obtained via exome sequencing, and enhanced-representation reduced bisulfite sequencing yielded genomic methylation data. Histone marks were highly conserved across chordoma samples regardless of site of origin or histopathology. Pathognomonic histone marks included hypermethylated lysine 27 on H3.1 (H3.1K27) compared to a cohort of 6 cancer cell lines (p = 4.8e-10), marks associated with transcriptional repression. Other significant alterations included H3K4 hypermethylation, predicted on the basis of brachyury overexpression. Genotype further predicted some degree of variability across chordoma samples, with CMG alterations including lysine demethylase loss associated with hypermethylation at the predicted residues. In this first utilization of mass spectrometric analysis of a solid tumor, chordoma harbors a histone code distinct from other profiled neoplastic and normal tissues.
Phase II study of interferon and thalidomide in metastatic renal cell carcinoma
Authors: R. R. Tripathi, B. Patel, L. Heilbrun, M. Hussain, L. Flaherty, U. N. Vaishampayan
Journal: Journal of Clinical Oncology (2004)

4712 Background: Immunomodulatory therapies are commonly the most effective systemic treatments in renal cell carcinoma (RCC). Interferon-alpha and thalidomide have both immunomodulatory and anti-angiogenic properties with few overlapping toxicities. Methods: 18 patients (pts) with locally advanced, recurrent or metastatic RCC were enrolled to receive 2 MU of interferon-alpha 2b subcutaneously and thalidomide 200 milligrams orally each day (28 days = 1 cycle) until progression. Results: Median age was 61 years and 14/18 patients had an ECOG performance status of 1. Most common sites of metastasis were lung (13/18), lymph nodes (11/18) and bone (6/18). 12/18 pts had two or more sites of metastasis and 11/18 pts were previously treated. There were no grade 4 toxicities or toxic deaths, but 3 of the 13 pts evaluated for toxicity had grade 3 fatigue. Other grade 3 toxicities seen were neutropenia, thrombocytopenia, infection, constipation, paresthesias, dizziness and leg pain. Grade 1 or 2 toxicities included lymphocytopenia in 7/13 pts, leucopenia in 6/13 pts and anorexia in 5/13 pts. Neutropenia, anemia and skin rash were each observed in 4/13 pts. Other Grade 1 and 2 toxicities, seen in less than 25% of pts, included constipation, drowsiness, paresthesias, fatigue, palmar erythema, shortness of breath, chills, itching, rise in creatinine, hyponatremia, hyperkalemia, hypercalcemia and hypoalbuminemia. Most pts did not discontinue treatment because of toxicity but rather progressive disease. 1 of the 12 pts evaluable for response had stable disease and received a total of 9 cycles. This patient had been heavily pre-treated. Conclusions: The toxicity of this combination is modest. To date, there have been no objective responses to this particular dose and schedule of interferon-alpha and thalidomide in the limited number of pre-treated (7) and untreated (5) pts evaluated. Author Disclosure Employment or Leadership Consultant or Advisory Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Celgene Celgene
Potential Usefulness of Leukotriene B4 (LTB4) on Mobilization of Hematopoietic Progenitor Cells (HPC).
Authors: Yeung-Chul Mun, Seung-Eun Lee, Kyung-Eun Lee, Eun-Sun Yoo, Eun Suk Kang, Sang min Lee, Jee-Young Ahn, Yun-Kyung Bae, Geun-Young Kim, Soon Nam Lee, Wha-Sun Chung, Min Kyoung Kim, Myung Soo Hyun, Jae-Hong Kim, Chu-Myong Seong
Journal: Blood (2005)