Nurses Alumni Association Bulletin, Fall 1993

Annual Meeting Calendar Inside Front & Back Cover 1994 Annual Luncheon-Meeting Notice. Inside Front & Back Cover 1993-1994 Meeting Dates Officers and Committee Chairs Bulletin Publication Committee The President\u27s Message Treasurer\u27s Report News About and From Our Graduates Seize the Day Psychology and Nursing Fiftieth Anniversary Resume of Minutes of Alumni Association Meetings Tribute to Mabel C. Prevost The Decade Fund Nursing Scholarship Happy Birthday Alumni Office News Jefferson Alumni Identification Card Committee Reports Bulletin Social Relief Fund Scholarship Finance In Memoriam, Names of Deceased Graduates Luncheon Photos Class News Relief Fund Application Scholarship Application Membership Application Pins, Transcripts, Class Address Lists, Change of Address For

Nurses Alumni Association Bulletin, Fall 1994

1994-1995 Meeting Dates Calendar 1995 Annual Luncheon - Meeting Notice Officers and Committee Chairs Bulletin Publication Committee 1994-1995 Meeting Dates Calendar The President\u27s Message Treasurer\u27s Report News About Our Graduates Fiftieth Anniversary Resume of Minutes of Alumni Association Meetings Department of Nursing 1993-1994 Alumni Office News Jefferson 2000 Fund The Women\u27s Center for Health Promotion Discount Parking for Alumni Cadet Nurse Corps Medical Anecdotes of Faith Ukranian-American Teacher Exchange Happy Birthday Committee Reports In Memoriam, Names of Deceased Graduates Luncheon Photos Class News Jefferson Alumni Identification Card Relief Fund Application Scholarship Application Membership Application Pins, Transcripts, Class Address Lists, Change of address Forms Campus Ma

Retreatment with brentuximab vedotin in patients with CD30-positive hematologic malignancies

BACKGROUND: Brentuximab vedotin is a CD30-directed antibody-drug conjugate. Retreatment with brentuximab vedotin monotherapy was investigated in patients with CD30-positive Hodgkin lymphoma (HL) or systemic anaplastic large cell lymphoma (ALCL) who relapsed after achieving complete or partial remission (CR or PR) with initial brentuximab vedotin therapy in a previous study (ClinicalTrials.gov NCT00947856). METHODS: Twenty-one patients with HL and 8 patients with systemic ALCL were retreated; 3 patients with systemic ALCL were retreated twice. Patients generally received brentuximab vedotin 1.8 mg/kg intravenously approximately every 3 weeks over 30 minutes as an outpatient infusion. The primary objectives of this study were to assess safety and to estimate antitumor activity of brentuximab vedotin retreatment. RESULTS: The objective response rate was 60% (30% CR) in HL patients and 88% (63% CR) in systemic ALCL patients. The estimated median duration of response for patients with an objective response was 9.5 months (range, 0.0+ to 28.0+ months) at the time of study closure. Of the 19 patients with objective response, 7 patients had not had an event of disease progression or death at the time of study closure; duration of response for these patients ranged from 3.5 to 28 months. Of the 11 patients with CR, 45% had response durations of over 1 year. Adverse events (AEs) occurring in ≥25% of patients during the retreatment period were generally similar in type and frequency to those observed in the pivotal trials of brentuximab vedotin monotherapy, with the exception of peripheral neuropathy, which is known to have a cumulative effect. Grade 3 or higher events were observed in 48% of patients; these were generally transient and managed by dose modifications or delays. Deaths due to AEs occurred in 3 HL patients; none were considered to be related to brentuximab vedotin retreatment. DISCUSSION: With the exception of a higher rate of peripheral motor neuropathy, retreatment with brentuximab vedotin was associated with similar side effects seen in the pivotal trials. CONCLUSIONS: Retreatment with brentuximab vedotin monotherapy is associated with response rates in 68% (39% CR) of patients with relapsed HL and systemic ALCL. TRIAL REGISTRATION: United States registry and results database ClinicalTrials.gov NCT00947856

Clinical Trials and Medical Care: Defining the Therapeutic Misconception

A key component of informed consent to participate in medical research includes understanding that research is not the same as treatment

Nurses Alumni Association Bulletin, Fall 1995

1995-1996 Meeting Dates Calendar 1996 Annual Luncheon-Meeting Notice Officers and Committee Chairs Bulletin Publication Committee 1995-1996 Meeting Dates Calendar The President\u27s Message Financial Report What\u27s New Fiftieth Anniversary Resume of Minutes of Alumni Association Meetings Scholarship Funds at Work CAHS Alumni Board/Diploma School Alumni Office News Jefferson Health System Oldest Veteran Dies 1OOth Anniversary Pearl Harbor Remembered Memories Janet Hindson Retires Happy Birthday Scholarship Fund donors for 1994 Committee Reports By-Laws Development Bulletin Relief Fund Satellite Social Scholarship In Memoriam, Names of Deceased Graduates Class News Luncheon Photos Jefferson Alumni Identification Card The Diploma School of Nursing Alumni Association-Mabel C. Prevost Letter of Appreciation Tribute To a Mother An End Must Come Stuff For Senior Citizens to Chuckle Over Membership Application Relief Fund Application To Order: A Chronological History and Alumni Directory From TJU Bookstore Scholarship Fund Application Pins, Transcripts, Class Address List, Change of Address Forms, Alumni Identification Card Campus Map Picture - Class of 1893-189

Phase 1 trial of rituximab, lenalidomide, and ibrutinib in previously untreated follicular lymphoma: Alliance A051103

Chemoimmunotherapy in follicular lymphoma is associated with significant toxicity. Targeted therapies are being investigated as potentially more efficacious and tolerable alternatives for this multiply-relapsing disease. Based on promising activity with rituximab and lenalidomide in previously untreated follicular lymphoma (overall response rate [ORR] 90%-96%) and ibrutinib in relapsed disease (ORR 30%-55%), the Alliance for Clinical Trials in Oncology conducted a phase 1 trial of rituximab, lenalidomide, and ibrutinib. Previously untreated patients with follicular lymphoma received rituximab 375 mg/m 2 on days 1, 8, 15, and 22 of cycle 1 and day 1 of cycles 4, 6, 8, and 10; lenalidomide as per cohort dose on days 1 to 21 of 28 for 18 cycles; and ibrutinib as per cohort dose daily until progression. Dose escalation used a 3+3 design from a starting dose level (DL) of lenalidomide 15 mg and ibrutinib 420 mg (DL0) to DL2 (lenalidomide 20 mg, ibrutinib 560 mg). Twenty-two patients were enrolled; DL2 was determined to be the recommended phase II dose. Although no protocol-defined dose-limiting toxicities were reported, a high incidence of rash was observed (all grades 82%, grade 3 36%). Eleven patients (50%) required dose reduction, 7 because of rash. The ORR for the entire cohort was 95%, and the 12-month progression-free survival was 80% (95% confidence interval, 57%-92%). Five patients developed new malignancies; 3 had known risk factors before enrollment. Given the increased toxicity and required dose modifications, as well as the apparent lack of additional clinical benefit to the rituximab-lenalidomide doublet, further investigation of the regimen in this setting seems unwarranted. The study was registered with www.ClinicalTrials.gov as #NCT01829568

Aptamer-based multiplexed proteomic technology for biomarker discovery

Interrogation of the human proteome in a highly multiplexed and efficient manner remains a coveted and challenging goal in biology. We present a new aptamer-based proteomic technology for biomarker discovery capable of simultaneously measuring thousands of proteins from small sample volumes (15 [mu]L of serum or plasma). Our current assay allows us to measure ~800 proteins with very low limits of detection (1 pM average), 7 logs of overall dynamic range, and 5% average coefficient of variation. This technology is enabled by a new generation of aptamers that contain chemically modified nucleotides, which greatly expand the physicochemical diversity of the large randomized nucleic acid libraries from which the aptamers are selected. Proteins in complex matrices such as plasma are measured with a process that transforms a signature of protein concentrations into a corresponding DNA aptamer concentration signature, which is then quantified with a DNA microarray. In essence, our assay takes advantage of the dual nature of aptamers as both folded binding entities with defined shapes and unique sequences recognizable by specific hybridization probes. To demonstrate the utility of our proteomics biomarker discovery technology, we applied it to a clinical study of chronic kidney disease (CKD). We identified two well known CKD biomarkers as well as an additional 58 potential CKD biomarkers. These results demonstrate the potential utility of our technology to discover unique protein signatures characteristic of various disease states. More generally, we describe a versatile and powerful tool that allows large-scale comparison of proteome profiles among discrete populations. This unbiased and highly multiplexed search engine will enable the discovery of novel biomarkers in a manner that is unencumbered by our incomplete knowledge of biology, thereby helping to advance the next generation of evidence-based medicine

Cancer therapy shapes the fitness landscape of clonal hematopoiesis.

Acquired mutations are pervasive across normal tissues. However, understanding of the processes that drive transformation of certain clones to cancer is limited. Here we study this phenomenon in the context of clonal hematopoiesis (CH) and the development of therapy-related myeloid neoplasms (tMNs). We find that mutations are selected differentially based on exposures. Mutations in ASXL1 are enriched in current or former smokers, whereas cancer therapy with radiation, platinum and topoisomerase II inhibitors preferentially selects for mutations in DNA damage response genes (TP53, PPM1D, CHEK2). Sequential sampling provides definitive evidence that DNA damage response clones outcompete other clones when exposed to certain therapies. Among cases in which CH was previously detected, the CH mutation was present at tMN diagnosis. We identify the molecular characteristics of CH that increase risk of tMN. The increasing implementation of clinical sequencing at diagnosis provides an opportunity to identify patients at risk of tMN for prevention strategies