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Jeffrey Crawford

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Jeffrey Crawford and George M. Rodgers

Myeloid growth factors can reduce the risk of chemotherapy-induced neutropenia (CIN) and thus impact the survival of patients with cancer. Patients should be assessed for risk, taking into consideration patient-related risk factors and chemotherapy regimens. Patients stratified as having at least a 20% risk for CIN should be considered for prophylactic growth factors. The NCCN Guidelines for Myeloid Growth Factors provide category 1 recommendations for the daily use of filgrastim, tbo-filgrastim, and pegfilgrastim. Cancer-related anemia can be treated with erythropoiesis-stimulating agents, red blood cell transfusion, or intravenous iron.

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David C. Dale, Gordon C. McCarter, Jeffrey Crawford and Gary H. Lyman

Delivery of cancer chemotherapy is often limited by myelotoxicity, primarily neutropenia. As part of an effort to create a model to predict the risk of chemotherapy-induced neutropenia, we reviewed the reports of randomized clinical trials with more than 50 patients per arm in early-stage breast cancer (ESBC) and non-Hodgkin's lymphoma (NHL) published between 1990 and 2000. We observed that no hematologic toxicity data were reported in 39% and 34% of the ESBC and NHL trials, respectively. The remaining trials reported on hematologic toxicity in 16 different ways. When reported, rates of neutropenia, leukopenia, and hematotoxicity varied widely with the same and similar chemotherapy regimens. Dose-intensity data were not reported in 39% and 54% of ESBC and NHL trials, respectively. The majority of the remaining studies reported incomplete dose-intensity data such as percentages of patients completing all cycles or receiving a given percentage of planned dose intensity. Only 28% reported the mean or median relative dose intensity received by patients. Based on this review, we conclude that current practices for reporting chemotherapy treatments are inadequate for describing the risk of chemotherapy to patients or for quantitatively assessing the risk of treatment alternatives. We recommend that standard procedures for documenting and reporting hematologic toxicity and dose intensity in cancer chemotherapy trials be required for publication of chemotherapy trials.

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Jeffrey Crawford, David C. Dale, Nicole M. Kuderer, Eva Culakova, Marek S. Poniewierski, Debra Wolff and Gary H. Lyman

This study was undertaken to describe the relationship between the occurrence and timing of neutropenic events and chemotherapy treatment in a community-based population of patients with cancer. The study included 2962 patients with breast, lung, colorectal, lymphoma, and ovarian cancers from a prospective U.S. registry of patients initiating a new chemotherapy regimen. Detailed patient-, disease-, and treatment-related data, including toxicities, were captured at baseline, the beginning of each cycle, and each midcycle blood draw for up to 4 cycles of treatment. Primary outcomes included febrile neutropenia (FN), severe neutropenia without fever/infection, and relative dose intensity (RDI). Thirty-seven percent of patients were aged 65 years or older, 43.5% had an Eastern Cooperative Oncology Group performance status of 1 or greater, and 27% had 1 or more comorbidities. Reductions in RDI to less than 85% of standard in the first cycle were planned in 23.6% of patients, whereas primary colony-stimulating factor prophylaxis was used in 18.2%. In the first 3 cycles of treatment, 10.7% of patients experienced FN, with most of these events (58.9%) occurring in the first cycle. This first-cycle pattern was consistently observed despite wide variations in event rates by tumor type, disease stage, chemotherapy regimen and dose, and patient characteristics. Despite frequent planned reductions from standard RDI, the incidence of FN remains high in community oncology practice in the United States. Improved methods of pretreatment assessment of patient risk factors for neutropenia are needed.

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Katy Winckworth-Prejsnar, Elizabeth A. Nardi, Lisa Korin Lentz, Jeffrey A. Crawford, C. Lyn Fitzgerald and Robert W. Carlson

Molecular testing and biosimilars offer the potential for increased access to targeted treatment options and reduction in healthcare costs, but come with significant challenges in ensuring patient access to innovation in cancer care while maintaining safe, effective, ethical, and affordable treatment options. As providers, payers, patients, and the larger healthcare systems become inundated with a wide variety of molecular diagnostics and an increased number of biosimilars coming to market, it will be important to understand regulatory guidance and policy implications relating to the appropriateness of molecular testing and the clinical use of biosimilars in cancer care. In September 2016, NCCN hosted the Molecular Testing and Biosimilars Policy Summit to address the challenges, issues, and opportunities in both the molecular testing and biosimilar landscapes. Keynote presentations and panelists further discussed the status and future of molecular testing and biosimilars within the oncology space, as well as patient access and education needs moving forward.

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Jeffrey Crawford, Jeffrey Allen, James Armitage, Douglas W. Blayney, Spero R. Cataland, Mark L. Heaney, Sally Htoy, Susan Hudock, Dwight D. Kloth, David J. Kuter, Gary H. Lyman, Brandon McMahon, David P. Steensma, Saroj Vadhan-Raj, Peter Westervelt and Michael Westmoreland

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Mary B. Daly, Jennifer E. Axilbund, Saundra Buys, Beth Crawford, Carolyn D. Farrell, Susan Friedman, Judy E. Garber, Salil Goorha, Stephen B. Gruber, Heather Hampel, Virginia Kaklamani, Wendy Kohlmann, Allison Kurian, Jennifer Litton, P. Kelly Marcom, Robert Nussbaum, Kenneth Offit, Tuya Pal, Boris Pasche, Robert Pilarski, Gwen Reiser, Kristen Mahoney Shannon, Jeffrey R. Smith, Elizabeth Swisher and Jeffrey N. Weitzel

Overview All cancers develop as a result of mutations in certain genes, such as those involved in the regulation of cell growth and/or DNA repair,1,2 but not all of these mutations are inherited from a parent. For example, sporadic mutations can occur in somatic/tumor cells only, and de novo mutations can occur for the first time in a germ cell (i.e., egg or sperm) or in the fertilized egg itself during early embryogenesis. However, family studies have long documented an increased risk for several forms of cancer among first-degree (i.e., parents, siblings, and children) and second-degree relatives (i.e., grandparents, aunts or uncles, grandchildren, and nieces or nephews) of affected individuals. These individuals may have an increased susceptibility to cancer as the result of 1 or more gene mutations present in parental germline cells; cancers developing in these individuals may be classified as hereditary or familial cancers. Hereditary cancers are often characterized by mutations associated with a high probability of cancer development (i.e., a high penetrance genotype), vertical transmission through either mother or father, and an association with other types of tumors.3,4 They often have an early age of onset and exhibit an autosomal dominant inheritance pattern (i.e., occur when the individual has a mutation in only 1 copy of a gene). Familial cancers share only some features of hereditary cancers. For example, although familial breast cancers occur in a given family more frequently than in the general population, they generally do not exhibit the inheritance patterns or onset age consistent...
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Mary B. Daly, Robert Pilarski, Jennifer E. Axilbund, Saundra S. Buys, Beth Crawford, Susan Friedman, Judy E. Garber, Carolyn Horton, Virginia Kaklamani, Catherine Klein, Wendy Kohlmann, Allison Kurian, Jennifer Litton, Lisa Madlensky, P. Kelly Marcom, Sofia D. Merajver, Kenneth Offit, Tuya Pal, Boris Pasche, Gwen Reiser, Kristen Mahoney Shannon, Elizabeth Swisher, Nicoleta C. Voian, Jeffrey N. Weitzel, Alison Whelan, Georgia L. Wiesner, Mary A. Dwyer and Rashmi Kumar

During the past few years, several genetic aberrations that may contribute to increased risks for development of breast and/or ovarian cancers have been identified. The NCCN Guidelines for Genetic/Familial High-Risk Assessment: Breast and Ovarian focus specifically on the assessment of genetic mutations in BRCA1/BRCA2, TP53, and PTEN, and recommend approaches to genetic testing/counseling and management strategies in individuals with these mutations. This portion of the NCCN Guidelines includes recommendations regarding diagnostic criteria and management of patients with Cowden Syndrome/PTEN hamartoma tumor syndrome.

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Jeffrey Crawford, James Armitage, Lodovico Balducci, Pamela Sue Becker, Douglas W. Blayney, Spero R. Cataland, Mark L. Heaney, Susan Hudock, Dwight D. Kloth, David J. Kuter, Gary H. Lyman, Brandon McMahon, Hope S. Rugo, Ayman A. Saad, Lee S. Schwartzberg, Sepideh Shayani, David P. Steensma, Mahsa Talbott, Saroj Vadhan-Raj, Peter Westervelt, Michael Westmoreland, Mary Dwyer and Maria Ho

Febrile neutropenia, a common side effect of myelosuppressive chemotherapy in patients with cancer, can result in prolonged hospitalization and broad-spectrum antibiotic use, often prompting treatment delays or dose reductions of drug regimens. Prophylactic use of myeloid growth factors (mainly the colony-stimulating factors filgrastim and pegfilgrastim) in patients of heightened risk can reduce the severity and duration of febrile neutropenia. The NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Myeloid Growth Factors provide recommendations on the use of these agents mainly in the oncology setting based on clinical evidence and expert consensus. This version includes revisions surrounding the issue of timing of pegfilgrastim administration. It also includes new sections on tbo-filgrastim, a recently approved agent that is biologically similar to filgrastim, and the role of myeloid growth factors in the hematopoietic cell transplant setting

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Jeffrey Crawford, James Armitage, Lodovico Balducci, Charles Bennett, Douglas W. Blayney, Spero R. Cataland, David C. Dale, George D. Demetri, Harry P. Erba, James Foran, Alison G. Freifeld, Marti Goemann, Mark L. Heaney, Sally Htoy, Susan Hudock, Dwight D. Kloth, David J. Kuter, Gary H. Lyman, Laura Boehnke Michaud, Sarah C. Miyata, Martin S. Tallman, Saroj Vadhan-Raj, Peter Westervelt and Michael K. Wong

Myeloid Growth Factors Clinical Practice Guidelines in Oncology NCCN Categories of Evidence and Consensus Category 1: The recommendation is based on high-level evidence (e.g., randomized controlled trials) and there is uniform NCCN consensus. Category 2A: The recommendation is based on lower-level evidence and there is uniform NCCN consensus. Category 2B: The recommendation is based on lower-level evidence and there is nonuniform NCCN consensus (but no major disagreement). Category 3: The recommendation is based on any level of evidence but reflects major disagreement. All recommendations are category 2A unless otherwise noted. Clinical trials: The NCCN believes that the best management for any cancer patient is in a clinical trial. Participation in clinical trials is especially encouraged. Overview Neutropenia (< 500 neutrophils/mcL or < 1000 neutrophils/mcL and a predicted decline to ≤ 500/mcL over the next 48 hours) and resulting febrile neutropenia (FN; ≥ 38.3°C orally or ≥ 38.0°C over 1 hour) can be induced by myelosuppressive chemotherapy. FN is a major dose-limiting toxicity of chemotherapy, often necessitating hospitalization for evaluation and empiric broad-spectrum antibiotics. These complications often result in dose reductions or treatment delays, which may compromise clinical outcomes. The prophylactic use of colony-stimulating factors (CSFs) can reduce the risk, severity, and duration of FN. Despite these benefits, CSFs are not administered to all patients under going myelosuppressive chemotherapy because of the costs associated with routine use. Selective use of CSFs in patients at increased risk for neutropenic complications may, however, enhance cost-effectiveness by directing treatment toward patients most likely to...