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  • Author: Kenneth B. Roberts x
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Erin Currin, Lanell M. Peterson, Erin K. Schubert, Jeanne M. Link, Kenneth A. Krohn, Robert B. Livingston, David A. Mankoff and Hannah M. Linden

Changes in estrogen receptor (ER) expression over the course of therapy may affect response to endocrine therapy. However, measuring temporal changes in ER expression requires serial biopsies, which are impractical and poorly tolerated by most patients. Functional ER imaging using 18F-fluoroestradiol (FES)-PET provides a noninvasive measure of regional ER expression and is ideally suited to serial studies. Additionally, lack of measurable FES uptake in metastatic sites of disease predict tumor progression in patients with ER-positive primary tumors treated with endocrine therapy. This report presents a case of restored sensitivity to endocrine therapy in a patient with bone-dominant breast cancer who underwent serial observational FES-PET imaging over the course of several treatments at our center, demonstrating the temporal heterogeneity of regional ER expression. Although loss and restoration of endocrine sensitivity in patients who have undergone prior hormonal and cytotoxic treatments has been reported, this is, to our knowledge, the first time the accompanying changes in ER expression have been documented by molecular imaging.

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Jacob P. Laubach, Constantine S. Mitsiades, Anuj Mahindra, Marlise R. Luskin, Jacalyn Rosenblatt, Irene M. Ghobrial, Robert L. Schlossman, David Avigan, Noopur Raje, Nikhil C. Munshi, Kenneth C. Anderson and Paul G. Richardson

Despite significant progress in the treatment of multiple myeloma (MM) over the past decade, this disease remains incurable and almost all patients ultimately experience relapse and become refractory to treatment over time. However, the outlook for patients with relapsed MM has improved markedly with the use of the immunomodulatory drugs thalidomide and lenalidomide, and the proteasome inhibitor bortezomib. Moreover, the development of new drug classes based on preclinical rationale and the introduction of next-generation agents is likely to further expand treatment options and improve outcomes for relapsed MM.

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Jacob P. Laubach, Constantine S. Mitsiades, Anuj Mahindra, Robert L. Schlossman, Teru Hideshima, Dharminder Chauhan, Nicole A. Carreau, Irene M. Ghobrial, Noopur Raje, Nikhil C. Munshi, Kenneth C. Anderson and Paul G. Richardson

Multiple myeloma (MM) is a clonal B-cell malignancy characterized by aberrant expansion of plasma cells within bone marrow and extramedullary sites. In 2009, 20,580 new cases of MM and 10,580 deaths from the disease occurred in the United States. Treatment traditionally consists of systemic chemotherapy, with adjunctive use of radiation or surgery in selected cases associated with extramedullary disease. The therapeutic landscape in MM has changed markedly in the past decade with the introduction of the novel immunomodulatory agents thalidomide and lenalidomide, and the first-in-class proteasome inhibitor bortezomib. Although MM remains an incurable malignancy, new approaches to therapy incorporating these agents have produced significantly higher response rates and improved intervals of both progression-free and overall survival in the context of randomized, controlled trials. In aggregate, the use of novel therapies in MM has been associated with substantial improvements in patient outcome.

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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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Therese B. Bevers, Deborah K. Armstrong, Banu Arun, Robert W. Carlson, Kenneth H. Cowan, Mary B. Daly, Irvin Fleming, Judy E. Garber, Mary Gemignani, William J. Gradishar, Helen Krontiras, Swati Kulkarni, Christine Laronga, Loretta Loftus, Deborah J. MacDonald, Martin C. Mahoney, Sofia D. Merajver, Ingrid Meszoely, Lisa Newman, Elizabeth Pritchard, Victoria Seewaldt, Rena V. Sellin, Charles L. Shapiro and John H. Ward

Breast cancer is the most commonly diagnosed cancer in American women with 209,060 and 54,010 estimated cases of invasive breast cancer and female carcinoma in situ, respectively, in 2010. Approximately 39,840 women will die of breast cancer in the United States in 2010.1Risk factors for the development of breast cancer can be grouped into categories, including familial/genetic factors (family history, known or suspected BRCA1/2, TP53, PTEN, or other gene mutation associated with breast cancer risk); factors related to demographics (e.g., age, ethnicity/race); reproductive history (age at menarche, parity, age at first live birth, age at menopause); environmental factors (prior thoracic irradiation before age 30 years [e.g., to treat Hodgkin disease], hormone replacement therapy [HRT], alcohol consumption); and other factors (e.g., number of breast biopsies, atypical hyperplasia or lobular carcinoma in situ [LCIS], breast density, body mass index).Estimating breast cancer risk for the individual woman is difficult, and most breast cancers are not attributable to risk factors other than female gender and increased age. The development of effective strategies for the reduction of breast cancer incidence has also been difficult because few of the existing risk factors are modifiable and some of the potentially modifiable risk factors have social implications extending beyond concerns for breast cancer (e.g., age at first live birth). Nevertheless, effective breast cancer risk reduction agents/strategies, such as tamoxifen, raloxifene, and risk reduction surgery, have been identified. However, women and their physicians who are considering interventions to reduce risk for breast cancer must balance the demonstrated...
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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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Mary B. Daly, Robert Pilarski, Jennifer E. Axilbund, Michael Berry, Saundra S. Buys, Beth Crawford, Meagan Farmer, Susan Friedman, Judy E. Garber, Seema Khan, Catherine Klein, Wendy Kohlmann, Allison Kurian, Jennifer K. Litton, Lisa Madlensky, P. Kelly Marcom, Sofia D. Merajver, Kenneth Offit, Tuya Pal, Huma Rana, Gwen Reiser, Mark E. Robson, Kristen Mahoney Shannon, Elizabeth Swisher, Nicoleta C. Voian, Jeffrey N. Weitzel, Alison Whelan, Myra J. Wick, Georgia L. Wiesner, Mary Dwyer, Rashmi Kumar and Susan Darlow

The NCCN Guidelines for Genetic/Familial High-Risk Assessment: Breast and Ovarian provide recommendations for genetic testing and counseling and risk assessment and management for hereditary cancer syndromes. Guidelines focus on syndromes associated with an increased risk of breast and/or ovarian cancer and are intended to assist with clinical and shared decision-making. These NCCN Guidelines Insights summarize major discussion points of the 2015 NCCN Genetic/Familial High-Risk Assessment: Breast and Ovarian panel meeting. Major discussion topics this year included multigene testing, risk management recommendations for less common genetic mutations, and salpingectomy for ovarian cancer risk reduction. The panel also discussed revisions to genetic testing criteria that take into account ovarian cancer histology and personal history of pancreatic cancer.

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Mary B. Daly, Robert Pilarski, Michael Berry, Saundra S. Buys, Meagan Farmer, Susan Friedman, Judy E. Garber, Noah D. Kauff, Seema Khan, Catherine Klein, Wendy Kohlmann, Allison Kurian, Jennifer K. Litton, Lisa Madlensky, Sofia D. Merajver, Kenneth Offit, Tuya Pal, Gwen Reiser, Kristen Mahoney Shannon, Elizabeth Swisher, Shaveta Vinayak, Nicoleta C. Voian, Jeffrey N. Weitzel, Myra J. Wick, Georgia L. Wiesner, Mary Dwyer and Susan Darlow

The NCCN Clinical Practice Guidelines in Oncology for Genetic/Familial High-Risk Assessment: Breast and Ovarian provide recommendations for genetic testing and counseling for hereditary cancer syndromes and risk management recommendations for patients who are diagnosed with a syndrome. Guidelines focus on syndromes associated with an increased risk of breast and/or ovarian cancer. The NCCN Genetic/Familial High-Risk Assessment: Breast and Ovarian panel meets at least annually to review comments from reviewers within their institutions, examine relevant new data from publications and abstracts, and reevaluate and update their recommendations. The NCCN Guidelines Insights summarize the panel's discussion and most recent recommendations regarding risk management for carriers of moderately penetrant genetic mutations associated with breast and/or ovarian cancer.

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Jaffer A. Ajani, David J. Bentrem, Stephen Besh, Thomas A. D’Amico, Prajnan Das, Crystal Denlinger, Marwan G. Fakih, Charles S. Fuchs, Hans Gerdes, Robert E. Glasgow, James A. Hayman, Wayne L. Hofstetter, David H. Ilson, Rajesh N. Keswani, Lawrence R. Kleinberg, W. Michael Korn, A. Craig Lockhart, Kenneth Meredith, Mary F. Mulcahy, Mark B. Orringer, James A. Posey, Aaron R. Sasson, Walter J. Scott, Vivian E. Strong, Thomas K. Varghese Jr, Graham Warren, Mary Kay Washington, Christopher Willett, Cameron D. Wright, Nicole R. McMillian and Hema Sundar

The NCCN Clinical Practice Guidelines in Oncology for Gastric Cancer provide evidence- and consensus-based recommendations for a multidisciplinary approach for the management of patients with gastric cancer. For patients with resectable locoregional cancer, the guidelines recommend gastrectomy with a D1+ or a modified D2 lymph node dissection (performed by experienced surgeons in high-volume centers). Postoperative chemoradiation is the preferred option after complete gastric resection for patients with T3-T4 tumors and node-positive T1-T2 tumors. Postoperative chemotherapy is included as an option after a modified D2 lymph node dissection for this group of patients. Trastuzumab with chemotherapy is recommended as first-line therapy for patients with HER2-positive advanced or metastatic cancer, confirmed by immunohistochemistry and, if needed, by fluorescence in situ hybridization for IHC 2+.

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NCCN Guidelines Insights: B-Cell Lymphomas, Version 3.2019

Featured Updates to the NCCN Guidelines

Andrew D. Zelenetz, Leo I. Gordon, Jeremy S. Abramson, Ranjana H. Advani, Nancy L. Bartlett, Paolo F. Caimi, Julie E. Chang, Julio C. Chavez, Beth Christian, Luis E. Fayad, Martha J. Glenn, Thomas M. Habermann, Nancy Lee Harris, Francisco Hernandez-Ilizaliturri, Mark S. Kaminski, Christopher R. Kelsey, Nadia Khan, Susan Krivacic, Ann S. LaCasce, Amitkumar Mehta, Auayporn Nademanee, Rachel Rabinovitch, Nishitha Reddy, Erin Reid, Kenneth B. Roberts, Stephen D. Smith, Erin D. Snyder, Lode J. Swinnen, Julie M. Vose, Mary A. Dwyer and Hema Sundar

Diffuse large B-cell lymphomas (DLBCLs) and follicular lymphoma (FL) are the most common subtypes of B-cell non-Hodgkin’s lymphomas in adults. Histologic transformation of FL to DLBCL (TFL) occurs in approximately 15% of patients and is generally associated with a poor clinical outcome. Phosphatidylinositol 3-kinase (PI3K) inhibitors have shown promising results in the treatment of relapsed/refractory FL. CAR T-cell therapy (axicabtagene ciloleucel and tisagenlecleucel) has emerged as a novel treatment option for relapsed/refractory DLBCL and TFL. These NCCN Guidelines Insights highlight important updates to the NCCN Guidelines for B-Cell Lymphomas regarding the treatment of TFL and relapsed/refractory FL and DLBCL.