Cancer

Kushner, Brian H.; Roberts, Stephen S.; Friedman, Danielle N.; Kuk, Deborah; Ostrovnaya, Irina; Modak, Shakeel; Kramer, Kim; Basu, Ellen M.; Cheung, Nai‐Kong V.

doi: 10.1002/cncr.29316pmid: 25728463

BACKGROUND Osteochondromas are benign bony protrusions that can be spontaneous or associated with radiotherapy (RT). Current treatment of high‐risk neuroblastoma includes dose‐intensive chemotherapy, local RT, an anti‐GD2 monoclonal antibody (MoAb), and isotretinoin. Late effects are emerging. METHODS The authors examined osteochondromas in 362 patients who were aged <10 years when diagnosed with neuroblastoma, had received a MoAb plus isotretinoin since 2000, and had survived >24 months from the time of the first dose of the MoAb. The incidence rate of osteochondroma was determined using the competing risks approach, in which the primary event was osteochondroma calculated from the date of neuroblastoma diagnosis and the competing event was death without osteochondroma. RESULTS A total of 21 osteochondroma cases were found among 14 patients who were aged 5.7 to 15.3 years (median, 10.4 years) and 3.1 to 11.2 years (median, 8.2 years) from the time of neuroblastoma diagnosis. The cumulative incidence rate was 0.6% at 5 years and 4.9% at 10 years from the neuroblastoma diagnosis. Nine osteochondromas were revealed incidentally during assessments of neuroblastoma disease status or bone age. Thirteen osteochondromas were detected outside RT portals and had characteristics of spontaneous forms. Complications were limited to pain necessitating surgical resection in 3 patients, but follow‐up was short at 0.3 to 7.7 years (median, 3.5 years). CONCLUSIONS Osteochondromas in long‐term survivors of neuroblastoma should be expected because these benign growths can be related to RT and these patients undergo radiologic studies over years, are monitored for late toxicities through and beyond adolescence, and receive special attention (because of concerns about disease recurrence) if they develop a bony protuberance. A pathogenic role for chemotherapy, anti‐GD2 MoAbs, or isotretinoin remains speculative. Cancer 2015. © 2015 American Cancer Society. Cancer 2015;121:2090–2096. © 2015 American Cancer Society.

Dean, Jennifer B.; Dome, Jeffrey S.

doi: 10.1002/cncr.29281pmid: 25712509

Chu, Haiyan; Xia, Liping; Qiu, Xiaonan; Gu, Dongying; Zhu, Linjun; Jin, Jing; Hui, Gaoyun; Hua, Qiuhan; Du, Mulong; Tong, Na; Chen, Jinfei; Zhang, Zhengdong; Wang, Meilin

doi: 10.1002/cncr.29314pmid:

Grant, William B.

doi: 10.1002/cncr.29276pmid: 25678245

Lamanna, Nicole

doi: 10.1002/cncr.29130pmid: 25690403

There has been a dramatic change in therapy for chronic lymphocytic leukemia (CLL) over the last 20 years. In 1990, available therapy produced complete responses in <5% of treated patients. This is in marked contrast to modern regimens, which are reported to reliably produce complete responses in approximately 40% to 50% of patients. This remarkable improvement has been attributable to combination chemoimmunotherapy agents that have contributed to the backbone of therapy for patients with CLL. However, the disease is still incurable and these modern treatment regimens have been somewhat limited to the treatment of younger, physically “fit” patients with CLL due to their increased toxicity, including enhanced myelosuppression and immunosuppression. In addition, because patients receive multiple therapies during the course of their lifetime, the mounting toxicities as well as decreased efficacy often limit the repeated use of these more aggressive combination therapies. Fortunately, over the past 5 years, there has been an explosion of new active agents that have demonstrated remarkable activity in patients with recurrent/refractory disease as well as those who harbor poor cytogenetic abnormalities. The current review focuses on some of the novel small molecules that have either been approved or are at the forefront of clinical development in the treatment of patients with CLL. Cancer 2015;121:1917–1926. © 2015 American Cancer Society.

Printz, Carrie

doi: 10.1002/cncr.29476pmid: 26042851

Sun, Weili; Gaynon, Paul S.; Sposto, Richard; Wayne, Alan S.

doi: 10.1002/cncr.29267pmid: 25678105

Leukemia is the most common pediatric cancer. Despite great progress in the development of curative therapy, leukemia remains a leading cause of death from disease in childhood, and survivors are at life‐long risk of complications of treatment. New agents are needed to further increase cure rates and decrease treatment‐associated toxicities. The complex biology and aggressive nature of childhood leukemia, coupled with the relatively small patient population available for study, pose specific challenges to the development of new therapies. In this review, the authors discuss strategies and initiatives designed to improve access to new agents in the treatment of pediatric leukemia. Cancer 2015;121:1927–1936. © 2015 American Cancer Society.

Printz, Carrie

doi: 10.1002/cncr.29477pmid: 26042853

Reuschenbach, Miriam; Huebbers, Christian U.; Prigge, Elena‐Sophie; Bermejo, Justo Lorenzo; Kalteis, Martin S.; Preuss, Simon F.; Seuthe, Inga M.C.; Kolligs, Jutta; Speel, Ernst‐Jan M.; Olthof, Nadine; Kremer, Bernd; Wagner, Steffen; Klussmann, Jens P.; Vinokurova, Svetlana;

Ademuyiwa, Foluso O.

doi: 10.1002/cncr.29280pmid: 25678364