ONJ has been increasingly suspected to be a potential complication of bisphosphonate therapy in recent years. Thus, the ASBMR leadership appointed a multidisciplinary task force to address key questions related to case definition, epidemiology, risk factors, diagnostic imaging, clinical management, and future areas for research related to the disorder. This report summarizes the findings and recommendations of the task force.

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In human cancers, bone is a common site for metastasis. It is well known that metastasis is the cause of morbidity and mortality in patients with cancer. Both breast and prostate carcinomas have a propensity to metastasize to bone. In general, metastatic breast cancers result in osteolytic lesions. On the other hand, prostate cancer metastases are osteoblastic and result in osteosclerosis. Thus, bone formation and bone resorption are at the crux of the cancer metastasis problem. For example, in the prostate, there is a vicious cycle of metastasis to bone (Fig. 1). Metastases to bone causes excruciating bone pain, pathological fractures, and eventually death, and therefore is a serious challenge to both bone biologists and cancer cell biologists. The stromal-epithelial interactions in breast and prostate are critical in initiation of carcinogenesis and the progression of the metastatic cascade to bone (Fig. 2)

The long latency period that occurs in some patients between initial treatment and evidence of metastases is attributed to tumor cell dormancy. Although the clinical occurrence of these late developing metastases has intrigued the medical community for years, there's a paucity of experimental data, especially among the solid tumors. Of clinical importance is that dormant tumor cells are highly refractory to chemotherapy. For these reasons, the NIH convened a small workshop in July 2006 of investigators with interests in this field to review the challenges and research opportunities. This report summarizes the key outcomes of this workshop. The mechanisms associated with tumor cell dormancy are poorly defined, in part because the dormant tumor cells have been extraordinarily difficult to isolate. New isolation and characterization techniques were presented. One of the critical limitations confronting the field is that molecular markers of dormancy are not now known. The workshop considered the role of the microenvironment in promoting and maintaining dormant tumor cells as well as events in the microenvironment that could activate the dormant cells. There was also discussion of new models of dormancy and new imaging modalities. Furthermore, the workshop reviewed studies of hematological tumor cell dormancy and how this insight could best be applied to the solid tumors. Finally, there was discussion related to the design of clinical trials for the study of tumor cell dormancy. The workshop concluded with an overall summary of the challenges and research opportunities associated with this field with recommendations for consideration by the NIH.

The Inflammation and Cancer Think Tank Meeting was organized by the National Cancer Institute with the purpose of identifying research advances, gaps, and opportunities for the study and clinical application of the role of inflammation on tumorigenesis. The format of this meeting consisted of brief presentations that focused on concepts, with extensive discussion periods to allow participants to identify issues and barriers limiting progress in this area. The strong relationship between inflammation and cancer in the gastrointestinal tract prompted several presentations that were focused on carcinogenesis within this organ system; however, many of the same immune mediators that influence esophageal, gastric, and colorectal carcinoma were also shown to influence inflammation-related malignancies at other anatomic sites. This article summarizes the findings of this Think Tank Meeting, which highlight the intimate relationship between malignant cells and their inflammatory microenvironment and specifically address opportunities to manipulate the host immune response and therefore intervene at different points along the tumorigenic cascade. (Cancer Res 2005; 65(19): 8583-7)

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The term androgen-independent cancer has now become a misnomer. Given that the androgen receptor can be activated by even low androgen concentrations or via protein modifications or other protein-protein interactions, a growing prostate cancer has the chance of assuming an androgen depletion-independent state, without necessarily bypassing the androgen signaling processes. It is thus suggested that "androgen-independent (AI)" cancer should be more accurately termed "androgen depletion-independent (ADI)" cancer.