Sources of hope in chronic illness.

Patients with many types of diagnosis find that hope is an important strategy in coping with their illness. One purpose of this study was to identify and explore the sources that patients with chronic illnesses report as being supportive of their hope. Another purpose was to determine if the sources differ between patients with cancer and patients with other chronic illnesses. A combination of Stotland's work on hope and Lazarus and Folkman's work on coping formed the conceptual framework for this study. Ninety patients, 45 with cancer and 45 with other chronic illnesses, were interviewed using an investigator-developed interview guide. Using chi-square and t-test analyses, no statistically significant differences were found between patients with cancer and patients with other chronic illnesses in any responses to the interview questions. The most commonly reported sources for supporting hopefulness were family, friends, and religious beliefs. Patients were able to identify specific ways in which these sources helped to support their hope. The majority of patients reported positive attitudes about their illnesses, with transient periods of lowered hope related to illness. They also described specific cognitive or behavioral strategies used for maintaining hope. The results of this study provide additional insight into the coping strategies of adults with a chronic illness.     

Chk1 is required to maintain claspin stability

Claspin is a Chk1-interacting protein that participates in the DNA replication checkpoint. Expression of Claspin fluctuates in a cell cycle-dependent manner, but the mechanisms involved in the regulation of Claspin protein levels have not been explored. In this study, we show that Claspin expression is downregulated by the proteasome-mediated degradation pathway and that Chk1 is required to maintain Claspin stability. Downregulation of Chk1 expression by siRNA or inhibition of Chk1 activity by UCN01 decreases Claspin levels in cells. Conversely, overexpression of Chk1 increases Claspin levels. These data indicate a role of Chk1 in regulating Claspin stability in the cell. Since Claspin has also been shown to participate in Chk1 activation following DNA damage, we further explored the exact role of Claspin during Chk1 activation following replication stress. We observed that while Rad17 is required for early Chk1 activation after hydroxyurea treatment, Claspin is only required to sustain Chk1 activation. Based on these findings, we propose that Claspin functions at late stages of Chk1 activation following DNA damage. Once Chk1 is activated, it stabilizes Claspin, which in turn helps to maintain Chk1 activation during replication stress. In summary, these data indicate that the interaction between Claspin and Chk1 is complex. These proteins regulate each other and thus ensure the proper cell cycle progression and replication checkpoint control.     

Natural resistance to cancer: A window of hope

As healthcare systems are improving and thereby the life expectancy of human populations is increasing, cancer is representing itself as the second leading cause of death. Although cancer biologists have put enormous effort on cancer research so far, we still have a long way to go before being able to treat cancers efficiently. One interesting approach in cancer biology is to learn from natural resistance and/or predisposition to cancer. Cancer-resistant species and tissues are thought-provoking models whose study shed light on the inherent cancer resistance mechanisms that arose during the course of evolution. On the other hand, there are some syndromes and factors that increase the risk of cancer development, and revealing their underlying mechanisms will increase our knowledge about the process of cancer formation. Here, we review natural resistance and predisposition to cancer and the known mechanisms at play. Further insights from these natural phenomena will help design future cancer research and could ultimately lead to the development of novel cancer therapeutic strategies.     

Achievable goals and relevant endpoints in cancer treatment.

The goals of cancer treatment range from eliminating cancer to prolonging the time to recurrence, controlling local disease, and palliating symptoms. For many cancer patients, disease elimination is an unrealistic treatment goal at the time of diagnosis due to the presence of metastatic disease and the lack of effective systemic treatment. For other patients, treatment options with similar survival expectation but differing side effects may complicate treatment selection. There is a clear need for new cancer treatment endpoints to be developed so that the effects of cancer treatment may be appropriately monitored. Some recently developed cancer treatment endpoints are described, and their use in clinical trials is advocated.