The Life and Death of Hopkins' Host-Selection Principle

Hopkins' host-selection principle (HHSP) refers to the observation that many adult insects demonstrate a preference for the host species on which they themselves developed as larvae. The meaning of HHSP has changed significantly since its first proposal in 1916. This review considers how the meaning of HHSP has changed over time and considers the various mechanisms that could contribute to a behavioral bias for the developmental host. The assumption that HHSP implies that the behavior of adult insects is conditioned by larval experience has resulted in widespread condemnation of HHSP. Despite a great deal of attention, there is still very little convincing evidence for preimaginal conditioning of host choice in insects. But growing evidence indicates that genetic variation in behavior and conditioning during the life span of an adult insect can contribute to a preference for the host on which an insect developed. Insects can acquire adult oviposition or feeding preferences through exposure to chemical residues from the environment of earlier life history stages. The concepts of host races and host fidelity have become familiar and acceptable, while the association of HHSP with preimaginal conditioning has led to a general rejection of the term.     

Tumor Dormancy: Death and Resurrection of Cancer As Seen through Transgenic Mouse Models

Cancer is caused by genetic changes that activate oncogenes or inactivate tumor suppressor genes. The repair or inactivation of mutant genes may be effective in the treatment of cancer. Drugs that target oncogenes have shown to be effective in the treatment of some cancers. However, it is still unclear why the inactivation of a single cancer associated gene would ever result in the elimination of tumor cells. In experimental transgenic mouse models the consequences of oncogene inactivation depend upon the genetic and cellular context. In some cases, oncogene inactivation results in the elimination of all or almost all tumor cells through apoptosis or terminal differentiation. However, in other cases, oncogene inactivation results in the apparent loss of the neoplastic properties of tumor cells, that now appear and behave like normal cells, however, upon oncogene reactivation rapidly recover their neoplastic phenotype. These observations illustrate that oncogene inactivation can result in a state of tumor dormancy. Understanding when and how oncogene inactivation induces sustained tumor regression will be important towards the development of successful therapeutic strategies for cancer.