It has been demonstrated by various workers in the past that glucocorticosteroids block hair growth. Using the mouse model for studying hair growth induction we reexamined the effect of topically applied steroids on hair growth to establish at what stage the steroid block acts. In accord with studies by others, we found that these steroids block hair growth at the point of anagen initiation, but that once the steroid applications are stopped, hair growth starts. Since steroid withdrawal alone did not induce hair growth, it is clear that these steroids do not block, either spontaneous or manipulated, hair growth induction, but they do block, the apparent next step, i.e., hair formation. Moreover, since hair growth could be induced even while the animals were being treated with the steroid, the induction step appears independent of the steroid block-These studies and those of others lead us to conclude that these steroids block the expression of hair-forming genes, but do not interfere with the signal(s) that initiates those genes. This system appears to be ideal for identifying the signals (perhaps, genes) responsible for initiating hair growth.

Purpose Hypomagnesemia is an adverse reaction associated with epidermal growth factor receptor (EGFR)-targeting monoclonal antibodies. Of the 2 EGFR antibodies approved by the US Food and Drug Administration—cetuximab and panitumumab—cetuximab-induced hypomagnesemia has been extensively characterized but panitumumab-induced hypomagnesemia has not. Methods In this retrospective study, the clinical course of hypomagnesemia is described in three 64- to 68-year-old men who received panitumumab monotherapy or panitumumab-plus-irinotecan therapy for colorectal cancer for 8 to 21 weeks. Results The onset of hypomagnesemia was variable, ranging from 1 week to 10 weeks following the initiation of panitumumab. Magnesium levels did not normalize until 4 to 8 weeks after discontinuation of the agent. Of the patients in the study, 2 had new onset of grade 3 hypomagnesemia 1 to 3 weeks after panitumumab was discontinued. Management was magnesium sulfate 2 g infusion weekly and magnesium oxide 1,200 mg oral repletion daily. With severe hypomagnesemia (grade 3 and higher) or significant diarrhea (grade 3 and higher), a daily infusion of magnesium sulfate 2 or 4 g was administered. Conclusion When administering panitumumab therapy, magnesium levels should be monitored from the initiation of the agent to at least 8 weeks following cessation. Hypomagnesemia usually can be managed with magnesium sulfate 2 to 4 g infusion weekly and magnesium oxide 1,200 mg oral repletion daily. Future research is warranted to identify simple and efficient strategies for monitoring and treating EGFR blockade with monoclonal antibody-associated hypomagnesemia.

Combination treatment with CS followed by IPHC in 15 patients with heterogeneous primary sources of intraabdominal malignancies resulted in a median survival time of 8.4 months.