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Graft-versus-host disease-associated angiomatosis (GVHD-AA) is an uncommon manifestation of chronic GVHD consisting of friable vascular proliferations. Using fluorescence in situ hybridization, we demonstrate the presence of donor-derived endothelial cells within areas of GVHD-AA. This is the first documented occurrence of a benign neoplastic growth in relationship to a form of chronic GVHD.

Amphibian tissues seem to resist oncogenesis in proportion to their regenerative capacity, a phenomenon most easily seen in relation to limb regeneration. There is evidence that mammalian tissues also possess, in addition to and distinct from the capacity for physiological renewal, a limited and not always overtly evident degree of amphibian-like capacity for regeneration (epimorphic regeneration). It is the thesis of this paper that cancer in mammals would seldom occur were it not for a local destruction or exhaustion, secondary to injury or aging, of this normal amphibian-like regenerative capacity.

Components of the renin-angiotensin system can be found in the vasculature, although in most cases it is unclear how much, if any, of this renin in the vasculature is locally synthesized. Over recent years, a variety of novel actions of angiotensin II have been delineated which suggest that in appropriate physiologic or pathologic circumstances vascular angiotensin II can play an important role in determining vascular structure. Moreover, angiotensin II may play a role in neoplastic growth of vascular and nonvascular tissues.

Myeloid sarcoma is a neoplastic growth of myeloid blasts that occur in a site other than the bone marrow. It has a male predilection and a median age of 56 years. The development of a megakaryoblastic myeloid sarcoma is very rare. Most cases arise from either a refractory anemia with excess blasts or a …

SYNOPSIS Chalones,inhibitors of cell dmsion have been isolated and studied from a number of mammalian tissues, most notably, the epidermis The epidermal rhalone is a glycoprotein It exhibits considerable, but not complete specificity The epidermal chalone decreases mitotic activity by inhibiting cells in the G 2 phase of the cell cycle from entering mitosis, and probably also by inhibiting ceils in the G 1 phase of the cell cycle from entering mitosis To inhibit cells in G 2 from entering mitosis the chilone requnes adrenalin, and for maximal activity hydrocortisone It is not known if idrenalin and hydrocortisone are required for chalone inhibition of cells in G 1 In addition to inhibiting cell division in normal epidermal cells the epidermal chalone can inhibit cell division in regenerating epidermal cells induced to proliferate by chemical damage The phase of the cell cycle in which the chalone inhibits legenerating epidermal cells from entering mitosis is not known Epidermal tumors contain a decreased amount of chalone Mitosis in epidermal tumors is inhibited by treatment with epidermal chalone Tumor cells are inhibitedfrom entering mitosis from either the G 1 or G 2 phases of the cell cycle Chalones are said to inhibit mitosis by a negative feedback mechanism However, experiments which presumably result in a decrease in chalone concentration do not result in an increase in mitotic activity It is suggested that if chalones are physiologi cal controllers of cell division they do not act by a simple negative feedback mechanism but require the action of a substance to decrease their concentration

Intrarectal administration of 0.5 ml of a 0.25 percent solution of N-methyl-N-nitrosourea twice seekly for 42 weeks to female inbred strain-2 guinea pigs induced large-bowel adenocarcinomas in 9 of 10 animals in 38-56 weeks. Controls did not show cancer. The lesions were infiltrative or constrictive, which distinguished them from chemically induced large-bowel cancers of rats and mice.