The Bacillus subtilis abh gene encodes a protein whose N-terminal domain has 74% identity to the DNAbinding domain of the global regulatory protein AbrB. Strains with a mutation in abh showed alterations in the production of antimicrobial compounds directed against some other Bacillus species and gram-positive microbes. Relative to its wild-type parental strain, the abh mutant was found deficient, enhanced, or unaffected for the production of antimicrobial activity. Using lacZ fusions, we examined the effects of abh upon the expression of 10 promoters known to be regulated by AbrB, including five that transcribe well-characterized antimicrobial functions (SdpC, SkfA, TasA, sublancin, and subtilosin). For an otherwise wild-type background, the results show that Abh plays a negative regulatory role in the expression of four of the promoters, a positive role for the expression of three, and no apparent regulatory role in the expression of the other three promoters. Binding of AbrB and Abh to the promoter regions was examined using DNase I footprinting, and the results revealed significant differences. The transcription of abh is not autoregulated, but it is subject to a degree of AbrB-afforded negative regulation. The results indicate that Abh is part of the complex interconnected regulatory system that controls gene expression during the transition from active growth to stationary phase.Upon entry into stationary phase and sporulation, strains of Bacillus subtilis cells produce different spectrums of various antibiotic and antimicrobial functions (36). Among the antimicrobials produced by B. subtilis 168 strains are sublancin (27), subtilosin A (2, 35), bacilysocin (46), bacilysin (20,22,48), the SdpC sporulation delay toxin (8,14), the SkfA sporulation killing factor (1, 14), and the TasA protein (37). The pleiotropic AbrB protein is known to play a role in regulating most of these antimicrobials in addition to numerous other genes expressed by postexponential-phase cells (22,31,36,37,54).The examination of over 60 chromosomal sites of AbrB binding has failed to uncover a consensus base sequence that has substantive predictive value and that can adequately explain target selection and affinity. High-affinity sites of AbrB-DNA interactions selected using in vitro methods do show convergence to a consensus, but sequences resembling this consensus are rarely found in the chromosomal sites (50, 53). It has been hypothesized that AbrB achieves binding specificity by recognizing three-dimensional DNA architectures that are shared by a finite subset of base sequences (5,40,42,45,53). A major factor accounting for what has been termed the "limited promiscuity" of AbrB-DNA interactions is believed to be the dynamic flexibility in the DNA-binding domain of the protein; this flexibility allows it to conform to different targets with thermodynamically favorable contacts (4, 6, 47).B. subtilis contains two AbrB paralogs: Abh (6, 23) andSpoVT (3). The abh gene codes for a protein of 92 amino acids, showing 58% overall identity...

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Metastases to the pancreas are rare at 1-2%. Among primaries metastasizing to the pancreas, lung cancer (LC) is frequently the culprit. Metastases to the lung from pancreatic cancer (PC) are significantly more common at about 45%, presenting striking differences in cancer behavior. There are conflicting reports regarding cancerogenicity and metastatic incidence between the lung and pancreas. Therefore, this review takes a fresh look at lung and pancreatic cancer behavior. Secondary metastases to the lung and pancreas are often indistinguishable from LC and PC primaries, and the seed and soil hypothesis is not always congruous with clinical interpretation of disease course. Sometimes single "seed" dissemination is thought to occur at the preneoplastic stage without any evidence of tumor invasion. Metastatic growth may become dormant, manifesting years later as cancer of unknown primary (CUP). Interestingly, CUPs are discovered to originate most frequently from LC and PC primaries at autopsy. The lung and pancreas are morphologically related through endoderm-level morphogenesis. The molecular basis of cancer regularity between them involves developmental signaling pathways including HEDGEHOG, NOTCH, WNT, and CXCL12/CXCR4, an evolving genetic background, and regulatory tumor-stromal interactions. Perhaps biomarkers that explain the regularity between them have been documented -as we peruse the bioscience literature for information, we may be reading through viable biomarkers and solutions and not seeing the forest for the trees. On the other hand, perhaps more research is warranted to explain cancer behavior between the lung and pancreas. Observations in this review provide a framework on which to extract clues for future work regarding organspecific metastasis between the lung and pancreas.