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Comment
. 2008 Jul;1(2):77-9.
doi: 10.1158/1940-6207.CAPR-08-0009. Epub 2008 Mar 19.

Colorectal neoplasia goes with the flow: prostaglandin transport and termination

Sanford D Markowitz  1
Affiliations
Comment

Colorectal neoplasia goes with the flow: prostaglandin transport and termination

Sanford D Markowitz. Cancer Prev Res (Phila). 2008 Jul.
No abstract available

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Figures

Fig. 1
Fig. 1
The flow of colorectal neoplasia passes through the prostaglandin E2 (PGE2) transporters. A, the PGE2 influx-dominated flow of normal colorectal cells; the dotted blue circular line represents the general pattern of this flow. B, the PGE2 efflux-dominated flow of neoplastic colorectal cells; the dotted red circular line represents the general pattern of this flow. C, a conceptual approach for preventing or treating colorectal cancer via molecular targeting of the processes shown in panels A and B. The colorectal neoplasia risk factors shown at the upper left in panel C are key early events associated with upregulated COX-2 and neoplasia in the colorectal region. The agent classes shown at the lower right in panel C are supported by PGT and/or 15-PGDH upregulation data. All of the processes suggested in panels A–C are well described toward the end of the text. 15-PGDH, 15-hydroxyprostaglandin dehydrogenase; AA, arachidonic acid; COX-1, cyclooxygenase 1; DNMT, DNA methyltransferase; MRP, multidrug resistance-associated protein; mPGES1, microsomal PGE synthase 1; PGT, PG transporter; ППAP-γ, peroxisome proliferator-activated receptor-γ.
Fig. 1
Fig. 1
The flow of colorectal neoplasia passes through the prostaglandin E2 (PGE2) transporters. A, the PGE2 influx-dominated flow of normal colorectal cells; the dotted blue circular line represents the general pattern of this flow. B, the PGE2 efflux-dominated flow of neoplastic colorectal cells; the dotted red circular line represents the general pattern of this flow. C, a conceptual approach for preventing or treating colorectal cancer via molecular targeting of the processes shown in panels A and B. The colorectal neoplasia risk factors shown at the upper left in panel C are key early events associated with upregulated COX-2 and neoplasia in the colorectal region. The agent classes shown at the lower right in panel C are supported by PGT and/or 15-PGDH upregulation data. All of the processes suggested in panels A–C are well described toward the end of the text. 15-PGDH, 15-hydroxyprostaglandin dehydrogenase; AA, arachidonic acid; COX-1, cyclooxygenase 1; DNMT, DNA methyltransferase; MRP, multidrug resistance-associated protein; mPGES1, microsomal PGE synthase 1; PGT, PG transporter; ППAP-γ, peroxisome proliferator-activated receptor-γ.
Fig. 1
Fig. 1
The flow of colorectal neoplasia passes through the prostaglandin E2 (PGE2) transporters. A, the PGE2 influx-dominated flow of normal colorectal cells; the dotted blue circular line represents the general pattern of this flow. B, the PGE2 efflux-dominated flow of neoplastic colorectal cells; the dotted red circular line represents the general pattern of this flow. C, a conceptual approach for preventing or treating colorectal cancer via molecular targeting of the processes shown in panels A and B. The colorectal neoplasia risk factors shown at the upper left in panel C are key early events associated with upregulated COX-2 and neoplasia in the colorectal region. The agent classes shown at the lower right in panel C are supported by PGT and/or 15-PGDH upregulation data. All of the processes suggested in panels A–C are well described toward the end of the text. 15-PGDH, 15-hydroxyprostaglandin dehydrogenase; AA, arachidonic acid; COX-1, cyclooxygenase 1; DNMT, DNA methyltransferase; MRP, multidrug resistance-associated protein; mPGES1, microsomal PGE synthase 1; PGT, PG transporter; ППAP-γ, peroxisome proliferator-activated receptor-γ.
See this image and copyright information in PMC

Comment on

References

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