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Curr Top Med Chem. An improved synthesis of substituted [ 11 C]toluenes via Suzuki coupling with [ 11 C]methyl iodide. J Labelled Comp Radiopharm. Synthesis, in vitro and in vivo evaluation of fluorine labelled FE-GW as a PET tracer for type 2 cannabinoid receptor imaging. Bioorg Med Chem. A PET brain reporter gene system based on type 2 cannabinoid receptors.

Chem Commun Camb ; 49 —6. Synthesis of the Cyanine 7 labeled neutrophil-specific agents for noninvasive near infrared fluorescence imaging. Bioorg Med Chem Lett. Bioconjugate Chem. Synthesis of novel neutrophil-specific imaging agents for positron emission tomography PET imaging. Hum Antibodies. Hawkey CJ. COX-2 inhibitors. Katori M, Majima M. Cyclooxygenase its rich diversity of roles and possible application of its selective inhibitors.

Inflamm Res. Minghetti L. Cyclooxygenase-2 COX-2 in inflammatory and degenerative brain diseases. J Neuropathol Exp Neurol. Evaluation of [ 11 C]rofecoxib as PET tracer for cyclooxygenase 2 overexpression in rat models of inflammation. In vivo expression of cyclooxygenase-1 in activated microglia and macrophages during neuroinflammation visualized by PET with 11 C-ketoprofen methyl ester. Can celecoxib affect P-glycoprotein-mediated drug efflux? A microPET study. Synthesis and preliminary in vitro biological evaluation of new carbonlabeled celecoxib derivatives as candidate PET tracers for imaging of COX-2 expression in cancer.

Eur J Med Chem. Synthesis and evaluation in vitro and in vivo of a 11 C-labeled cyclooxygenase-2 COX-2 inhibitor. Cancer Prev Res Phila ; 4 — Egeblad M, Werb Z. New functions for the matrix metalloproteinases in cancer progression. Nat Rev Cancer. Measurement of MMP activity in synovial fluid in cases of osteoarthritis and acute inflammatory conditions of the knee joints using a fluorogenic peptide probe-immobilized diagnostic kit. Optical imaging of cancer-related proteases using near-infrared fluorescence matrix metalloproteinase-sensitive and cathepsin B-sensitive probes.

Real-time video imaging of protease expression in vivo. J Control Release. Mol Pharm. J Nucl Cardiol. Scintigraphic imaging of matrix metalloproteinase activity in the arterial wall in vivo.


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Imaging with radiolabelled anti-membrane type 1 matrix metalloproteinase MT1-MMP antibody: potentials for characterizing atherosclerotic plaques. In vitro and in vivo investigation of matrix metalloproteinase expression in metastatic tumor models. NuclMed Biol. Targeting of matrix metalloproteinase activation for noninvasive detection of vulnerable atherosclerotic lesions.

European journal of nuclear medicine and molecular imaging. T-lymphocyte infiltration in visceral adipose tissue: a primary event in adipose tissue inflammation and the development of obesity-mediated insulin resistance. Nucl Med Comm. Imaging active lymphocytic infiltration in coeliac disease with iodineinterleukin-2 and the response to diet. Pharmacokinetic modelling of N- 4-[ 18 F]fluorobenzoyl interleukin-2 binding to activated lymphocytes in an xenograft model of inflammation.

Bench to bedside: tumor necrosis factor-alpha: from inflammation to resuscitation. Acad Emerg Med. PET imaging of acute and chronic inflammation in living mice. Integrins in cancer: biological implications and therapeutic opportunities. Hodivala-Dilke K. Curr Opin Cell Biol. Regulation of macrophage foam cell formation by alphaVbeta3 integrin: potential role in human atherosclerosis. Am J Pathol. J Cell Physiol. Niu G, Chen X. Why integrin as a primary target for imaging and therapy.

Radiolabelled RGD peptides for imaging and therapy. Angiogenesis as a novel component of inflammatory bowel disease pathogenesis. Wilder RL. Integrin alpha V beta 3 as a target for treatment of rheumatoid arthritis and related rheumatic diseases. Ann Rheum Dis. MFG-E8 attenuates intestinal inflammation in murine experimental colitis by modulating osteopontin-dependent alphavbeta3 integrin signaling. J Immunol. Evaluation of alphavbeta3 integrin-targeted positron emission tomography tracer 18 F-galacto-RGD for imaging of vascular inflammation in atherosclerotic mice. Circ Cardiovas Imaging.

Salmi M, Jalkanen S. VAP an adhesin and an enzyme. Trends Immunol. Clin Physiol Funct Imaging. Siglec-9 is a novel leukocyte ligand for vascular adhesion protein-1 and can be used in PET imaging of inflammation and cancer. Synthesis, 68 Ga labeling and preliminary evaluation of DOTA peptide binding vascular adhesion protein a potential PET imaging agent for diagnosing osteomyelitis. In Vivo. Ley K, Huo Y. VCAM-1 is critical in atherosclerosis. J Clin Invest. Tsan MF. Mechanism of gallium accumulation in inflammatory lesions. Ross R. Atherosclerosis--an inflammatory disease.

N Engl J Med. The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases. Brain Res Brain Res Rev. Inflammation as a tumor promoter in cancer induction. Semin Cancer Biol. Hiari N, Rudd JH. Curr Cardiol Rep. Sheikine Y, Akram K. Microglia and neuroinflammation: a pathological perspective. J Neuroinflammation. Jacobs AH, Tavitian B.

Noninvasive molecular imaging of neuroinflammation. J Cereb Blood Flow Metab. In vivo changes in microglial activation and amyloid deposits in brain regions with hypometabolism in Alzheimer's disease. Age and disease related changes in the translocator protein TSPO system in the human brain: positron emission tomography measurements with [ 11 C]vinpocetine. Microglial activation and amyloid deposition in mild cognitive impairment: a PET study. Neurobiol Dis. Microglia, amyloid, and glucose metabolism in Parkinson's disease with and without dementia. The temporal dynamics of poststroke neuroinflammation: a longitudinal diffusion tensor imaging-guided PET study with 11 C-PK in acute subcortical stroke.

Inflammation after trauma: microglial activation and traumatic brain injury. Ann Neurol. PET tracers for the peripheral benzodiazepine receptor and uses thereof. Drug Discov Today. Glial cell-mediated deterioration and repair of the nervous system after traumatic brain injury in a rat model as assessed by positron emission tomography.

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J Neurotrauma. Increased cerebral R -[ 11 C]PK uptake and glutamate release in a rat model of traumatic brain injury: a longitudinal pilot study.


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Microglial activation in regions related to cognitive function predicts disease onset in Huntington's disease: a multimodal imaging study. Hum Brain Mapp. Cancer-related inflammation. Tumor-associated macrophages TAM as major players of the cancer-related inflammation. J Leukoc Biol. Depletion of tumor-associated macrophages enhances the effect of Sorafenib in metastatic liver cancer models by antimetastatic and antiangiogenic effects. Clin Cancer Res. MR imaging of tumor-associated macrophages.

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A nonpeptidic cathepsin S activity-based probe for noninvasive optical imaging of tumor-associated macrophages. Chem Biol. PET imaging of tumor associated macrophages using mannose coated 64 Cu liposomes. Nanobody-based targeting of the macrophage mannose receptor for effective in vivo imaging of tumor-associated macrophages.

Cancer Res. Hybrid PET-optical imaging using targeted probes. Differential expression of the 18 kDa translocator protein TSPO by neoplastic and inflammatory cells in mouse tumors of breast cancer. Proliferation markers for the differential diagnosis of tumor and inflammation. Curr Pharm Des. Comparison of 2-amino-[3- 11 C]isobutyric acid and 2-deoxy[ 18 F]fluoro-D-glucose in nude mice with xenografted tumors and acute inflammation. Specific PET imaging of xC- transporter activity using a 18 F-labeled glutamate derivative reveals a dominant pathway in tumor metabolism.

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We also recommend that a new baseline PET be obtained before initiation of a new therapeutic regimen. Should a biopsy be necessary, PET may also help guide the biopsy to the relevant part of a tumor mass. Early identification of non-responders is certainly a major goal. No one wants to expose a patient to any treatment if he or she is not going to derive significant benefit from it.

I think that imaging has a role to play soon after initiation of drug therapy to allow for an earlier change to alternative therapy and to avoid unnecessary toxicity in patients who are not responding. I also believe that PET imaging has propelled science forward — particularly in patients with GIST — by giving us a simple, noninvasive, and rapid way to demonstrate biologic effects on the tumor as early as hours after a single dose of the drug, as we have shown with imatinib.

These profound metabolic changes within the tumor are consistent with response to therapy and precede significant changes in tumor size by weeks and months. If we can see what works and what does not early on, we can direct our energies and research dollars accordingly. The use of functional imaging with PET has already shortened the length of several clinical trials, with the result that new drugs became available to the public sooner than would otherwise have been the case, and development costs were re duced.

We demonstrated this with sunitinib and helped bring the drug to the market six months ahead of schedule based on feedback from the company. I also anticipate that imaging, and in particular functional imaging with PET, will play a major role in the future in the delivery of personalized medicine. I think that imaging can lead to significant cost savings by helping identify the right patient for the right drug.

So the facilitation of clinical trials, drug development, and personalized medicine through the use of imaging would be other major goals. Metabolic changes tend to precede structural changes within the tumor and are predictive of both clinical and subsequent radiologic responses. Qualitative and quantitative imaging methods can be used to assess metabolic response to therapy.

A complete metabolic response by either qualitative or quantitative evaluation is highly predictive of good outcome. Conversely, persistent metabolic activity suggests residual tumor, and recurrent tumor activity in an area that had previously shown response may be indicative of secondary resistance. Several quantitative and semi-quantitative methods can be used to assess metabolic response, but these vary in complexity and reproducibility and are mainly used in the context of clinical trials.

Because the metabolic response to drug treatment precedes the anatomic response, reductions in tumor activity may be seen in as little as 24 hours — long before physical shrinkage is visible on CT or MRI. Thus, PET is a really efficient tool for determining how well a drug is working in a particular patient. If the CT scan shows stability or shrinkage, that is probably all the information the oncologist needs to know to assess if the drug is working, and if you should stay on that drug.

Where PET is really valuable is in resolving discrepancies between the CT scan and clinical findings: for example, the CT may show an increase in tumor growth but other clinical information suggests that the patient is actually doing well. A negative PET scan will confirm that this is the case. Conversely, tumors may look stable in size on CT but show small nodular development within the wall of the mass. PET can also be very helpful in guiding the biopsy to these sites of active tumor metabolism and possible secondary resistance. FDG-PET is an ideal imaging tool in GIST for staging the disease, assessing therapeutic response, evaluating primary and secondary resistance, and resolving discrepant results between CT and the clinical findings.