review of literature on clinical pancreatology - The Pancreapedia

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1.14 to 4.10), although the p27 polymorphism alone was not associated with pancreaticcancer risk. These results indicate that the p21 polymorphism may contribute to susceptibilityto pancreatic cancer, particularly among p27 homozygous wild-type carriers and nonsmokers[391].p53With the aim <strong>of</strong> improving early detection <strong>of</strong> pancreatic carcinoma, it was attempted to makecorrelations among positive immunohistochemical detection <strong>of</strong> p53 expression, mutations inthe p53 gene, and detailed histologic features <strong>of</strong> pancreatic carcinoma. Seven cases <strong>of</strong>invasive pancreatic ductal carcinoma demonstrating p53 overexpression were analyzed.Serial 4- and 20-microm sections from paraffin blocks were used for immunodetection <strong>of</strong> p53protein and microdissection, respectively. It was used direct sequencing <strong>of</strong> polymerase chainreaction at 101 p53-positive and 10 p53-negative sites to sequence exons 5 to 8 <strong>of</strong> p53 andthen analyzed these results in concert with detailed histologic features. Regardless <strong>of</strong> thedegree <strong>of</strong> p53 overexpression, it was detected p53 point mutations in all p53-positive lesions,including 22 noninvasive sites, 17 invasive areas, and 1 lymph node metastasis. Nosignificant correlations were measured between specific p53 mutations and histologicfeatures. Within individual tumors, the same p53 mutation was generally, but not always,detected in different areas in invasive and noninvasive lesions. The results demonstrate thatp53 mutation is an early genetic event affecting a diversity <strong>of</strong> molecular pathways inpancreatic carcinogenesis and indicates a possibility <strong>of</strong> early diagnosis <strong>of</strong> pancreaticcarcinoma by detecting a few p53-positive cells obtained from the pancreatic fluid [392].Pain and nerve growth factorPerineural invasion is one <strong>of</strong> the most common routes <strong>of</strong> invasion in pancreatic cancer andthe exact mechanism is still not clear. The aim <strong>of</strong> one study was to investigate the effect <strong>of</strong>nerve growth factor (NGF) and tyrosine kinase receptor A (TrkA) on perineural invasion andto clarify the possible mechanism <strong>of</strong> perineural invasion in pancreatic cancer. Expressions <strong>of</strong>NGF/TrkA were examined in 51 human primary pancreatic cancer usingimmunohistochemistry (IHC) and reverse transcription polymerase chain reaction (RT-PCR).Immunohistochemical analysis indicated that the presence and kind <strong>of</strong> perineural invasionare prognostic parameters. Tumors with high NGF expression exhibited significantly morefrequent presence <strong>of</strong> perineural invasion. NGF expression was significantly correlated withmetastasis <strong>of</strong> lymph nodes and involvement <strong>of</strong> surgical margins. TrkA expression wassignificantly correlated with degree <strong>of</strong> perineural invasion. Negative correlations were foundbetween expression <strong>of</strong> NGF/TrkA and Ki-67. As shown by RT-PCR, mRNA levels <strong>of</strong>NGF/TrkA with perineural invasion were significantly higher than that without perineuralinvasion. It was concluded that in pancreatic cancer, overexpression <strong>of</strong> NGF may contributeto perineural invasion by prompting the hyperplasia <strong>of</strong> nerves, restraining the apoptosis <strong>of</strong>tumor cells and specifically combining NGF and TrkA [393].PPARGThe Pro12Ala variant in the peroxisome proliferator-activated receptor-gamma (PPARG)gene has been associated with diabetes and several cancers. A pilot study tested for theassociation between Pro12Ala and pancreatic cancer risk in a high-risk sample <strong>of</strong> smokers.A nested case-control study was conducted in 83 incident cases <strong>of</strong> pancreatic cancer and166 matched controls originally recruited into a cohort chemoprevention study <strong>of</strong> lung cancer.Associations between Pro12Ala and pancreatic cancer risk were measured using conditionallogistic regression. Carriers <strong>of</strong> the G allele (Ala) <strong>of</strong> the Pro12Ala variant had a borderlineincreased relative risk <strong>of</strong> pancreatic cancer compared with homozygous carriers <strong>of</strong> the Callele (Pro), with an odds ratio <strong>of</strong> 1.79 (95 % confidence interval 0.96-3.33). Among subjects
andomized to high-dose vitamin A, the odds ratio was 2.80 versus 1.20 in the placebogroup. A haplotype including Pro12Ala was also significantly associated with pancreaticcancer risk in all subjects and in subjects randomized to vitamin A. The analysis presentsevidence that PPARG may be associated with pancreatic cancer risk [394].Plasminogen activatorThe serine protease urokinase-type plasminogen activator (uPA) and its receptor (uPAR) areknown to be involved in the invasion and metastasis <strong>of</strong> many solid tumors. In one study, itwas analyzed the role <strong>of</strong> the uPAR/uPA system in both the development and progression <strong>of</strong>pancreatic cancer in invasive ductal adenocarcinomas <strong>of</strong> the pancreas and theirpremalignant precursors (PanIN lesions) in 50 patients with long-term clinical follow-up. Itwas found overexpression <strong>of</strong> the uPAR in 48 <strong>of</strong> 50 invasive carcinomas as well as in a largeproportion <strong>of</strong> high-grade PanIN lesions by immunohistochemistry and in situ hybridization.Fluorescence in situ hybridization analysis showed both high- and low-level amplification <strong>of</strong>the uPAR gene in approximately 50 percent <strong>of</strong> cases with strictly identical patterns betweeninvasive cancers and their accompanying precursor lesions. These results suggest thatpancreatic cancer may develop from PanIN lesions along an alternative rather than asequential molecular pathway. The detection <strong>of</strong> the gene amplification <strong>of</strong> uPAR was a highlysignificant, adverse prognostic parameter because it likely renders the tumors more sensitiveto uPA and its proproliferative and anti-apoptotic signals. It was concluded that the activation<strong>of</strong> the uPAR/uPA system is an early event in the development <strong>of</strong> PDA and that uPAR geneamplifications identify a subgroup <strong>of</strong> particularly aggressive tumors, making the uPAR/uPAsystem a critical and highly promising target for therapeutic interventions [395].REG4Preoperative chemoradiotherapy is one <strong>of</strong> the key strategies for the improvement <strong>of</strong> survivalin pancreatic cancer; however, no method to predict the response has yet been established.The aim <strong>of</strong> one study was to prospectively evaluate the predictive value <strong>of</strong> REG4, a newmember <strong>of</strong> the regenerating (REG) islet-derived family <strong>of</strong> proteins. Stably REG4-expressingcells were established from a pancreatic cancer cell line and exposed in vitro to gamma-rayor gemcitabine to investigate the relevance <strong>of</strong> REG4 to the resistance to chemotherapy orradiotherapy. In 23 patients with resectable pancreatic cancer, the serum concentration <strong>of</strong>REG4 was measured before preoperative chemoradiotherapy, and the histologic responsewas evaluated after the surgery. A 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazoliumbromide assay and fluorescence activated cell scanning (FACS) revealed that REG4-overexpressing cells were resistant to [gamma]-radiation but showed a modest resistance togemcitabine. The patients with a higher REG4 level, but not carcinoembryonic antigen or CA-19-9, showed an unfavorable histologic response to chemoradiotherapy. The patientsshowing a higher REG4 level experienced local recurrence postoperatively [396].RosiglitazoneEvaluate the effect <strong>of</strong> fen<strong>of</strong>ibrate, bezafibrate, and rosiglitazone on nonalcoholic fattypancreatic disease and islet peroxisome proliferator-activated receptor-alpha (PPAR-alpha)and PPAR-beta immunostain in mice fed high-fat high-sucrose (HFHS) diet. Two-month-oldmale mice were fed standard chow (n=10) or HFHS chow (n=40) for 6 weeks. Afterward,HFHS mice were grouped by treatment: untreated HFHS and HFHS treated withrosiglitazone (HFHS-Ro), fen<strong>of</strong>ibrate (HFHS-Fe), or bezafibrate (HFHS-Bz). Medicationswere administered for 5 weeks. After treatment, the pancreas was removed and analyzed bymorphometry, stereology, and immunohistochemistry. Results: The HFHS-fed mice showedaltered fasting glucose (+33 %) and insulin (+138 %); increased body (+20 %) and pancreas(+28 %) masses, pancreatic fat (+700 %), islet hypertrophy (+38 %); and decreased GLUT2
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REVIEW OF LITERATURE ONCLINICAL PAN
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ABBREVIATIONAAPacute alcoholicABPac
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FMF AIPfocal mass-forming autoimmun
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ODPopen distal pancreatectomyOForga
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USUTDTVESDVTEZESWHOXIAPUnited State
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Ectopic pancreasCircumportal annula
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SymptomsEndocopic ultrasography (EU
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HSP27HuRIGF-1 receptorIntegrinesInt
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HemodialysisSerous cystadenomasSero
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CRPC-reactive proteinCRTchemoradiot
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ITNPintrathecal narcotics pumpJCGAI
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QSRquantitative systematic
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PANCREATIC HISTORYEarly conceptsPan
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derived from broadly Harveian anato
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acute appendicitis, intestinal obst
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dogma and its implied presence <str
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In the late 19th century, explorato
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performed. In 1880, Carl Thiersch <
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cancer was reported by Nestor Dimit
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Modern pancreatic historyHoward Reb
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PANCREATIC DEVELOPMENT, EMBRYOLOGY
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preparations. They were also employ
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pancreas can be diagnosed without t
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PANCREATIC PHYSIOLOGYSphincter <str
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acid profile and d
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hormones. The roles of</str
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ACUTE PANCREATITISAcute pancreatiti
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necrosis or a severe course, and lo
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of 245 cases <stro
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plasty of the mino
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no significant difference. The stro
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Urinary trypsinogen-2There is not a
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groups. None of th
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evaluated the presence or absence <
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adical, etc, further studies are st
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Precut at sphincterotomyPrecut is p
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indications [204].Hypercalcemia-ind
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endoscopic retrograde cholangiopanc
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(before ERCP), serum TAP was detect
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concentration and clinical symptoms
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However, the recipients of<
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less safe for predominantly cephali
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increased mortality. Mortality in p
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Epidemiology and demographyChinaCHR
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for the first time the significance
Page 91 and 92: endoscopic ultrasound accurately de
Page 93 and 94: possible to at least reduce relapse
Page 95 and 96: etiologies have been proposed and a
Page 97 and 98: patients, can be performed with mod
Page 99 and 100: negative binomial model. One hundre
Page 101 and 102: Halofuginone did n
Page 103 and 104: years, the risk of
Page 105 and 106: patients with a proven exocrine pan
Page 107 and 108: high-risk patients [296].Cystic fib
Page 109 and 110: TNF-alpha promoter were performed.
Page 111 and 112: were validated in another series <s
Page 113 and 114: vascular invasion (14/15). Abnormal
Page 115 and 116: and other lymph nodes, salivary gla
Page 117 and 118: HEREDITARY PANCREATITISPatients wit
Page 119 and 120: Classification of
Page 121 and 122: historically, but recent life-style
Page 123 and 124: carcinogen exposure with cancer ris
Page 125 and 126: the risk of pancre
Page 127 and 128: conducted a cohort analysis <strong
Page 129 and 130: emain to be solved in screening for
Page 131 and 132: considered for women with Lynch syn
Page 133 and 134: Annexin A5Protein misfolding is a c
Page 135 and 136: CTNNB1To use fluorescence in situ h
Page 137 and 138: expression was not associated with
Page 139 and 140: (ECM) are not fully understood. In
Page 141: lines. However, the role of
Page 145 and 146: Synuclein-gammaPerineural invasion
Page 147 and 148: interventions. Cancer nests were ma
Page 149 and 150: the optimal combination of<
Page 151 and 152: which is essential in tumor and nod
Page 153 and 154: provide conclusive evidence for the
Page 155 and 156: MD-CT is suitable for evaluating tu
Page 157 and 158: approved study and imaged during sh
Page 159 and 160: Quantum dotsIt was reported the suc
Page 161 and 162: clearly have a very high incidence
Page 163 and 164: patients for operation and when cou
Page 165 and 166: demonstrated using the confocal mic
Page 167 and 168: cancer [468].To evaluate pancreatic
Page 169 and 170: pancreaticoduodenectomy (PD). The s
Page 171 and 172: safe option as an interposition gra
Page 173 and 174: a curative surgery, while double-by
Page 175 and 176: %), pseudocyst (3 %), and trauma (3
Page 177 and 178: procedure is failing to progress la
Page 179 and 180: Glucos metabolism after pancreatect
Page 181 and 182: Quality of lifeOne
Page 183 and 184: was observed in the NACRT group. Th
Page 185 and 186: interval 0.80 to 0.96]. On subgroup
Page 187 and 188: ate in patients with pancreatic can
Page 189 and 190: median survival time was 7 versus 7
Page 191 and 192: and the endoscopic ultrasound-guide
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local recurrence of1.5 cm (odds ratio 2.4), and
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adenocarcinoma must be addressed at
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Molecular biologyCD44v6The purpose
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IPMN were studied. Two-dimensional
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the NT-IPMN-Br group. Eleven patien
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metastatic neoplasms showing cystic
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Solid pseudopapillary neoplasms <st
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The tumor cells were negative for p
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Duodenal tumorsColorectal polyposis
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Colorectal carcinomaPancreatic meta
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It was described a case of<
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evaluation. The purpose of<
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perforation of a p
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the 28 had pancreatic duct injury <
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ENDOCRINE PANCREATIC TUMORSHistoryA
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25-111 pg/mL). Mean Hemoglobin A1C
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clinical features, misdiagnosis occ
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achieved in selected cases by tissu
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Overall survivalPancreatic neuroend
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REFERENCES001. Metter CC. History <
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044. Fitz RH. The symptomatology an
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089. McClusky DA, Skandalakis LJ, C
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126. Toouli J. Sphincter of
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162. Deshpande AV, Thomas G, Shun A
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196. Park JH, Lee TH, Cheon SL, Sun
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226. Botoi G, Andercou A. Early and
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260. Nakamura H, Morifuji M, Muraka
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292. Borak GD, Romagnuolo J, Alsola
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324. Oh HC, Kim MH, Choi KS, Moon S
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358. Koornstra JJ, Mourits MJ, Sijm
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391. Chen JY, Amos CI, Merriman KW,
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421. Horwhat JD, Gerke H, Acosta RD
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451. Zamboni G, Capelli P, Scarpa A
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483. Rosa F, Pacelli F, Papa V, Tor
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517. Isayama H, Nakai Y, Togawa O,
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545. Pino MS, Milella M, Gelibter A
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576. Tanno S, Sasajima J, Koizumi K
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605. Ayadi L, Ellouze S, Khabir A,
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637. Nagar AM, Raut AA, Morani AC,
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670. Lejonklou M, Edfeldt K, Johans
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