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bibo:doi: 10.1101%2Fgad.228452.113
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Subject Item: _:vb27795316
rdf:type: n4:Section
dc:title: translational applications
n4:contains: _:vb27795317 _:vb27795318

Subject Item: _:vb27795317
rdf:type: n2:Context
rdf:value: Clinical screening approaches segregate into noninvasive imaging of the pancreas (magnetic resonance imaging [MRI] or computerized tomography [CT]) or invasive methodologies, such as endoscopic ultrasound (Canto et al. >>2012<<). One study found that in asymptomatic patients with familial pancreatic cancer, 7% had pancreatic cancer, and 16% had IPMN (Poley et al. 2009), suggesting that screening may be effective to detect preneoplastic or early stage neoplastic
n2:mentions: n3:22245846

Subject Item: _:vb27795318
rdf:type: n2:Context
rdf:value: However, the age at which to start (and stop) screening, the subsequent frequency of screening, and how to manage ambiguous lesions are not clear (Canto et al. >>2013<<).
n2:mentions: n3:23135763

Subject Item: _:vb27795319
rdf:type: n4:Section
dc:title: hereditary pancreatitis
n4:contains: _:vb27795320 _:vb27795321 _:vb27795322 _:vb27795323 _:vb27795324 _:vb27795325 _:vb27795326 _:vb27795327 _:vb27795328 _:vb27795329 _:vb27795330 _:vb27795331 _:vb27795332

Subject Item: _:vb27795320
rdf:type: n2:Context
rdf:value: The most appreciated and recognized risk factor for sporadic PDAC is chronic pancreatitis, which is triggered by acinar cell damage followed by autodigestion, a proinflammatory milieu, and fibrosis (Lowenfels et al. >>1993<<; Yadav and Lowenfels 2013). Chronic pancreatitis results in manifestations of exocrine insufficiency and endocrine insufficiency, the latter typically following the former.
n2:mentions: n3:8479461

Subject Item: _:vb27795321
rdf:type: n2:Context
rdf:value: appreciated and recognized risk factor for sporadic PDAC is chronic pancreatitis, which is triggered by acinar cell damage followed by autodigestion, a proinflammatory milieu, and fibrosis (Lowenfels et al. 1993; Yadav and Lowenfels >>2013<<). Chronic pancreatitis results in manifestations of exocrine insufficiency and endocrine insufficiency, the latter typically following the former.
n2:mentions: n3:23622135

Subject Item: _:vb27795322
rdf:type: n2:Context
rdf:value: An uncommon form of chronic pancreatitis is hereditary pancreatitis, which is an autosomal dominant inherited disorder and highly penetrant (>80%) and typically manifests prior to the age of 30 (Whitcomb >>2013<<), although this may be dependent on ancestral origin in the family.
n2:mentions: n3:23622139

Subject Item: _:vb27795323
rdf:type: n2:Context
rdf:value: Germline mutations in PRSS1 (protease, Ser1 [chromosome 7q35]), which encodes the cationic trypsinogen protein, are associated with hereditary pancreatitis (Whitcomb et al. >>1996<<). Trypsinogen is abundant in acinar cells. It hydrolyzes dietary proteins at lysine and arginine residues, thereby activating proenzymes.
n2:mentions: n3:8841182

Subject Item: _:vb27795324
rdf:type: n2:Context
rdf:value: R116C is a rare mutation that may result in misfolding of the protein and present an alternative cause of activation (Kereszturi et al. >>2009<<). Patients with hereditary pancreatitis have recurrent acute pancreatitis, which can often evolve into chronic pancreatitis. Their lifetime risk for PDAC is 35-fold (or more) by ages 70–75. Patients with hereditary pancreatitis may
n2:mentions: n3:19191323

Subject Item: _:vb27795325
rdf:type: n2:Context
rdf:value: Modeling of hereditary pancreatitis has revealed that pancreata from Elastase-R122H (mPRSS1) transgenic mice display early-onset acinar cell injury and inflammatory cell infiltration (Archer et al. >>2006<<). With age, the transgenic mice develop pancreatic fibrosis and display acinar cell dedifferentiation and an augmented response to cerulein-induced pancreatitis.
n2:mentions: n3:17087933

Subject Item: _:vb27795326
rdf:type: n2:Context
rdf:value: Chymotrypsin C (CTRC) gene (chromosome 1p36.21) mutations can be found in chronic pancreatitis (Rosendahl et al. >>2008<<). CTRC mutations appear to boost the effects of the mutant forms of cationic trypsinogen (Fig.
n2:mentions: n3:18059268

Subject Item: _:vb27795327
rdf:type: n2:Context
rdf:value: 1; Szabo and Sahin-Toth >>2012<<). Two alterations in the CTRC gene, R254W and K247_R254del, were significantly overrepresented in a study of cohorts of patients with idiopathic chronic pancreatitis and hereditary pancreatitis (Rosendahl et al. 2008).
n2:mentions: n3:22539344

Subject Item: _:vb27795328
rdf:type: n2:Context
rdf:value: Two alterations in the CTRC gene, R254W and K247_R254del, were significantly overrepresented in a study of cohorts of patients with idiopathic chronic pancreatitis and hereditary pancreatitis (Rosendahl et al. >>2008<<). Functional analysis of the CTRC variants showed impaired activity and/or reduced secretion, which resulted in “removal” of the normal negative degradative influence of CTRC on trypsin levels.
n2:mentions: n3:18059268

Subject Item: _:vb27795329
rdf:type: n2:Context
rdf:value: Similarly, heterozygous mutations in the cystic fibrosis transmembrane receptor (CFTR) gene may be found in a subset of these patients (Cohn et al. >>1998<<, 2000; Sharer et al. 1998).
n2:mentions: n3:9725922

Subject Item: _:vb27795330
rdf:type: n2:Context
rdf:value: Similarly, heterozygous mutations in the cystic fibrosis transmembrane receptor (CFTR) gene may be found in a subset of these patients (Cohn et al. 1998, >>2000<<; Sharer et al. 1998).
n2:mentions: n3:10872419

Subject Item: _:vb27795331
rdf:type: n2:Context
rdf:value: Similarly, heterozygous mutations in the cystic fibrosis transmembrane receptor (CFTR) gene may be found in a subset of these patients (Cohn et al. 1998, 2000; Sharer et al. >>1998<<). CFTR is an ion channel involved in the transport of chloride and thiocyanate. While CFTR gene mutations are traditionally associated with cystic fibrosis, they may also contribute to chronic pancreatitis. CFTR mutations lead to impaired
n2:mentions: n3:9725921

Subject Item: _:vb27795332
rdf:type: n2:Context
rdf:value: CFTR mutations lead to impaired chloride secretion and/or loss of bicarbonate secretion across ductal epithelial cells, which causes the accumulation of protein-rich materials, damage to acini, and subsequent fibrosis (Ooi et al. >>2011<<).
n2:mentions: n3:20923678

Subject Item: _:vb27795333
rdf:type: n4:Section
dc:title: familial atypical mole and multiple melanoma (fammm) syndrome
n4:contains: _:vb27795334 _:vb27795335 _:vb27795336 _:vb27795337 _:vb27795338

Subject Item: _:vb27795334
rdf:type: n2:Context
rdf:value: Three original descriptions in different kindreds implicated germline mutations or microdeletions in CDNK2 (chromosome 9p21.3), in particular restricted to the p16INK4a isoform (chromosome 9p21.3), as causative for FAMMM (Gruis et al. >>1995<<; Ranade et al. 1995). These mutant p16 proteins cannot inhibit the cyclin D1/CDK4 or cyclin D1/CDK6 complex.
n2:mentions: n3:7670475

Subject Item: _:vb27795335
rdf:type: n2:Context
rdf:value: in different kindreds implicated germline mutations or microdeletions in CDNK2 (chromosome 9p21.3), in particular restricted to the p16INK4a isoform (chromosome 9p21.3), as causative for FAMMM (Gruis et al. 1995; Ranade et al. >>1995<<). These mutant p16 proteins cannot inhibit the cyclin D1/CDK4 or cyclin D1/CDK6 complex.
n2:mentions: n3:7647780

Subject Item: _:vb27795336
rdf:type: n2:Context
rdf:value: In one study, there was a 25% increased risk of pancreatic cancer in FAMMM kindreds, and in another study, a cohort showed a 13-fold to 22-fold increase in pancreatic cancer (Lynch et al. >>2008<<). The age of onset of pancreatic cancer in FAMMM is quite variable, perhaps reflecting incomplete penetrance. Importantly, nearly 90% of sporadic PDACs harbor alterations (promoter hypermethylation, mutations, and microdeletions) in
n2:mentions: n3:17992582

Subject Item: _:vb27795337
rdf:type: n2:Context
rdf:value: Interestingly, CDK4 mutations that occur in the CDKN2-binding domain have been reported in FAMMM kindreds (Zuo et al. >>1996<<). Abnormal cell cycle progression and proliferation in FAMMM is evident also in sporadic PDAC. The reasons underlying the tissue-specific functional consequences of mutant p16 protein in FAMMM are not clear. It is likely that mutant p16
n2:mentions: n3:8528263

Subject Item: _:vb27795338
rdf:type: n2:Context
rdf:value: It is likely that mutant p16 protein promotes genomic instability in sporadic PDAC by virtue of its contribution to uncontrolled cell division (Campbell et al. >>2010<<).
n2:mentions: n3:20981101

Subject Item: _:vb27795339
rdf:type: n4:Section
dc:title: peutz-jeghers (pj) syndrome and other colon cancer syndromes: associations with pancreatic cancer
n4:contains: _:vb27795340 _:vb27795341 _:vb27795342 _:vb27795343 _:vb27795344

Subject Item: _:vb27795340
rdf:type: n2:Context
rdf:value: As an autosomal dominant disorder characterized by germline STK11 (LKB1) gene mutations, patients have early onset of large, multiple small intestinal and colonic polyps with increased risk of cancers at these sites (Rustgi >>2007<<). As patients age, they have an increased risk of breast, lung, pancreatic, cervical, and other cancers.
n2:mentions: n3:17938238

Subject Item: _:vb27795341
rdf:type: n2:Context
rdf:value: The types of pancreatic cancers include PDAC, IPMN, and serous cystadenocarcinomas (Sato et al. >>2001<<). One comprehensive Dutch study of PJ syndrome patients revealed a 26% increased risk of pancreatic cancer by age 70 yr and relative risk of 76 (Korsse et al. 2013). Patients may also present with ampullary cancer or distal bile duct
n2:mentions: n3:11733352

Subject Item: _:vb27795342
rdf:type: n2:Context
rdf:value: One comprehensive Dutch study of PJ syndrome patients revealed a 26% increased risk of pancreatic cancer by age 70 yr and relative risk of 76 (Korsse et al. >>2013<<). Patients may also present with ampullary cancer or distal bile duct cancer. Conditional deletion of Lkb1 in the mouse pancreas results in postnatal acinar cell degeneration, acinar-to-ductal metaplasia, and serous cystadenomas (Hezel et
n2:mentions: n3:23240097

Subject Item: _:vb27795343
rdf:type: n2:Context
rdf:value: Conditional deletion of Lkb1 in the mouse pancreas results in postnatal acinar cell degeneration, acinar-to-ductal metaplasia, and serous cystadenomas (Hezel et al. >>2008<<), suggesting some discordance between the pancreatic phenotype observed in PJ syndrome patients and this particular mouse model.
n2:mentions: n3:18227155

Subject Item: _:vb27795344
rdf:type: n2:Context
rdf:value: In a study of 147 families with germline MMR gene mutations, the cumulative risk of pancreatic cancer was 1.31% up to age 50 yr and 3.68% up to age 70 yr, an 8.6-fold increase compared with the general population (Kastrinos et al. >>2009<<). However, MSI is not common in sporadic PDAC.
n2:mentions: n3:19861671

Subject Item: _:vb27795345
rdf:type: n4:Section
dc:title: dna repair defects: a potential unifying theme in a subset of familial pancreatic cancer
n4:contains: _:vb27795346 _:vb27795347 _:vb27795348 _:vb27795349 _:vb27795350 _:vb27795351 _:vb27795352 _:vb27795353 _:vb27795354 _:vb27795355 _:vb27795356 _:vb27795357

Subject Item: _:vb27795346
rdf:type: n2:Context
rdf:value: This resection of one strand of DNA creates a single-stranded element onto which RAD51 is loaded by BRCA2 and PALB2 (Zhang et al. >>2009<<). RAD51 then helps pair this strand with the template on the double-strand sister chromatid to replace damaged segments through replication and recombination (Fig. 2). Germline mutations in some of the DNA repair genes have been
n2:mentions: n3:19268590

Subject Item: _:vb27795347
rdf:type: n2:Context
rdf:value: In a study of 173 families with germline BRCA2 mutations and breast/ovarian cancers, representing a cohort of 3728 individuals, the relative risk of pancreatic cancer was 3.51 (Goldgar >>1995<<). This risk is particularly evident in families of Ashkenazi Jewish descent, where a germline 6174delT BRCA2 mutation has been reported (Ozçelik et al. 1997). Some estimates indicate that up to 10% of familial pancreatic cancer may be
n2:mentions: n3:8788017

Subject Item: _:vb27795348
rdf:type: n2:Context
rdf:value: This risk is particularly evident in families of Ashkenazi Jewish descent, where a germline 6174delT BRCA2 mutation has been reported (Ozçelik et al. >>1997<<). Some estimates indicate that up to 10% of familial pancreatic cancer may be attributable to germline BRCA2 mutations, although the age of onset may not be particularly early in life. In a separate study, the relative risk of pancreatic
n2:mentions: n3:9140390

Subject Item: _:vb27795349
rdf:type: n2:Context
rdf:value: In a separate study, the relative risk of pancreatic cancer was nearly 2.3 in BRCA1 mutation carriers (Thompson et al. >>2002<<). Analysis of conditional knockouts of Brca2 in the mouse pancreas has produced conflicting results on KRASG12D-driven pancreatic carcinogenesis. In one setting, Brca2 accelerates lesions in KRASG12D-expressing mice irrespective of Trp53
n2:mentions: n3:12237281

Subject Item: _:vb27795350
rdf:type: n2:Context
rdf:value: In one setting, Brca2 accelerates lesions in KRASG12D-expressing mice irrespective of Trp53 status, with evidence of only loss of one allele of Brca2 being necessary (Skoulidis et al. >>2010<<). In another mouse model, Brca2 loss decelerates KRASG12D-driven pancreatic carcinogenesis but accelerates it when combined with Trp53 mutation (Rowley et al. 2011), again underscoring the careful interpretation that is necessary of some
n2:mentions: n3:21056012

Subject Item: _:vb27795351
rdf:type: n2:Context
rdf:value: In another mouse model, Brca2 loss decelerates KRASG12D-driven pancreatic carcinogenesis but accelerates it when combined with Trp53 mutation (Rowley et al. >>2011<<), again underscoring the careful interpretation that is necessary of some mouse models to correlate with human pancreatic cancer.
n2:mentions: n3:21199651

Subject Item: _:vb27795352
rdf:type: n2:Context
rdf:value: sequencing analysis of nearly 170 families with familial pancreatic cancer, two families were identified as having germline heterozygous ATM mutations, and four families had deleterious homozygous ATM mutations (Roberts et al. >>2012<<). PALB2 performs its tumor suppressor role at least in part by supporting HR-type DSB repair (HR-DSBR) through physical interactions with BRCA1, BRCA2, and RAD51 (Zhang et al. 2009).
n2:mentions: n3:22585167

Subject Item: _:vb27795353
rdf:type: n2:Context
rdf:value: PALB2 performs its tumor suppressor role at least in part by supporting HR-type DSB repair (HR-DSBR) through physical interactions with BRCA1, BRCA2, and RAD51 (Zhang et al. >>2009<<). In an analysis of nearly 100 families with familial pancreatic cancer, four families had evidence of protein-truncating mutations in PALB2 (Jones et al. 2009), confirmed in another study (Tischkowitz et al. 2009). The role of the Palb2
n2:mentions: n3:19268590

Subject Item: _:vb27795354
rdf:type: n2:Context
rdf:value: In an analysis of nearly 100 families with familial pancreatic cancer, four families had evidence of protein-truncating mutations in PALB2 (Jones et al. >>2009<<), confirmed in another study (Tischkowitz et al. 2009).
n2:mentions: n3:19264984

Subject Item: _:vb27795355
rdf:type: n2:Context
rdf:value: In an analysis of nearly 100 families with familial pancreatic cancer, four families had evidence of protein-truncating mutations in PALB2 (Jones et al. 2009), confirmed in another study (Tischkowitz et al. >>2009<<). The role of the Palb2 mutation in the initiation of pancreatic cancer via loss of its chromosome integrity maintenance role has not been investigated to date in mouse pancreata. However, Palb2 is known to play an important
n2:mentions: n3:19635604

Subject Item: _:vb27795356
rdf:type: n2:Context
rdf:value: However, Palb2 is known to play an important cancer-suppressive role in another tissue (namely, the breast), as it synergizes with Trp53 to limit mammary tumors in mice (Bowman-Colin et al. >>2013<<). It is likely that germline BRCA2, ATM, or PALB2 mutations in human familial pancreatic cancer contribute to defective DNA repair, accumulation of damaged DNA, genomic instability, and eventual cancer formation. Genomic instability is a
n2:mentions: n3:23657012

Subject Item: _:vb27795357
rdf:type: n2:Context
rdf:value: Genomic instability is a hallmark feature of sporadic PDAC (Campbell et al. >>2010<<), and understanding defective DNA repair mechanisms may shed light on the molecular pathogenesis of sporadic PDAC.
n2:mentions: n3:20981101

Subject Item: _:vb27795358
rdf:type: n4:Section
dc:title: approaches to discovery of new gene mutations
n4:contains: _:vb27795359 _:vb27795360 _:vb27795361 _:vb27795362

Subject Item: _:vb27795359
rdf:type: n2:Context
rdf:value: In an initial study of 57 familial pancreatic cancer kindreds, a total of 56 unique genomic regions with CNVs were identified that were not present in controls, including 31 amplifications and 25 deletions (Lucito et al. >>2007<<). In a subsequent study of 120 familial pancreatic cancer cases (and 1194 controls), a total of 93 nonredundant familial pancreatic cancer-specific CNVs (53 losses and 40 gains) were identified in 50 cases, with each CNV present in a
n2:mentions: n3:17912030

Subject Item: _:vb27795360
rdf:type: n2:Context
rdf:value: pancreatic cancer cases (and 1194 controls), a total of 93 nonredundant familial pancreatic cancer-specific CNVs (53 losses and 40 gains) were identified in 50 cases, with each CNV present in a single individual (Al-Sukhni et al. >>2012<<).
n2:mentions: n3:22665139

Subject Item: _:vb27795361
rdf:type: n2:Context
rdf:value: Genome-wide associations studies (GWASs) in patients with sporadic PDAC may highlight gene loci that could be tested for linkage in familial pancreatic cancer (Petersen et al. >>2010<<; Wu et al. 2011). To that end, susceptibility loci have been identified, although differences in results may be attributable to the evaluation of different populations (Table 1).
n2:mentions: n3:20101243

Subject Item: _:vb27795362
rdf:type: n2:Context
rdf:value: Genome-wide associations studies (GWASs) in patients with sporadic PDAC may highlight gene loci that could be tested for linkage in familial pancreatic cancer (Petersen et al. 2010; Wu et al. >>2011<<). To that end, susceptibility loci have been identified, although differences in results may be attributable to the evaluation of different populations (Table 1).
n2:mentions: n3:22158540

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