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Vietri, M.T. Pancreatic Cancer with Mutation. Encyclopedia. Available online: https://encyclopedia.pub/entry/19653 (accessed on 18 December 2025).
Vietri MT. Pancreatic Cancer with Mutation. Encyclopedia. Available at: https://encyclopedia.pub/entry/19653. Accessed December 18, 2025.
Vietri, Maria Teresa. "Pancreatic Cancer with Mutation" Encyclopedia, https://encyclopedia.pub/entry/19653 (accessed December 18, 2025).
Vietri, M.T. (2022, February 19). Pancreatic Cancer with Mutation. In Encyclopedia. https://encyclopedia.pub/entry/19653
Vietri, Maria Teresa. "Pancreatic Cancer with Mutation." Encyclopedia. Web. 19 February, 2022.
Pancreatic Cancer with Mutation
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This entry is adapted from the peer-reviewed paper 10.3390/genes13020321

Pancreatic ductal adenocarcinoma (PDAC) is the seventh leading cause of cancer death worldwide; most of cases are sporadic, however about 5% to 10% report a hereditary predisposition. Several hereditary syndromes have been associated with familial pancreatic cancer (FPC) onset, including hereditary breast and ovarian cancer syndrome (HBOC), Lynch syndrome (LS), Familial atypical multiple mole melanoma (FAMMM), Familial adenomatous polyposis (FAP), Li–Fraumeni syndrome (LFS), Peutz–Jeghers syndrome (PJS), and Hereditary pancreatitis (HP).

pancreatic ductal adenocarcinoma hereditary breast and ovarian cancer syndrome hereditary nonpolyposis colon cancer syndrome

1. Introduction

Pancreatic ductal adenocarcinoma (PDAC) is the twelfthmost common tumor and the seventh main cause of cancer death worldwide [1]. It represents about 5% of all malignancy cases, with the overall survival (OS) 5 years worse than other cancers [2]. Recently, a 2.3-fold increase has been seen in the global number of cases and deaths from PDAC, with a 3 times higher incidence in most developed countries [3]. Most of the PDAC cases are sporadic, but about 5% to 10% report a hereditary predisposition [4].
Pancreatic cancer arises in several hereditary syndromes, including Hereditary breast and ovarian cancer (HBOC), Lynch syndrome (LS), Familial atypical multiple mole melanoma (FAMMM), Familial adenomatous polyposis (FAP), Li–Fraumeni syndrome (LFS), Peutz–Jeghers syndrome (PJS), and Hereditary pancreatitis (HP) [5][6][7][8]. Most familial pancreatic cancer (FPC) is attributable to HBOC syndrome that results from germline mutations in BRCA1/2 genes and other genes such as ATM, BRIP1, CHEK2, RAD50, and RAD51C [9][10]. In FPC belonging to HBOC, BRCA2 mutations are the most common genetic alteration, observed in about 5–10% of cases [11].
It was shown that about half of the patients with PDAC report pathogenic germline variants, even if they do not have a family history of pancreatic carcinoma. Moreover, the mutation presence could have therapeutic implications [12]. The American Society of Clinical Oncology (ASCO) and National Comprehensive Cancer Network (NCCN) guidelines to date recommend universal germline tests for all patients with PDAC [13] in order to identify germline mutation in patients that may benefit from alternative treatments. Moreover, identification of germline mutations in a patient will allow for testing family members at risk ofthe same or other associated cancers.
Immunetherapies or molecularly targeted agents have been recently introduced into cancer clinical practice [14][15][16], but it is still unclear whether they promote benefits in PDAC patients. For patients with BRCA mutation, positive results data have been shown in clinical trials on poly (ADP-ribose) polymerase (PARP) inhibitors, as in use of anti-PD-1 antibodies for patients with mismatch repair (MMR) mutation [17]. In a retrospective analysis, patients with PDAC, with a BRCA mutation, after treatment with the combination regimen of leucovorin calcium, fluorouracil, irinotecan hydrochloride, and oxaliplatin (FOLFIRINOX), had a longer OS than those without the mutations [18]. No differences in survival outcomes were observed in patients treated with Gemcitabine/nab-paclitaxel and FOLFIRINOX, so alternative treatments could be considered in patients with PDAC [19].

2. HBOC Families

Out of 56 HBOC probands, 16 (28.6%) reported a pathogenic mutation, particularly 6/56 (10.7%) in BRCA1, 9/56 (16.1%) in BRCA2, and 1/56 (1.8%) reported a double mutation (DM), both in BRCA2.
The number and percentage of cancers type that occur in mutated HBOC families are reported in Figure 1A; PDAC is the second recurrent cancer, resulting in 13% of cases. Table 1 shows the frequency of cancer types that occur in mutated and non-mutated HBOC families. A statistically significant difference is observed in OC onset.
Genes 13 00321 g001
Figure 1. Cancer types that occur in HBOC mutated families (A). Cancer types that occur in LS mutated families (B). Cancer types that occur in FAP mutated family(C). BC: Breast cancer; PDAC: Pancreatic ductal adenocarcinoma; OC: Ovarian cancer; LC: Lung cancer; LVC: Liver cancer; GC: Gastric cancer; EC: Endometrial cancer; CC: Colon cancer; BLC: Bladder cancer; PC: Prostate cancer; LEU: Leukemia; bBC: Bilateral Breast cancer; LAC: Laryngeal cancer; MEL: Melanoma; KC: Kidney cancer; ESC: Esophageal cancer; BRC: Brain cancer; and TC: Thyroid cancer.
Table 1. Number and percentage of cancers type that occur in mutated and non-mutated HBOC families.
Type of Cancer Cancer Number in Family Non Mutated PDAC Patients Mutated PDAC Patients p-Value
BC 0 2 (4%) 2 (11%) 0.27
1 15 (33%) 2 (11%)
2 13 (28%) 4 (22%)
3 10 (22%) 5 (28%)
≥4 6 (13%) 5 (28%)
PDAC 1 34 (74%) 14 (78%) 0.75
2 12 (26%) 4 (22%)
OC 0 33 (72%) 8 (44%) 0.042
1 11 (24%) 6 (33%)
2 2 (4%) 4 (22%)
LC 0 23 (50%) 10 (56%) 0.30
1 18 (39%) 4 (22%)
2 4 (9%) 3 (17%)
3 1 (2%) 0 (0%)
4 0 (0%) 1 (6%)
LVC 0 34 (74%) 13 (72%) 0.34
1 10 (22%) 4 (22%)
2 2 (4%) 0 (0%)
3 0 (0%) 1 (6%)
GC 0 27 (59%) 11 (61%) 0.93
1 15 (33%) 6 (33%)
2 3 (7%) 1 (6%)
4 1 (2%) 0 (0%)
EC 0 33 (72%) 15 (83%) 0.71
1 7 (15%) 1 (6%)
2 4 (9%) 1 (6%)
3 2 (4%) 1 (6%)
CC 0 34 (74%) 14 (78%) 0.78
1 6 (13%) 3 (17%)
2 4 (9%) 1 (6%)
3 2 (4%) 0 (0%)
BLC 0 37 (80%) 15 (83%) 0.35
1 8 (17%) 2 (11%)
2 0 (0%) 1 (6%)
3 1 (2%) 0 (0%)
PC 0 40 (87%) 14 (78%) 0.62
1 5 (11%) 3 (17%)
2 1 (2%) 1 (6%)
LEU 0 41 (89%) 15 (83%) 0.53
1 5 (11%) 3 (17%)
bBC 0 44 (96%) 15 (83%) 0.099
1 2 (4%) 3 (17%)
LAC 0 39 (85%) 15 (83%) 0.77
1 6 (13%) 3 (17%)
2 1 (2%) 0 (0%)
MEL 0 43 (93%) 16 (89%) 0.54
1 3 (7%) 2 (11%)
KC 0 43 (93%) 17 (94%) 0.89
1 3 (7%) 1 (6%)
ESC 0 45 (98%) 16 (89%) 0.13
1 1 (2%) 2 (11%)
BRC 0 43 (93%) 17 (94%) 0.81
1 2 (4%) 1 (6%)
2 1 (2%) 0 (0%)
TC 0 42 (91%) 18 (100%) 0.20
1 4 (9%) 0 (0%)
BC: Breast cancer; PDAC: Pancreatic ductal adenocarcinoma; OC: Ovarian cancer; LC: Lung cancer; LVC: Liver cancer; GC: Gastric cancer; EC: Endometrial cancer; CC: Colon cancer; BLC: Bladder cancer; PC: Prostate cancer; LEU: Leukemia; bBC: Bilateral Breast cancer; LAC: Laryngeal cancer; MEL: Melanoma; KC: Kidney cancer; ESC: Esophageal cancer; BRC: Brain cancer; and TC: Thyroid cancer.
One of the BRCA2 mutations, specifically c.5511delT (p.Phe1837LeufsX3), was a novel germline mutation, not previously reported in any database, previously observedas somatic mutation in tissue of mucoepidermoid carcinoma [20]. This mutation, localized in exon 11, consists of a thymine deletion at nucleotide 5511, which results in the introduction of a premature stop codon at position 1840 (Figure 2A). It was identified in a 46-year-old woman affected with breast cancer diagnosed at the age of 45. Figure 2B reports the pedigree of the proband; her mother was affected with pancreatic cancer. Moreover, the analysis was extended in the sisters of 48 and 43 years, that carried the mutation. Finally, the analysis was conducted to daughters of 23 and 19 years and it revealed the presence of mutation only in the daughter of 19 years.
Genes 13 00321 g002
Figure 2. (A) Partial electropherogram of BRCA2 exon 11. The novel germline mutation c.5511delT (p.Phe1837LeufsX3) results in chain termination at codon 1840. (B) Pedigree of the proband carrying the BRCA2 novel mutation c.5511delT (p.Phe1837LeufsX3). The ages at diagnosis are indicated in brackets. Her mother died at 80 years old, was affected with PDAC.
Figure 3 shows the location through BRCA1/2 genes of the mutations found. The mutations are located throughout the length of gene, in BRCA2 most of them fall in exon 11.
Genes 13 00321 g003
Figure 3. Mutations found in HBOC, LS, and FAP families with PDAC localized trough BRCA1, BRCA2, MLH1, and APC genes.
Mutational analysis was extended to 60 family members of 16 mutated patients, both healthy and cancer affected. The results of genetic test were summarized in Table 2. Twenty-sixfamily members resulted wild-type and 34 inherited the proband’s mutation, of these 11 with cancer and 23 unaffected.
Table 2. Mutations identified and results of mutational analysis conducted in family members of 16HBOC mutated patients, 2LS mutated patients, and 1 FAP mutated patient. Name of mutation was reported in bold.
Family Gene Mutation Exon Family Members
(Diagnosis)		 Age Mutational Analysis
1 BRCA1 c.181T>G
(p.Cys61Gly)		 5 Proband (Ovarian Cancer) 72 Mutated
Sister (Breast Cancer) 64 Mutated
Daughter (Unaffected) 48 Wild Type
2 BRCA1 c.917delT
(p.Leu306ArgfsTer27)		 11 Proband (Breast/Ovarian Cancer) 56 Mutated
Son (Unaffected) 28 Mutated
Brother (Unaffected) 61 Mutated
Sister (Unaffected) 65 Wild Type
3 BRCA1 c.5123C>A
(p.Ala1708Glu)		 18 Proband (Pancreatic cancer) 67 Mutated
Sister (Ovarian cancer) 63 Mutated
Nephew (Unaffected) 38 Wild Type
Niece (Unaffected) 40 Mutated
4 BRCA1 c.5266dupC
(p.Gln1756Profs)		 20 Proband (Breast and Ovarian cancer) 64 Mutated
Daugheter (Unaffected) 62 Wild Type
Son (Unaffected) 38 Mutated
Brother (Unaffected) 66 Mutated
Niece (Breast cancer) 32 Mutated
Niece (Unaffected) 41 Mutated
5 BRCA1 c.5266dupC
(p.Gln1756Profs)		 20 Proband (Pancreatic Cancer) 73 Mutated
Sister (Breast Cancer) 72 Mutated
6 BRCA1 c.5397_5398del
(p.Leu1800Trpfs*29)		 22 Proband (Ovarian Cancer) 63 Mutated
Son (Unaffected) 33 Wild Type
Daughter (Unaffected) 41 Wild Type
7 BRCA2 c.3545_3546del
(p.Gln1181_Phe1182insTer)		 11 Proband (Ovarian cancer) 57 Mutated
Daugheter (Unaffected) 32 Wild Type
Daugheter (Unaffected) 23 Wild Type
Son (Unaffected) 28 Wild Type
Brother (Unaffected) 58 Wild Type
Sister (Ovarian cancer) 62 Mutated
Niece (Unaffected) 34 Mutated
Nephew (Unaffected) 30 Mutated
8 BRCA2 c.4284dupT
(p.Gln1429Serfs)		 11 Proband (Breast cancer) 85 Mutated
Daugheter (Unaffected) 57 Wild Type
Daugheter (Unaffected) 56 Mutated
Son(Unaffected) 52 Wild Type
Son(Unaffected) 50 Mutated
Sister (Unaffected) 83 Mutated
Niece (Unaffected) 48 Mutated
Nephew (Unaffected) 42 Mutated
Nephew (Unaffected) 45 Mutated
Nephew (Unaffected) 36 Wild Type
9 BRCA2 c.5511delT
(p.Phe1837LeufsX3)		 11 Proband (Breast cancer) 46 Mutated
Sister (Unaffected) 48 Mutated
Sister (Unaffected) 43 Mutated
Daughter (Unaffected) 23 Wild Type
Daughter (Unaffected) 19 Mutated
10 BRCA2 c.5722_5723delCT
(p.L1908RfsX2)		 11 Proband (Breast cancer) 62 Mutated
Brother (Unaffected) 61 Wild Type
11 BRCA2 c.6037A>T
(p.Lys2013Ter)		 11 Proband (Ovarian cancer) 52 Mutated
Daugheter (Unaffected) 25 Mutated
Son (Unaffected) 21 Wild type
Sister (Unaffected) 58 Mutated
Niece (Unaffected) 32 Wild type
Niece (Unaffected) 28 Wild type
12 BRCA2 c.6450dup
(p.Val2151fs)		 11 Proband (Breast cancer) 54 Mutated
Son (Unaffected) 24 Wild Type
Daughter (Unaffected) 21 Mutated
13 BRCA2 c.6468_6469delTC
(p.Gln2157Ilefs)		 11 Proband (Breast Cancer) 47 Mutated
Father (Unaffected) 75 Mutated
Sister (Unaffected) 46 Mutated
Sister (Unaffected) 41 Wild type
14 BRCA2 c.6468_6469delTC
(p.Gln2157Ilefs)		 11 Proband (Pancreatic Cancer) 61 Mutated
Sister (Breast and EndometrialCancer) 62 Mutated
Sister (Ovarian Cancer) 54 Mutated
Nephew (Unaffected) 26 Wild type
15 BRCA2 c.7857G>A
(p.Trp2619Ter)		 17 Proband (Breast Cancer) 45 Mutated
Sister (Unaffected) 48 Wild Type
16 BRCA2
BRCA2		 c.631G>A
(p.Val221Ile)

c.7008-2A>T
(IVS13-2A>T)		 7

14		 Proband (Breast Cancer) 62 Mutated
Daugheter (Unaffected) 41 Wild type
Daugheter (Unaffected) 35 Mutated
Brother (Unaffected) 59 Wild Type
Sister (Bilateral Breast Cancer) 56 Mutated
Niece (Unaffected) 35 Wild Type
Niece (Unaffected) 30 Wild Type
Niece (Breast cancer) 33 † Mutated
Cousin (Breast cancer) 70 Mutated
1 MLH1 c.2181_2182delCA
(p.Ile728Serfs)		 5 Proband (Colon Cancer) 25 Mutated
Brother (Unaffected) 29 Wild Type
Aunt (Breast Cancer) 58 Wild Type
Aunt (Unaffected) 54 Wild Type
2 MLH1 c.229T>C
(p.Cys77Arg)		 3 Proband (Colon Cancer) 48 Mutated
No family members   -
1 APC c.6709C>T
(p.Arg2237Ter)		   Proband (Pancreatic Cancer) 52 † Mutated
Brother (Cerebral angiomas) 65 Mutated
Sister (Pancreatic Cancer) 48 † Mutated
Sister (Colon Cancer) 55 Mutated
Sister (Colon Cancer) 57 Mutated
Sister (Unaffected) 67 Wild Type
Sister (Unaffected) 66 Wild Type

3. LS Families

Out of sevenprobands, two (28.6%) reported a pathogenic mutation in MLH1 gene. The mean age of pancreatic cancer onset was 62.5 years in mutated patients and 57.3 years in non-mutated patients.
The number and percentage of cancers type that occur in LS mutated families were reported in Figure 1B. PDAC is the third recurrent cancer and happen in 6.9% of cases.
The mutations found were in exon 3 and 5 of MLH1 gene, as shown in Figure 3.
Mutational analysis was extended to three family members of one mutated patient, both healthy and cancer affected; in the second family, no family member was available for genetic testing. The results of genetic test were summarized in Table 2; no family member inherited the mutation.

4. FAP Families

Out of three probands, one (33.3%) reported a pathogenic mutation in APC gene. The mean age of pancreatic cancer onset was 47.5 years in mutated patient and 49.6 years in non-mutated patients.
The number and percentage of cancers type that occur in APC mutated family were reported in Figure 1C. PDAC is the second recurrent cancer and occurred in 44.4% of cases.
The mutation found was in exon 15 of APC gene, as showed in Figure 3.
Mutational analysis was extended to six family members, both healthy and cancer affected, of mutated patient; four inherited the proband’s mutation (Table 2).

References

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