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\begin{document}

\title{Long-term survival in pancreatic ductal adenocarcinoma with lung and
brain metastases: a case report}



\author[1]{Yutaro Ohgaki}%
\author[1]{Makoto Takahashi}%
\author[1]{Yasuhiro Morita}%
\author[1]{Tatsuya Hayashi}%
\author[1]{Keishi Kawasaki}%
\author[1]{Takuma Kikkawa}%
\author[1]{Daisuke Sato}%
\author[1]{Takahiro Ota}%
\author[1]{Sachiko Izumi}%
\author[1]{Haruka Okada}%
\affil[1]{Tokyo Metropolitan Tama Medical Center}%


\vspace{-1em}



  
  \date{June 07, 2024}


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\textbf{1. Introduction}

Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis, with a
5-year survival rate of approximately 10\% \textsuperscript{1}.
Unfortunately, surgical resection is indicated in \textless{} 20\% of
patients \textsuperscript{2}. Many of these patients have distant
metastases, which decreases the median overall survival time to
\textless{} 1 year, and most die within 2 years \textsuperscript{3}.
PDAC most frequently metastasizes to the liver (76\%), followed by the
lungs (19.9\%). The brain (0.6\%) is extremely rare site of
metastasis\textsuperscript{4}. However, in a few cases, long-term
survival has been achieved via multidisciplinary treatment including
chemotherapy, radiotherapy, and local excision, even after distant
metastasis, such as lung and brain metastases, was observed
\textsuperscript{5,6}. Herein, we report the case of a patient with PDAC
who achieved long-term survival after pylorus-preserving
pancreaticoduodenectomy~(PpPD) despite metachronous lung and brain
metastases.

\textbf{2. Case report}

A 70-year-old male patient who was referred to our hospital, for the
treatment of obstructive jaundice was diagnosed with pancreatic head
cancer. He was 168 cm tall, weighed 71.6 kg, had a body mass index of
25.4 kg/m\textsuperscript{2}, did not smoke or drink alcohol, and had no
history of chronic pancreatitis or diabetes. His blood test results were
as follows: total bilirubin, 15.0 mg/dL (0.3--1.2); direct bilirubin,
11.4 mg/dL (\textless{}0.4); aspartate aminotransferase, 125 U/L
(10--40); alanine aminotransferase, 218 U/L (5--40); carbohydrate
antigen 19--9 (CA19-9), 38.2 U/mL (\textless{}37.0); carcinoembryonic
antigen (CEA), 4.4 ng/mL (5.0); duke pancreatic monoclonal antigen type
2 (DUPAN-2), \textgreater{}1600 U/mL (\textless{}150); and s-pancreas-1
antigen (SPan1), 240 U/mL (\textless{}30). Computed tomography (CT)
revealed a low-density mass (27 mm in diameter) with no major vessel
involvement in the pancreatic head (Fig. 1) and no distant metastases.
Endoscopic retrograde cholangiopancreatography was performed for biliary
drainage, and the pancreatic tumor was pathologically diagnosed as a
PDAC. The clinical stage was T3N1M0, stage IIB, according to the eighth
edition of the TNM classification of the American Joint Committee on
Cancer (AJCC) /Union for International Cancer Control (UICC). The tumor
was considered resectable and the patient underwent PpPD. Because tumor
invasion was observed in the superior mesenteric vein (SMV), combined
resection and reconstruction of the SMV was performed. No postoperative
complications were observed and the patient was discharged on the 21st
postoperative day.

Macroscopic examination revealed a whitish solid mass, 50\selectlanguage{ngerman}×40×30 mm in
size, located in the pancreatic head (\textbf{Fig. 2A and 2B} ). The
mass was histologically diagnosed as a well-differentiated
adenocarcinoma, T3 N1(7/38) M0, stage IIB, according to the eighth
edition of the TNM classification of the AJCC/UICC (\textbf{Fig. 2C} ).
The lymphatic invasion was severe, vascular invasion was moderate, and
neural invasion was severe. Biliary, duodenal, anterior tissue,
retoroperitoneal tissue, superior mesenteric vein, and extrapancreatic
nerve plexus invasions were observed.

One month after surgery, the patient received gemcitabine and S-1 (GS:
gemcitabine at a dose of 800 mg/m\textsuperscript{2} on days 1 and 8
plus S-1 at a dose of 100 mg/body twice daily on days 1--14 of a 21-day
cycle) as postoperative adjuvant chemotherapy. At the time, only
gemcitabine was recommended for adjuvant chemotherapy after PDAC surgery
in Japan, and S1 was not yet recommended\textsuperscript{7}. In
addition, since there have been some reports that GS therapy is
effective as adjuvant chemotherapy\textsuperscript{89}, GS therapy was
not standard clinical treatment at that time, but selected after
providing sufficient explanation to the patient and obtaining informed
consent. Eleven months post-PpPD, multiple microscopic bilateral
pulmonary metastases were suspected on CT. Since the lesions suspected
to be multiple lung metastases remained almost unchanged in size and
only gemcitabine was the chemotherapy medication recommended for
unresectable PDAC in Japan at that time \textsuperscript{7}, GS therapy
was continued with sufficient informed consent for an extended period,
even after lung metastasis recurrence.

At 4 years and 6 months post-PpPD, only one lesion in the right lower
lung grew rapidly (\textbf{Fig. 3A} ), and bronchoscopy revealed class V
cytopathology (\textbf{Fig. 3B} ). Whole-body dynamic CT showed no
metastasis except in the lung, and since the possibility of primary lung
cancer could not be ruled out, the bottom portion of the right lung was
thoracoscopically resected 5 years and 5 months post-PpPD. Other
pulmonary lesions showed almost no change in size; therefore, we
concluded that chemotherapy was effective. In addition, they were not
resected because they were numerous and complete resection was
impossible.

The lesion was pathologically diagnosed as an adenocarcinoma, similar to
the primary lesion (\textbf{Fig. 4A} ). Immunostaining was positive for
CK7 (\textbf{Fig. 4B} ), and negative for CK20 (\textbf{Fig. 4C} ) and
TTF-1 (\textbf{Fig. 4D} ). This indicated a low likelihood of primary
lung cancer. Based on these findings, metastatic PDAC was diagnosed. In
addition, multiple lung lesions were obscured, and after obtaining
sufficient informed consent from the patient, he was followed up without
chemotherapy. However, 6 months after the second surgery (5 years and 10
months after PpPD), CT revealed a nodule in the upper lobe of the right
lung. Although GS was resumed, the number of lung metastases increased.
Seven years and five months post-PpPD, the treatment regimen was
switched to a combination therapy of gemcitabine plus nab-paclitaxel
(GEM + nab-PTX: gemcitabine at a dose of 450 mg/m\textsuperscript{2} and
nab-PTX at a dose of 115 mg/m\textsuperscript{2} on days 1 and 8 of a
21-day cycle). Eleven years and one month post-PpPD, FOLFIRINOX (a
combination of folinic acid, fluorouracil, irinotecan hydrochloride, and
oxaliplatin) was required to stem the growth of the lung metastases.
However, the resulting adverse effects compelled the physicians to
discontinue the treatment after only one course, and the patient was
subsequently treated with S-1 alone (at a dose of 80 mg/body twice daily
on days 1--14 of a 21-day cycle).

11 years and 2 months post-PpPD, the patient was readmitted because of
dizziness and left hemiplegia. Contrast-enhanced magnetic resonance
imaging (MRI) revealed a 23×22×20-mm neoplasm in the right inferior
parietal lobule. A strong contrast effect was evident at the edges and
center, and mulberry-like papillary structures were observed within the
lesion (\textbf{Fig. 5A} ). A 5-mm ring-shaped contrast effect was also
observed in the right cingulate gyrus. Metastatic brain tumors were
suspected in the right inferior parietal lobule and right cingulate
gyrus. Only the right inferior parietal lobe lesion was resected to
relieve symptoms at 11 years and 4 months post-PpPD.

Histopathological analysis revealed metastatic PDAC in the brain
(\textbf{Fig. 5B} ). Six weeks after the third surgery, S-1 treatment
was resumed (at a dose of 100 mg/body twice daily on days 1--14 of a
21-day cycle).

MRI performed at this time demonstrated numerous small lesions in the
brain, and a tumor appeared in the meninges at the site of the previous
surgery. Subsequently, the patient underwent whole-brain irradiation,
and his condition improved to the point where he was able to walk
without assistance. However, the patient died of PDAC recurrence 6
months after the craniotomy (11 years and 8 months after the first
surgery).

The CA19-9, CEA, SPan1, and DUPAN-2 levels were measured monthly. CA19-9
was slightly elevated only at the first visit but remained low
throughout the observation period, and CEA only spiked just before
death. SPan1 and DUPAN-2 levels increased as metastasis increased and
decreased as the chemotherapy regimen was changed (\textbf{Fig. 6} ).

\textbf{3. Discussion}

Although PDAC outcomes have been improving owing to progress in
multidisciplinary treatments, the 5-year survival rate remains
\textless{} 5\% \textsuperscript{10}. As previously reported,
approximately 75\% of patients with resectable PDAC who have undergone
radical resection experience tumor relapse and have an overall survival
time of \textless{} 30 months \textsuperscript{11}.

Surgery is usually not indicated for postoperative recurrence of PDAC,
except when it occurs in the remnant pancreas \textsuperscript{12}. In
such cases, systemic chemotherapy (such as FOLFIRINOX or combination
therapy consisting of GEM + nab-PTX) is
preferred\textsuperscript{13,14}. However, surgical treatment may also
be considered if chemotherapy is successful and metastasis can be
controlled for a sufficient period. Our previous report described a
patient in whom long-term survival was achieved via surgery for
gallbladder and stomach metastases following surgery for
PDAC\textsuperscript{15}.

Recurrence of lung metastases after surgery for PDAC is known to have a
better prognosis than recurrence at other sites, and previous studies
have reported successful resection of lung metastases. Zheng \emph{et
al.} reported that primary tumor recurrence in the lungs was associated
with longer median disease-free survival (15 months) and longer median
overall survival after detection (20 months) than any other type of
primary recurrence. Moreover, patients with primary recurrence in the
lungs have the longest median survival (36 months) among all patients
with tumor recurrence \textsuperscript{16}. Kurahara \emph{et
al.}reported that the median survival time of seven patients with
postoperative lung metastases of PDAC who underwent lung resection was
36.5 months, which exceeded that of patients receiving either
chemotherapy or the best supportive care \textsuperscript{5}.

Many case reports on lung metastases of PDAC have shown that local
resection prolongs patient survival. Furthermore, a long interval
between the initial resection for PDAC and subsequent lung resection has
been associated with long-term survival (13-15). However, currently
available evidence on the effectiveness of resection for pulmonary
metastases of PDAC is insufficient to establish general recommendations,
and indications for surgery should be carefully weighed in each case.
Okui \emph{et al.} reported that surgery for lung metastasis should be
considered under the following conditions: 1) the patient will be able
to tolerate the surgery, 2) the primary lesion is under control, 3) no
other metastases are present outside the lungs, and 4) multiple lung
metastases can be resected \textsuperscript{17}.

Brain metastases from PDAC are rare and have poor prognosis. Treatment
is usually palliative in these cases; however, a previous study has
reported that aggressive surgery can result in long-term survival.
Lemke\emph{et al.} reported that patients with PDAC who achieved
long-term survival were initially treated with cancer-directed surgery
with curative intent and had solitary metachronous brain metastasis for
which complete (R0) resection followed by adjuvant therapy could be
performed. Therefore, surgery for metachronous metastatic PDAC lesions
may be considered a viable option in some cases \textsuperscript{18}.
Kumar et al. reported a 9-year survival case after
craniotomy\textsuperscript{6}. Matsumoto \emph{et al.} reported that
local resection failed to prolong survival in their patient. However, it
improved the patient's neurological symptoms and allowed him to spend
the remainder of his life meaningfully, without neurological
deficits\textsuperscript{19}. Therefore, surgical resection may confer
benefits to some patients.

In the present case, brain metastases were observed in the right
inferior parietal lobule and right cingulate gyrus. The former was the
cause of the left hemiplegia, which prompted craniotomy. As a result,
neurological symptoms improved significantly and the patient recovered
sufficiently to walk unassisted.

Gamma knife treatment was also considered, but craniotomy was chosen for
the following reasons: 1) the lesion occurred 11 years after surgery for
PDAC, and pathological diagnosis by resection was necessary; 2) the
lesion was located in the inferior parietal lobule of the non-dominant
hemisphere, was present on the brain surface, and was safely resected;
and 3) severe peri-tumor edema worsens after gamma knife treatment. The
patient's days were numbered; therefore, prompt improvement of
neurological symptoms was required.

Thirteen of the 31 case reports of pancreatic cancer with brain
metastasis retrieved in a PubMed search involved surgical resection. Of
the 13 patients who underwent surgery, nine underwent radical resection
and four underwent palliative surgery, with some patients in both groups
experiencing an improvement in prognosis and quality of
life\textsuperscript{18} \textsuperscript{19} \textsuperscript{2021}.

A previous report revealed that the incidence of PDAC in patients with
brain metastasis and complicated lung metastases was higher than that of
overall pancreatic cancer patients (29--37.5\% vs. 19.9\%).
Sasaki\emph{et al.} reported that lung metastasis may be a risk factor
for brain metastasis in patients with PDAC \textsuperscript{21}.

In the present case, lung resection was performed for lung metastasis 5
years and 5 months post-PpPD, craniotomy was performed for brain
metastasis 11 years and 4 months post-PpPD, and GS, GEM + nab-PTX,
FOLFIRINOX, and S-1 were administered at various time points during the
disease course. Considering the transition in tumor markers in Fig. 6,
chemotherapy contributed the most to this patient. However, resection of
rapidly growing lung metastases and brain tumors that had caused
paralysis had significant effects in prolonging the patient's life
prognosis and maintaining his quality of life. Although the prognosis of
PDAC remains poor in some patients, it can be improved using multimodal
therapy that combines chemotherapy and local excision.

\textbf{4. Conclusion}

Multimodal treatment involving local excision and chemotherapy for
postoperative metastases has the potential to extend the survival of
PDAC patients.

\textbf{Authors' contributions}

\textbf{Ohgaki Yutaro:} Drafted the manuscript.

\textbf{Makoto Takahashi:} Revised the manuscript.

\textbf{Yasuhiro Morita:} Contributed to the preoperative examinations
and diagnosis, and performed the first operation and followed-up on the
patient.

\textbf{Tatsuya Hayashi:} Followed-up on the patient.

\textbf{Takuma Kikkawa} : Performed the lung surgery.

\textbf{Takahiro Ota:} Planned the craniotomy for the brain tumor, and

\textbf{Daisuke Sato:} Performed the craniotomy.

\textbf{Sachiko Izumi:} Administered the radiation treatment.

\textbf{Haruka Okada:} Pathologically diagnosed the disease.

All the authors have read and approved the final manuscript.

\textbf{ACKNOWLEDGEMENTS}

Not applicable.

\textbf{FUNDING INFORMATION}

None.

\textbf{CONFLICT OF INTEREST}

None declared.

\textbf{CONSENT}

Written informed consent was obtained from the patient to publish this
report in accordance with the journal's patient consent policy.

\textbf{REFERENCES}

1. Siegel RL, Miller KD, Fuchs HE, Jemal A. 2022. Cancer statistics,
2022. \emph{CA Cancer J Clin} . 72(1):7-33.

2. Konstantinidis IT, Warshaw AL, Allen JN, et al. 2013. Pancreatic
ductal adenocarcinoma: is there a survival difference for R1 resections
versus locally advanced unresectable tumors? What is a ''true'' R0
resection? \emph{Ann Surg} . 257(4):731-736.

3. Ryan DP, Hong TS, Bardeesy N. 2014. Pancreatic adenocarcinoma.\emph{N
Engl J Med} . 371(11):1039-1049.

4. Oweira H, Petrausch U, Helbling D, et al. 2017. Prognostic value of
site-specific metastases in pancreatic adenocarcinoma: A Surveillance
Epidemiology and End Results database analysis. \emph{World J
Gastroenterol} . 23(10):1872-1880.

5. Kurahara H, Maemura K, Mataki Y, et al. 2020. Lung recurrence and its
therapeutic strategy in patients with pancreatic
cancer.\emph{Pancreatology} . 20(1):89-94.

6. Kumar A, Dagar M, Herman J, Iacobuzio-Donahue C, Laheru D. 2015. CNS
involvement in pancreatic adenocarcinoma: a report of eight cases from
the Johns Hopkins Hospital and review of literature. \emph{J
Gastrointest Cancer} . 46(1):5-8.

7. Yamaguchi K, Tanaka M. 2011. EBM-based Clinical Guidelines for
Pancreatic Cancer 2009 from the Japan Pancreas Society: a
synopsis.\emph{Jpn J Clin Oncol} . 41(7):836-840.

8. Murakami Y, Uemura K, Sudo T, et al. 2008. Adjuvant gemcitabine plus
S-1 chemotherapy after surgical resection for pancreatic
adenocarcinoma.\emph{Am J Surg} . 195(6):757-762.

9. Murakami Y, Uemura K, Sudo T, et al. 2009. Impact of adjuvant
gemcitabine plus S-1 chemotherapy after surgical resection for
adenocarcinoma of the body or tail of the pancreas. \emph{J Gastrointest
Surg} . 13(1):85-92.

10. Buscail L. 2017. Commentary: Pancreatic cancer: is the worst to
come? \emph{Int J Epidemiol} . 46(6):1774-1775.

11. Takahashi M, Nojima H, Kuboki S, et al. 2020. Comparing prognostic
factors of Glut-1 expression and maximum standardized uptake value by
FDG-PET in patients with resectable pancreatic
cancer.\emph{Pancreatology} . 20(6):1205-1212.

12. Miyazaki M, Yoshitomi H, Shimizu H, et al. 2014. Repeat
pancreatectomy for pancreatic ductal cancer recurrence in the remnant
pancreas after initial pancreatectomy: is it worthwhile? \emph{Surgery}
. 155(1):58-66.

13. Conroy T, Desseigne F, Ychou M, et al. 2011. FOLFIRINOX versus
gemcitabine for metastatic pancreatic cancer. \emph{N Engl J Med} .
364(19):1817-1825.

14. Von Hoff DD, Ervin T, Arena FP, et al. 2013. Increased survival in
pancreatic cancer with nab-paclitaxel plus gemcitabine. \emph{N Engl J
Med} . 369(18):1691-1703.

15. Takahashi M, Yoshitomi H, Kato A, et al. 2019. A case of
successfully resected metachronous gastric and gallbladder metastases
from pancreatic body cancer. \emph{Surg Case Rep} . 5(1):21.

16. Zheng B, Ohuchida K, Yan Z, Okumura T, Ohtsuka T, Nakamura M. 2017.
Primary Recurrence in the Lung is Related to Favorable Prognosis in
Patients with Pancreatic Cancer and Postoperative Recurrence.\emph{World
J Surg} . 41(11):2858-2866.

17. Okui M, Yamamichi T, Asakawa A, Harada M, Horio H. 2017. Resection
for Pancreatic Cancer Lung Metastases. \emph{Korean J Thorac Cardiovasc
Surg} . 50(5):326-328.

18. Lemke J, Scheele J, Kapapa T, Wirtz CR, Henne-Bruns D, Korn\{Lemke
m, M. 2013. Brain metastasis in pancreatic cancer. \emph{Int J Mol Sci}
. 14(2):4163-4173.

19. Matsumoto H, Yoshida Y. 2015. Brain metastasis from pancreatic
cancer: A case report and literature review. \emph{Asian J Neurosurg} .
10(1):35-39.

20. Oka Y, Takano S, Kouchi Y, et al. 2021. Simultaneous brain and lung
metastases of pancreatic ductal adenocarcinoma after curative
pancreatectomy: a case report and literature review. \emph{BMC
Gastroenterol} . 21(1):9.

21. Sasaki T, Sato T, Nakai Y, Sasahira N, Isayama H, Koike K. 2019.
Brain metastasis in pancreatic cancer: Two case reports. \emph{Medicine
(Baltimore)} . 98(4):e14227.

\textbf{Figure legends}

\textbf{Figure 1:} Computed tomography scan showing a 27-mm mass (arrow)
and no major vessel involvement in the pancreatic head.

\textbf{Figure 2: A, B)} A whitish, solid, 50-mm mass (arrow) in the
pancreatic head. \textbf{C)} Pathological findings showing cells with
nuclear atypia including ductal and papillary structures. The lesion was
diagnosed as a well-differentiated tubular adenocarcinoma.

\textbf{Figure 3: A)} Computed tomography scan showing growth of the
mass at the bottom of the right lung. \textbf{B)} The cytological
diagnosis was adenocarcinoma.

\textbf{Figure 4:} \textbf{A)} Pathological analysis showed an
adenocarcinoma similar to the primary lesion, round-shaped enlarged
nucleus, and mucin-producing columnar tumor cells proliferating in a
tubular or papillary manner. \textbf{B)} Immunostaining is positive for
CK7. \textbf{C)} Immunostaining is negative for CK20.
\textbf{D)}Immunostaining is negative for TTF-1, indicating a low
likelihood of primary lung cancer.

\textbf{Figure 5: A)} Magnetic resonance imaging showing a 23×22×20-mm
neoplasm in the right inferior parietal lobule (arrow).
\textbf{B)}Pathological findings showing a tumor similar to the primary
lesion, cells with atypical nuclei, and a high N/C ratio, indicating
papillary, fused ductal structures and solid arrangements, which are
findings of adenocarcinoma.

\textbf{Figure. 6)} Tumor markers (CA19-9, CEA, DUPAN-2, and SPan1) were
measured regularly during the course of the study; DUPAN-2 and SPan1
reflected disease activity.

Both decreased markedly after the PpPD, but not after pulmonary
resection or after craniotomy, and decreased when chemotherapy was
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