Progressive Development of Pseudomyxoma Peritonel After Resection of Low-Grade Mucinous Adenocarcinoma of the Appendix

2014 ◽  
Vol 109 ◽  
pp. S341
Author(s):  
Damodar Pandey ◽  
Kamran Zahid ◽  
Hilary Hertan
2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Yingbo Gong ◽  
Xin Wang ◽  
Zhi Zhu

Background. Pseudomyxoma peritonei (PMP) is a rare neoplasm involving the peritoneum. Most PMPs are low-grade appendicular mucinous neoplasms (LAMNs). There have been no reports of PMP originating from a transverse colonic mucinous adenocarcinoma and causing metastatic mucinous adenocarcinoma. Case Presentation. We report a 46-year-old woman who presented with a right abdominal mass of more than 4-month duration. Transverse colonic mucinous adenocarcinoma, PMP, and ovarian metastatic mucinous adenocarcinoma were diagnosed. The patient’s diet was normal, and she had no abdominal pain or bloating. The abdomen mass increased in the month before treatment. After chemotherapy, the transverse colon mass and ovarian giant cyst were resected and about 2000 mL of gelatinous tumor tissue was removed. Postoperative histology confirmed PMP from the transverse colonic mucinous adenocarcinoma, ovarian metastatic mucinous adenocarcinoma, and mesocolon metastatic cancer. Multiple lung metastases appeared 8 months after surgery. The patient died 29 months after surgery because of an inability to eat and poor nutrition. A systematic literature review of the management and outcome of all known similar cases is also presented. Conclusions. This is the first report of PMP originating from a transverse colonic mucinous adenocarcinoma. It was diagnosed during resective surgery, involved ovarian metastasis, and survival was short. We did an extensive literature review in order to describe the clinical characteristics, histopathological findings, genetic profile, and potential treatments of PMP caused by nonappendiceal mucinous adenocarcinoma.


2017 ◽  
Vol 24 (7) ◽  
pp. 1783-1786 ◽  
Author(s):  
Vladimir Milovanov ◽  
Armando Sardi ◽  
Nail Aydin ◽  
Carol Nieroda ◽  
Michelle Sittig ◽  
...  

2019 ◽  
Vol 27 (1) ◽  
pp. 165-170 ◽  
Author(s):  
Arvind Sabesan ◽  
Seth Felder ◽  
Sebastian Feuerlein ◽  
Cesar Lam ◽  
Melissa McGettigan ◽  
...  

2017 ◽  
Vol 24 (S3) ◽  
pp. 627-627 ◽  
Author(s):  
Sean P. Dineen ◽  
Richard E. Royal ◽  
Paul F. Mansfield ◽  
Keith F. Fournier

2019 ◽  
Vol 218 (6) ◽  
pp. 1239-1243 ◽  
Author(s):  
Yosef Y. Nasseri ◽  
Ruoyan Zhu ◽  
Christine Sutanto ◽  
Christina Wai ◽  
Jason S. Cohen ◽  
...  

2017 ◽  
Vol 4 (4) ◽  
pp. 17
Author(s):  
Mahmoud L. Soliman ◽  
Shi Yang ◽  
John Cho Lee

A 58-year old male has a past medical history of a rectal low-grade mucinous adenocarcinoma with a KRAS codon 12/13 mutation (GGT>GAT), for which he received neoadjuvant chemotherapy and radiation.  Five months after diagnosis, the patient underwent a low anterior resection showing persistent tumor with the pathological staging being (ypT3, ypN0, ypMx).  Six months after surgery, follow-up PET scan showed two right upper lung nodules measuring 1.0 and 1.8 cm.  Subsequent video-assisted thoracic surgery with a lung wedge resection revealed two tumors: a mucinous adenocarcinoma and an acinar-predominant adenocarcinoma.  The mucinous adenocarcinoma showed similar cytologic features as the rectal tumor; however, it showed more of a lepidic pattern.  The immunohictochemical profile of the lung mucinous adenocarcinoma was positive CK7 (cytoplasmic), negative CK20, TTF1, napsin-A, and CDX2.  KRAS codon 12/13 analysis also showed a mutation in the lung, however it was different compared to the previous rectal tumor and showed a GGT>AGT mutation.  The acinar adenocarcinoma had a wild-type KRAS.  In this case, we favored a primary lung mucinous carcinoma over a metastasis from the rectum based on the lepidic morphology, CK20 negativity and differing KRAS codon 12 mutations.  A year after the resection of the lung adenocarcinomas, the patient presented with dyspnea and abnormal liver functions.  Abdominal US and MRI revealed multiple liver lesions (up to 1.9 cm).  Core liver biopsies showed a poorly-differentiated mucinous adenocarcinoma with positive CK7 (cytoplasmic) and negative CK20, TTF-1, napsin-A, CDX2 and HSA.  KRAS codon 12/13 analysis also showed a mutation GGT>AGT, similar to that of the lung mucinous adenocarcinoma.  The immunohistochemical profile and the KRAS mutation sequence of the hepatic tumor suggests a metastasis from the lung primary and corroborates the earlier premise that the lung tumor is distinct from the rectal one.  In conclusion, in the unusual circumstance of a lung mucinous adenocarcinoma in a patient with established gastrointestinal mucinous primary, KRAS mutation analysis sequencing could help distinguish whether the lung mucinous is a primary tumor or metastasis from colorectal origin.


Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 706 ◽  
Author(s):  
Justin Hou Ming Yung ◽  
Adria Giacca

Obesity has been described as a global epidemic and is a low-grade chronic inflammatory disease that arises as a consequence of energy imbalance. Obesity increases the risk of type 2 diabetes (T2D), by mechanisms that are not entirely clarified. Elevated circulating pro-inflammatory cytokines and free fatty acids (FFA) during obesity cause insulin resistance and ß-cell dysfunction, the two main features of T2D, which are both aggravated with the progressive development of hyperglycemia. The inflammatory kinase c-jun N-terminal kinase (JNK) responds to various cellular stress signals activated by cytokines, free fatty acids and hyperglycemia, and is a key mediator in the transition between obesity and T2D. Specifically, JNK mediates both insulin resistance and ß-cell dysfunction, and is therefore a potential target for T2D therapy.


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