Aging affects regrowth of stealthperitoneal dissemination of advanced ovarian cancer: a multicenter retrospective cohort study.

Ovarian cancer (OvCa) is one of the most lethal gynecological malignancies, and most patients are diagnosed at advanced stage with peritoneal dissemination. Although age at diagnosis is considered an independent prognostic factor, its impact on peritoneal recurrence after combined cytoreductive surgery and chemotherapy is not clear. The objective of this study was to investigate the impact of aging on peritoneal recurrence from stealth dissemination and gain insight of the pathophysiology of OvCa in elderly patients. A total of 243 patients with pT2b-pT3 epithelial ovarian who achieved complete surgery, no-residual tumor at first surgery, were selected to be analyzed the risk of peritoneal seeding and recurrence. We found that age over 65 years was independently associated with an increased risk of peritoneum-specific (PS) recurrence (. Furthermore, pT3 stages and positive ascites cytology also worsen the PS-relapse-free survival. Collectively, our findings suggest that age, especially over 65 years, predicts reduced peritoneum-specific tumor recurrence in patients with advanced ovarian cancer after complete cytoreduction surgery, particularly those with pT3 tumors and positive ascites cytology.

PAR1 Is a Candidate Target for the Treatment of Peritoneal Dissemination in Gastric Cancer.

BACKGROUND/AIM: Peritoneal dissemination (PD) is a frequent cause of death in gastric cancer (GC), and there is evidence of an association between protease-activated receptor-1 (PAR1) and the development of PD. This study hypothesized that PD in GC might be influenced by PAR1. MATERIALS AND METHODS: The cytotoxic effect of paclitaxel (PTX) on PAR1-transfected MKN45 (MKN45/PAR1) cells was analyzed using the MTT assay, and IC50 values were determined. In female athymic nude mice, MKN45/PAR1 cells were suspended in 0.05 ml phosphate-buffered saline (PBS) medium and inoculated into the stomach mid-wall. In each group, intraperitoneal injections of PBS, PTX, SCH79797 (PAR1-antagonist), or PTX plus SCH79797 were administered on days 8, 15, and 22 following tumor inoculation. At 56 days after tumor inoculation, mice were examined for both abdominal tumor nodule status and size and weight of the tumors. RESULTS: The IC50 of PTX for MKN45/PAR1 cells was 0.0697 µM and that of SCH79797 was 0.0145 µM. Mean survival of the MKN45/PAR1 mice in the PBS group was 28.75 days, whereas survival times for the mice treated with SCH79797, PTX, or a combination of PTX and SCH79797 were 31.2, 49.2, and 48.5 days, respectively. Tumor weight was smaller in the group receiving PTX and SCH79797 intraperitoneally compared with that in the PBS group (1,086±127.2 mg vs. 33.2±19.9 mg; p<0.001). CONCLUSION: The PAR1 antagonist was found to inhibit PD in a PAR1-expressing GC cell line. PAR1 may serve as a promising therapeutic target for managing PD in gastric cancer, as it plays a crucial role in its progression.

A Case Report of Long-Term Survival Achieved by Nivolumab and Hyperthermia With Multiple Local Therapies for the Peritoneal Dissemination of Gastric Cancer.

A 60-year-old male with recurrent metastatic gastric cancer achieved long-term survival with nivolumab, hyperthermia, and local multisite therapy. The patient had a history of multiple relapses despite receiving standard treatment. After the failure of multiple lines of chemotherapy, nivolumab and hyperthermia were initiated. During this combination therapy, local treatments including surgery and radiation therapy were administered to treat the progressive disease. Remarkably, the patient achieved more than five years of overall survival time after starting nivolumab and external repeated hyperthermia with local therapies and has shown no measurable disease on imaging for the past 24 months. This case suggests that a combination of nivolumab, hyperthermia, and local therapies may offer a potential therapeutic strategy for patients with advanced gastric cancer.

Robot-assisted extended rectal anterior resection for peritoneal dissemination of hepatocellular carcinoma invading rectum after atezolizumab plus bevacizumab combined therapy.

The prognosis for patients with hepatocellular carcinoma (HCC) with extrahepatic metastasis remains poor. In recent years, the combination therapy of atezolizumab plus bevacizumab (ATZ/BEV) has demonstrated remarkable antitumor efficacy against HCC. Conversion surgery following chemotherapy emerges as a promising strategy for initially unresectable HCC. A 74-year-old man was referred to our department with disseminated HCC in the rectovesical pouch. He underwent hepatic subsegmental resection for primary HCC with abdominal wall invasion on the background of chronic hepatitis B 7 years ago. Intrahepatic recurrence was emerged 5 and 2 years ago, which was successfully managed with transarterial chemoembolization and radiofrequency ablation, respectively. Subsequently, 4 cm peritoneal dissemination appeared in the rectovesical pouch, invading the rectum, right pelvic neural plexus, and right seminal vesicle. ATZ/BEV therapy was initiated, but bevacizumab had to be discontinued due to fistula formation between the rectum and the tumor after two courses, and atezolizumab monotherapy was continued. After 1 year of ATZ/BEV combined therapy followed by atezolizumab monotherapy, the disseminated tumor, though still visible, exhibited a significant reduction, with no new intra- or extrahepatic lesions. To confirm the absence of other disseminated lesions, a diagnostic laparoscopy was performed. Subsequently, robot-assisted extended rectal anterior resection with the right seminal vesicle and right pelvic neural plexus, and permanent colostomy (Hartmann's procedure) were performed. Histopathological examination revealed disseminated HCC with a 4 mm resection margin to achieve R0 resection. We present a case of disseminated HCC successfully undergoing curative surgery through robot-assisted extended rectal anterior resection following ATZ/BEV combined therapy. Supplementary Information: The online version contains supplementary material available at 10.1007/s13691-024-00688-0.

An actinomycosis infection resembling peritoneal dissemination of rectal cancer: a case report.

BACKGROUND: Actinomycosis is a suppurative and granulomatous inflammation commonly caused by Actinomyces israelii. Due to its rarity and the paucity of characteristic clinical features, diagnosis of intra-abdominal actinomycosis is challenging, especially when the patient has a treatment history of abdominal cancer. CASE PRESENTATION: The patient is a 72-year-old man who has a history of multiple abdominal surgeries for rectal cancer, including low anterior resection for primary rectal cancer, partial hepatic resection for metachronous liver metastasis, and Hartmann surgery for local recurrence. The patient has also undergone parastomal hernia repair using the Sugarbaker method. One year after hernia repair, computed tomography (CT) identified a mass lesion between the abdominal wall and the mesh, suggesting the possibility of peritoneal recurrence of rectal cancer. The accumulation of fluorodeoxyglucose (FDG) was evident via positron emission tomography-CT (PET-CT), while tumor marker levels were within the normal range. On laparotomy, the small intestine, abdominal wall, mesh, colon, and stoma were observed to be associated with the mass lesion, and en bloc resection was carried out. However, postoperative histopathological examination revealed an actinomyces infection without any cancerous cells. CONCLUSIONS: This case highlights the challenges faced by surgeons regarding preoperative diagnosis of actinomycosis, especially when it occurs after the resection of abdominal cancer. Also, this case reminds us of the importance of a histopathological examination for abdominal masses or nodules before starting chemotherapy.

A Case Study of a High-Grade Serous Carcinoma of the Fallopian Tube Transformed into Carcinosarcoma at the Site of Peritoneal Dissemination With Immunohistological Evidence of an Epithelial-Mesenchymal Transition.

We report a patient in whom a primary high-grade serous carcinoma (HGSC) of the fallopian tube transformed into a carcinosarcoma at the site of peritoneal dissemination, and immunohistological analysis suggested the involvement of an epithelial-mesenchymal transition (EMT). The patient, a 70-year-old woman, had an abdominal mass palpated on admission, and a laparotomy was performed after a close examination. The resected right fallopian tube was cystically dilated, and a solid mass was observed in its lumen. The histological diagnosis was HGSC of the right fallopian tube with a papillary or complex tubular structure composed of tumor cells with marked nuclear irregularities. p53 was overexpressed, and no mesenchymal tumor component was observed. The resected left-sided abdominal mass of the omentum was a solid with a long diameter of 100 mm. Microscopically, the tumor exhibited a mixture of HGSC and high-grade sarcoma with nonspecific differentiation. Furthermore, a heterologous chondrosarcoma was subsequently observed from the high-grade sarcoma. The HGSC component was E-cadherin positive. The high-grade sarcoma component was positive for EMT-related proteins such as zinc finger E-box-binding homeobox 1 (ZEB1) and twist family bHLH transcription factor 1 (TWIST1). The chondrosarcoma component was ZEB1 positive and TWIST1 negative. p53 overexpression was found in all 3 components. The tumor of the omentum suggested that an EMT phenomenon was involved in the tumorigenesis. In this scenario, the primary HGSC of the fallopian tube with obvious invasion demonstrated that the conversion from carcinoma to sarcoma by EMT occurs only with peritoneal dissemination.

Effects of Hyperbaric Oxygen Therapy for Malignant Bowel Obstruction Caused by Peritoneal Dissemination.

INTRODUCTION: This study aimed to investigate the efficacy of hyperbaric oxygen therapy (HBOT) in patients presenting with malignant bowel obstruction (MBO) and peritoneal dissemination. MATERIALS AND METHODS: We retrospectively examined whether HBOT affects prognosis following MBO with peritoneal dissemination. This study included 44 patients diagnosed with MBO secondary to peritoneal dissemination at our hospital between January 2013 and December 2022. Among these patients, 30 underwent HBOT. The treatment protocol involved daily HBOT administration, comprising 100% oxygen at 2.5 atmospheres absolute for 60 min. RESULTS: In a univariate analysis of HBOT and non-HBOT groups, the proportion of patients able to resume eating was significantly higher in the HBOT group. Therefore, the percentage of patients in the non-HBOT group whose MBO did not improve was significantly higher than that in the HBOT group. The percentage of patients undergoing surgery or receiving anticancer treatment did not differ significantly between the groups, whereas overall survival was significantly longer in the HBOT group. Furthermore, when examining inoperable patients, significantly more individuals in the HBOT group could resume eating, and their overall survival was significantly prolonged. CONCLUSIONS: HBOT may increase the spontaneous resolution rate and improve long-term prognoses of patients with MBO secondary to peritoneal dissemination.

Molecular mechanisms driving the interactions between platelet and gastric cancer cells during peritoneal dissemination.

Platelets (PLTs) facilitate tumor progression and the spread of metastasis. They also interact with cancer cells in various cancer types. Furthermore, PLTs form complexes with gastric cancer (GC) cells via direct contact and promote their malignant behaviors. The objective of the present study was to explore the molecular mechanisms driving these interactions and to evaluate the potential for preventing peritoneal dissemination by inhibiting PLT activation in GC cells. The present study examined the roles of PLT activation pathways in the increased malignancy of GC cells facilitated by PLT-cancer cells. Transforming growth factor-ß receptor kinase inhibitor (TRKI), Src family kinase inhibitor (PP2) and Syk inhibitor (R406) were used to identify the molecules influencing these interactions. Their therapeutic effects were verified via cell experiments and validated using a mouse GC peritoneal dissemination model. Notably, only the PLT activation pathway-related inhibitors TRKI and PP2, but not R406, inhibited the PLT-enhanced migration and invasion of GC cells. In vivo analyses revealed that PLT-enhanced peritoneal dissemination was suppressed by PP2. Overall, the present study revealed the important role of the Srk family in the interactions between PLTs and GC cells, suggesting kinase inhibitors as promising therapeutic agents to mitigate the progression of peritoneal metastasis in patients with GC.

Anti-tumor effect of antibody-drug conjugate targeting cell adhesion molecule 1 on GIST cells representing small intestinal GIST.

Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the alimentary tract. The prognosis depends on the primary site, and small intestinal GISTs have a worse prognosis than gastric GISTs. Molecularly targeted drugs to inhibit tyrosine kinase activity of KIT were used for unresectable or recurrent GISTs. However, secondary resistance to the drugs is often acquired, and treatments based on other mechanisms are needed. Previously, we reported that cell adhesion molecule 1 (CADM1) was highly expressed in most of small intestinal GISTs but not in most of gastric GISTs. In the present study, we examined whether the antibody-drug conjugate (ADC) with anti-CADM1 antibody and monomethyl auristatin E (anti-CAD-ADC) shows anti-tumor effect on CADM1-expressing human GIST cells. The ADC adhibited in this study was previously used for CADM1-expressing human mesothelioma cells and showed anti-tumor effect for them in vitro. GIST-T1 cell line of gastric origin which scarcely expresses CADM1 and GIST-T1 cells transfected with CADM1 cDNA (GIST-T1-CAD cells) which highly expresses CADM1 and represents small intestinal GIST were used. In vitro, anti-CAD-ADC showed remarkable cytotoxic activity on GIST-T1-CAD cells, but control ADC did not. Both anti-CAD-ADC and control ADC did not show anti-tumor effect on original GIST-T1 cells. When GIST-T1-CAD cells were subcutaneously injected to the nude mice, intravenous administration of anti-CAD-ADC showed inhibitory effect for tumor enlargement. Tumor of GIST-T1 cells grew even after anti-CAD-ADC injection. When GIST-T1-CAD cells were injected into peritoneal cavity of the SCID mice, intraperitoneal administration of anti-CAD-ADC showed reduction of the peritoneal tumor. On the other hand, peritoneal tumor grew after control ADC administration. Tissue and organ damage due to administration of anti-CAD-ADC was not apparent by macroscopic and histological examinations in mice. These results indicate that anti-CAD-ADC could have apparent anti-tumor effect on CADM1-expressing human GIST cells both in in vitro and in vivo mouse models.

High expression of B3GALT5 suppresses the galectin-4-mediated peritoneal dissemination of poorly differentiated gastric cancer cells.

Peritoneal metastasis frequently accompanies metastatic and/or recurrent gastric cancer, leading to a poor prognosis owing to a lack of effective treatment. Hence, there is a pressing need to enhance our understanding of the mechanisms and molecules driving peritoneal metastasis. In a previous study, galectin-4 inhibition impeded peritoneal metastasis in a murine model. This study examined the glycan profiles of cell surface proteins and glycosphingolipids (GSLs) in cells with varying tumorigenic potentials to understand the intricate mechanisms underlying galectin-4-mediated regulation, particularly glycosylation. Detailed mass spectrometry analysis showed that galectin-4 knockout cells exhibit increased expression of lacto-series GSLs with ß1,3-linked galactose while showing no significant alterations in neolacto-series GSLs. We conducted real-time polymerase chain reaction (PCR) analysis to identify candidate glycosyltransferases that synthesize increased levels of GSLs. Subsequently, we introduced the candidate B3GALT5 gene and selected the clones with high expression levels. B3GALT5 gene-expressing clones showed GSL glycan profiles like those of knockout cells and significantly reduced tumorigenic ability in mouse models. These clones exhibited diminished proliferative capacity and showed reduced expression of galectin-4 and activated AKT. Moreover, co-localization of galectin-4 with flotillin-2 (a raft marker) decreased in B3GALT5-expressing cells, implicating GSLs in galectin-4 localization to lipid rafts. D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (a GSL synthase inhibitor) also affected galectin-4 localization in rafts, suggesting the involvement of GSL microdomains. We discovered that B3GALT5 plays a crucial role in regulating peritoneal metastasis of malignant gastric cancer cells by suppressing cell proliferation and modulating lipid rafts and galectin-4 via mechanisms that are yet to be elucidated.

G-CSF induces neutrophil extracellular traps formation and promotes ovarian cancer peritoneal dissemination.

Epithelial ovarian cancer is characterized by aggressive peritoneal dissemination. Neutrophils are mobilized to peritoneal cavity in some patients with ovarian cancer dissemination; however, its pathological significance remains unknown. This study aimed to investigate the role of neutrophil extracellular traps (NETs) in ovarian cancer dissemination. We conducted a retrospective analysis of clinical data and samples from 340 patients with ovarian cancer who underwent primary surgery between 2007 and 2016 at the Osaka University Hospital. In vitro, NETs formation was induced by stimulating human peripheral neutrophils. The human ovarian cancer cell line, OVCAR8, was cocultured with NETs. For an ovarian cancer dissemination mouse model, we performed an intraperitoneal injection of OVCAR8 cells into nude mice. The association between NETs and peritoneal dissemination was explored, and model mice were treated with the PAD4 inhibitor GSK484 to assess antitumor efficacy. Neutrophilia (neutrophil count >7000/mm3) correlated with shorter survival, advanced peritoneal dissemination, elevated granulocyte colony-stimulating factor (G-CSF) levels, increased neutrophil count in ascites, and augmented NETs foci in peritoneal dissemination sites. In vitro assays revealed that G-CSF stimulated neutrophils to form NETs, promoting cancer cell adhesion. In vivo investigations revealed that G-CSF-producing tumor-bearing mice had accelerated peritoneal dissemination and poor prognosis. NETs formation was pathologically observed at the peritoneal dissemination sites. Inhibition of NETs formation by GSK484 significantly delayed peritoneal dissemination in vivo. In conclusion, G-CSF was associated with intra-abdominal NETs formation and increased peritoneal dissemination. NETs represent potential therapeutic targets for ovarian cancer, particularly in patients with neutrophilia.

Diffuse peritoneal dissemination of intracranial pure germinoma via ventriculoperitoneal shunt.

Germinomas frequently cause hydrocephalus, and ventriculoperitoneal shunts (VPS) have been commonly used for their management. Although VPS can potentially serve as a route for peritoneal dissemination of germinomas, the abdominal imaging characteristics of this rare yet important complication remain unknown. In this article, we report the computed tomography imaging findings of diffuse peritoneal dissemination of intracranial germinoma.

Claudin-18 status and its correlation with HER2 and PD-L1 expression in gastric cancer with peritoneal dissemination.

BACKGROUND: Gastric cancer with peritoneal dissemination (PD) has a dismal prognosis, and current treatments have shown little efficacy. CLDN18.2-targeted therapies have shown promising efficacy against gastric cancers that express high levels of CLDN18. Because of the limited information regarding CLDN18.2 status in PD, we analyzed PD-positive gastric cancers for CLDN18 status in both primary and PD, along with HER2 and PD-L1 combined positive score (CPS). METHODS: Immunohistochemical analyses were performed on 84 gastric cancer cases using paired primary and PD tissue samples. RESULTS: At 40% cut-off, CLDN18 was positive in 57% (48/84) primary tumors and in 44% (37/84) PDs. At 75% cut-off, 28.6% (24/84) primary tumors and 20.2% (17/84) PDs were CLDN18-positive. The concordance rate between primary tumors and PD was 79.8% at 40% cut-off and 75% at 75% cut-off. When comparing biopsy and surgical specimens, the concordance rates were 87.5% at 40% cut-off and 81.3% at 75% cut-off. Within a tumor, the superficial area tended to have a higher CLDN18-positive rate than the invasive front (P = 0.001). Although HER2 -positivity was only 11.9% in this cohort, CLDN18 positivity in HER2-negative tumors (n = 74) was relatively high: 60.8% at 40% cut-off and 28.4% at 75% cut-off. Among double-negative (HER2 - and PD-L1 CPS < 1) tumors, CLDN18 positivity was 67.6% at 40% cut-off and 26.5% at 75% cut-off. CONCLUSIONS: CLDN18 expression is generally maintained in PD and is relatively high even in double-negative tumors, making it a promising therapeutic target for PD-positive gastric cancer.

RAC1-mediated integrin alpha-6 expression in E-cadherin-deficient gastric cancer cells promotes interactions with the stroma and peritoneal dissemination.

Diffuse-type gastric cancer (DGC) is a subtype of gastric cancer that is prone to peritoneal dissemination, with poor patient prognosis. Although intercellular adhesion loss between cancer cells is a major characteristic of DGCs, the mechanism underlying the alteration in cell-to-extracellular matrix (ECM) adhesion is unclear. We investigated how DGCs progress and cause peritoneal dissemination through interactions between DGC cells and the tumour microenvironment (TME). P53 knockout and KRASG12V-expressing (GAN-KP) cells and Cdh1-deleted GAN-KP (GAN-KPC) cells were orthotopically transplanted into the gastric wall to mimic peritoneal dissemination. The GAN-KPC tumour morphology was similar to that of human DGCs containing abundant stroma. RNA sequencing revealed that pathways related to Rho GTPases and integrin-ECM interactions were specifically increased in GAN-KPC cells compared with GAN-KP cells. Notably, we found that Rac Family Small GTPase 1 (RAC1) induces Integrin Subunit Alpha 6 (ITGA6) trafficking, leading to its enrichment on the GC cell membrane. Fibroblasts activate the FAK/AKT pathway in GC cells by mediating extracellular matrix (ECM)-Itga6 interactions, exacerbating the malignant phenotype. In turn, GC cells induce abnormal expression of fibroblast collagen and its transformation into cancer-associated fibroblasts (CAFs), resulting in DGC-like subtypes. These findings indicate that Cdh1 gene loss leads to abnormal expression and changes in the subcellular localization of ITGA6 through RAC1 signalling. The latter, through interactions with CAFs, allows for peritoneal dissemination.

Patient-Derived Exosomes as siRNA Carriers in Ovarian Cancer Treatment.

RNA interference is a powerful gene-silencing tool with potential clinical applications. However, its therapeutic use is challenging because suitable carriers are unavailable. Exosomes are stable small endogenous vesicles that can transport functional molecules to target cells, making them ideal small interfering RNA (siRNA) carriers. Herein, we elucidated the therapeutic potential of patient-derived exosomes as an siRNA carrier for ovarian cancer (OC) treatment. The exosomes were extracted from the culture medium of primary fibroblasts collected from the omentum of patients with OC during surgery. MET proto-oncogene, receptor tyrosine kinase (MET) was selected for gene silencing, c-Met siRNAs were synthesized and loaded into the exosomes (Met-siExosomes) via electroporation, and the treatment effect of the Met-siExosomes was assessed in vitro and in vivo. The Met-siExosomes downregulated the c-Met protein levels and inhibited OC cell proliferation, migration, and invasion. In xenograft experiments using SKOV3-13 and ES-2 cells, Met-siExosomes were selectively extracted from peritoneally disseminated tumors. Intraperitoneal treatment suppressed the c-Met downstream targets in cancer cells and prolonged mouse survival. The synthesized siRNAs were successfully and selectively delivered via the exosomes to intraperitoneally disseminated tumors. As patients with OC routinely undergo omentectomy and abundant fibroblasts can be easily collected from the omentum, patient-derived exosomes may represent a promising therapeutic siRNA carrier to treat OC.

A case of disseminated peritoneal metastases after 2-year conservative treatment for intramucosal colon carcinoma due to a perforation during endoscopic submucosal dissection.

A 70-year-old man was admitted to our hospital for the treatment of a large granular-type laterally spreading tumor in the splenic flexure of the descending colon. The preoperative diagnosis was intramucosal colon carcinoma and endoscopic submucosal dissection was performed. During treatment, a small perforation occurred accidentally. After conservative treatment with endoscopic suturing, the patient was discharged without additional surgery. The pathological diagnosis was an intramucosal carcinoma. One year after treatment, no local recurrence was observed on endoscopy, and abdominal computed tomography showed no obvious metastasis. Two years later, fluorodeoxyglucose-positron emission tomography/computed tomography, laparoscopic findings, and histopathologic findings by experimental excision of omentum revealed several disseminated peritoneal metastases from previously treated colon carcinoma. To the best of our knowledge, this is the first report of peritoneal dissemination after a small perforation during endoscopic submucosal dissection and conservative therapy for early-stage colon carcinoma. This report suggests the possibility of tumor dissemination in patients with small perforations during endoscopic procedures. Endoscopists should be aware of these rare potential risks and perform later surveillance carefully.

Peritoneal dissemination of appendiceal goblet cell adenocarcinoma mimicking white pus caused by peritonitis following appendicitis: an instructive case report.

BACKGROUND: Goblet cell adenocarcinoma is an extremely rare tumor in which the same cells exhibit both mucinous and neuroendocrine differentiation. It is considered more aggressive compared to conventional carcinoids and more likely to cause metastasis. CASE PRESENTATION: We report a case of goblet cell adenocarcinoma with peritoneal metastases. A 62-year-old man underwent appendectomy for acute appendicitis. Intraoperatively, inflammatory white pus and a small amount of dirty ascites were observed in the lower abdomen with severely inflamed appendix. Histopathological examination of the specimen collected during appendectomy revealed goblet cell adenocarcinoma with a positive surgical margin. One month later, additional ileal resection was planned. Laparoscopic examination revealed disseminated nodules throughout the abdominal cavity. Therefore, the patient underwent resection of the peritoneal nodules. The peritoneal specimens confirmed the histopathological findings. Thus we diagnosed the patient with peritoneal dissemination of appendiceal goblet cell adenocarcinoma. CONCLUSIONS: In cases wherein white pus is observed during surgery for acute appendicitis, considering the possibility of dissemination, collecting samples for histopathological examination, and initiating early treatment are crucial.

A Case of Cervical Squamous Cell Carcinoma Developing 33 Years After Conization.

We report a fatal case of early postoperative peritoneal dissemination in a patient who was diagnosed with cervical squamous cell carcinoma after laparoscopic hysterectomy for hematometra. A 73-year-old multiparous woman with pyometra and lower abdominal pain was referred to our hospital. Her medical history was remarkable for four open surgeries and conization at the age of 40 years. The cytology obtained from the mucosa of the palpated cervix was negative. The cytology and bacterial culture of the mucus collected from the uterine cavity were negative. Increasing fluid accumulation in the uterine cavity started to cause severe abdominal pain. A laparoscopy was performed. The small intestine showed extensive adhesions to the abdominal wall, which were dissected. A total hysterectomy was performed, and the uterus was placed in a collection bag, cut inside the bag, and retrieved transvaginally. Histopathological examination revealed nests of squamous cell carcinoma that replaced the entire uterine myometrium, and the tumor cells showed diffuse positivity for p16 on immunostaining. The patient was diagnosed with squamous cell carcinoma of the uterine cervix with invasion of the uterine myometrium. Three months later, the patient suffered from small bowel obstruction. A laparotomy was performed, and it revealed numerous disseminated lesions in the pelvic peritoneum and mesentery of the small intestine. Bypass surgery was performed. A biopsy of a disseminated lesion near the vaginal cuff revealed squamous cell carcinoma. The patient died within three weeks of bypass surgery.

Three-year progression-free survival of a patient with concomitant mucinous adenocarcinoma of the colon with peritoneal dissemination and multiple myeloma who received lenalidomide: a case report.

BACKGROUND: Concomitant multiple myeloma (MM) and other primary malignancies is rare. Therefore, the treatment outcomes of patients with these conditions have not been well discussed. Lenalidomide is an oral thalidomide analog drug used for MM. Recently, the antitumor effect of lenalidomide has been gaining attention, and lenalidomide has been applied for managing solid tumors. The current case showed the treatment course of a patient treated with lenalidomide for concomitant MM and colon cancer with peritoneal dissemination. CASE PRESENTATION: A 74-year-old female patient receiving treatment for MM was diagnosed with mucinous adenocarcinoma of the transverse colon. The patient was clinically diagnosed with stage IIIC T4aN2M0 disease. Subsequently, laparoscopic colectomy with lymph node dissection was planned. However, intraperitoneal observation revealed peritoneal dissemination that had sporadically and widely spread. Therefore, palliative partial colectomy was performed to prevent future hemorrhage or obstruction. The patient was discharged on the 10th postoperative day without postoperative complication. Based on the patient's preference, lenalidomide was continually administered for MM without systemic chemotherapy. The patient survived for > 36 months without any signs of tumor progression. CONCLUSION: The current case first showed the treatment course of concomitant MM and colon cancer. The antitumor effect of lenalidomide can possibly contribute to 3-year progression-free survival in patients with mucinous adenocarcinoma of the colon with peritoneal dissemination.

A case of metachronous oligo-hepatic and peritoneal metastases of pancreatic cancer with a favorable outcome after conversion surgery combined with perioperative sequential chemotherapy.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies, and the prognosis for its recurrence after surgery is very poor. Here, we report a case of metachronous oligo-hepatic and peritoneal metastases in a patient who survived without recurrence for 3 years after conversion surgery combined with perioperative sequential chemotherapy using gemcitabine plus nab-paclitaxel (GnP) and modified FOLFIRINOX (mFOLFIRINOX). The patient was a 70-year-old man with pancreatic ductal carcinoma, classified as cT3N0M0, cStage IIA, who underwent a distal pancreatosplenectomy. At 1 year and 4 months later, two liver metastases and one peritoneal metastasis were detected. A systemic 9-month course of chemotherapy was administered with GnP and mFOLFIRINOX as the first- and second-line chemotherapeutic agents, respectively. The two liver metastases were judged as showing a partial response, but one dissemination was considered stable disease. After receiving informed consent from the patient, we performed resection of the disseminated tumor and lateral segmentectomy of the liver. Adjuvant chemotherapy using mFOLFIRINOX and GnP was administered for 10 months. The patient has now been alive for 5 years and 6 months after the initial pancreatosplenectomy, and 3 years and 3 months after the conversion surgery, without subsequent tumor recurrence. Thus, a multidisciplinary treatment approach including surgery and perioperative sequential chemotherapy using GnP and mFOLFIRINOX may be beneficial for treating metachronous oligo-hepatic and peritoneal metastases, depending on the patient's condition.