Cerebellar abscess secondary to metastatic lung adenocarcinoma: a case report.

BACKGROUND: Cerebellar abscesses are rare, life-threatening infections often originating from bacterial sources, while metastatic brain lesions from lung adenocarcinoma are relatively common. However, the coexistence of a cerebellar abscess secondary to metastatic lung adenocarcinoma is exceedingly rare and presents unique diagnostic and management challenges. CASE PRESENTATION: We report a case of a 35 year-old Pakistani female patient with persistent headaches, nausea, and vertigo, who was found to have a large cerebellar mass with features suggestive of metastatic lung adenocarcinoma. Further investigation revealed a concomitant cerebellar abscess. Surgical excision and broad-spectrum antibiotics were initiated, resulting in a favorable outcome. CONCLUSION: This case showcases the rarity and complexity of cerebellar abscesses due to metastatic lung adenocarcinoma. Timely intervention, including surgery and targeted therapy, is crucial for successful management. Further research is needed to enhance treatment strategies.

The mechanism of ITGB4 in tumor migration and invasion.

Integrin ß4 (ITGB4) is a transmembrane protein that functions as a mechanosensor, mediating the bidirectional exchange of information between the intracellular and extracellular matrices. ITGB4 plays a critical role in cell adhesion, migration, and signaling. Numerous studies have implicated ITGB4 as a key facilitator of tumor migration and invasion. This review provides a foundational description of the mechanisms by which ITGB4 regulates tumor migration and invasion through pathways involving focal adhesion kinase (FAK), protein kinase B (AKT), and matrix metalloproteinases (MMPs). These mechanisms encompass epithelial-mesenchymal transition (EMT), phosphorylation, and methylation of associated molecules. Additionally, this review explores the role of ITGB4 in the migration and invasion of prevalent clinical tumors, including those of the digestive system, breast, and prostate.

Anti-angiogenic activity of a novel angiostatin-like plasminogen fragment produced by a bacterial metalloproteinase.

Tumor growth depends on angiogenesis, a process by which new blood vessel are formed from pre-existing normal blood vessels. Proteolytic fragments of plasminogen, containing varying numbers of plasminogen kringle domains, collectively known as angiostatin, are a naturally occurring inhibitor of angiogenesis and inhibit tumor growth. We have developed an "affinity-capture reactor" that enables a single-step method for the production/purification of an angiostatin-like plasminogen fragment from human plasma using an immobilized bacterial metalloproteinase. The resulting fragment, named BL-angiostatin, contains one or two glycosyl chains and the N-terminal PAN module, which are not present in canonical angiostatins tested for cancer treatment. BL-angiostatin inhibited angiogenesis in vitro at 20 nM and the growth of both allograft and human xenograft tumors as well as lung metastasis of primary tumors mice at 0.3-10 mg kg-1. Derivatives of BL angiostatin lacking the PAN module or the terminal sialic acids in the glycosyl chains showed reduced anti-angiogenic activity in vivo, suggesting a role for these functions in activity, possibly via conferring a pharmacokinetic advantage to BL angiostatin compared to recombinant angiostatin lacking both features. These results highlight the potential of BL-angiostatin for therapeutic applications.

Cancer metastases: Tailoring the targets.

Metastasis is an intricate and formidable pathophysiological process encompassing the dissemination of cancer cells from the primary tumour body to distant organs. It stands as a profound and devastating phenomenon that constitutes the primary driver of cancer-related mortality. Despite great strides of advancements in cancer research and treatment, tailored anti-metastasis therapies are either lacking or have shown limited success, necessitating a deeper understanding of the intrinsic elements driving cancer invasiveness. This comprehensive review presents a contemporary elucidation of pivotal facets within the realm of cancer metastasis, commencing with the intricate processes of homing and invasion. The process of angiogenesis, which supports tumour growth and metastasis, is addressed, along with the pre-metastatic niche, wherein the primary tumour prepares for a favorable microenvironment at distant sites for subsequent metastatic colonization. The landscape of metastasis-related genetic and epigenetic mechanisms, involvement of metastasis genes and metastasis suppressor genes, and microRNAs (miRNA) are also discussed. Furthermore, immune modulators' impact on metastasis and their potential as therapeutic targets are addressed. The interplay between cancer cells and the immune system, including immune evasion mechanisms employed by metastatic cells, is discussed, highlighting the importance of targeting immune modulation in arresting metastatic progression. Finally, this review presents promising treatment opportunities derived from the insights gained into the mechanisms of metastasis. Identifying novel therapeutic targets and developing innovative strategies to disrupt the metastatic cascade holds excellent potential for improving patient outcomes and ultimately reducing cancer-related mortality.

Comparative analysis of the mutational landscape and evolutionary patterns of pancreatic ductal adenocarcinoma metastases in the liver or peritoneum.

Background: Pancreatic ductal adenocarcinoma (PDAC) often presents with liver or peritoneal metastases at diagnosis. Despite similar treatment approaches, patient outcomes vary between these metastatic sites. To improve targeted therapies for metastatic PDAC, a comprehensive analysis of the genetic profiles and evolutionary patterns at these distinct metastatic locations is essential. Methods: We performed whole exome sequencing on 44 tissue samples from 27 PDAC patients, including primary tumours and matched liver or peritoneal metastases. We analysed somatic mutation profiles, signatures, and affected pathways for each group, and examined clonal evolution using subclonal architectures and phylogenetic trees. Results: KRAS mutations remained the predominant driver alteration, with a prevalence of 89 % across all tumours. Notably, we observed site-specific differences in mutation frequencies, with KRAS alterations detected in 77.8 % (7/9) of peritoneal metastases and 87.5 % (7/8) of liver metastases. TP53 mutations exhibited a similar pattern, occurring in 55.6 % (5/9) of peritoneal and 37.5 % (3/8) of liver metastases. Intriguingly, we identified site-specific alterations in DNA repair pathway genes, including ATM and BRCA1, with distinct mutational profiles in liver versus peritoneal metastases. Furthermore, liver metastases demonstrated a significantly higher tumor mutational burden (TMB) compared to peritoneal metastases (median [IQR]: 2.14 [1.77-2.71] vs. 1.29 [1.21-1.69] mutations/Mb; P = 0.048). Conclusions: In conclusion, metastasis of pancreatic cancer may be influenced by variables other than KRAS mutations, such as TP53. PDAC peritoneal and liver metastases may differ in potential therapeutic biomarkers. Further inquiry is needed on the biological mechanisms underlying metastasis and the treatment of diverse metastases.

A rare case of anterior sternal metastasis in ovarian cancer: A case report.

A subcutaneous mass in the anterior region of the thorax, (presternal region). Subcutaneous metastases in ovarian cancer are rare, occurring in 0.9% to 5.8% of cases. They are usually a late manifestation that arises several years after the initial diagnosis and often serve as a poor prognostic indicator. Their presence suggests a reported median survival ranging from 3 to 18 months. subcutaneous metastases can be categorized into umbilical metastases, commonly referred to as Sister Joseph's nodules (SJN) the most prevalent type, and non-SJN cutaneous metastases. We present the unusual case of a 57-year-old woman who underwent surgical intervention and received adjuvant chemotherapy for serous ovarian adenocarcinoma. She presented for consultation 5 years later with a painful presternal mass, and the histopathological examination of the mass revealed a metastasis of the primary ovarian tumor.

Unveiling Oral Malignant Melanoma: Clinicopathological Details of a Case.

Oral malignant melanoma is a rare tumor of the oral cavity. It is more common among Negros and Japanese people. Initial symptoms are frequently overlooked, resulting in a delayed diagnosis and poor prognosis with a 5-year survival rate. Unlike melanomas in other sites, it is uncommon and thus lacks a well-defined classification system and treatment regimen. The survival rate is mainly correlated with early diagnosis and treatment. A 54-year-old male reported to our department with a de novo fast-growing exophytic proliferative pigmented lesion for six months. After proper radiographic analysis, an incisional biopsy was done which revealed the presence of nests and fascicles of pleomorphic spindle cells with hyperchromatic nuclei and abundant brown pigments rendering it a provisional diagnosis of oral malignant melanoma which was later confirmed by immunohistochemistry (IHC). PET-CT scan revealed widespread metastasis. This article stresses the importance of identification of initial symptoms which are frequently overlooked, resulting in a delayed diagnosis and poor prognosis.

Research progress on the effect of pyroptosis on the occurrence, development, invasion and metastasis of colorectal cancer.

Pyroptosis is a type of programmed cell death mediated by gasdermines (GSDMs). The N-terminal domain of GSDMs forms pores in the plasma membrane, causing cell membrane rupture and the release of cell contents, leading to an inflammatory response and mediating pyrodeath. Pyroptosis plays an important role in inflammatory diseases and malignant tumors. With the further study of pyroptosis, an increasing number of studies have shown that the pyroptosis pathway can regulate the tumor microenvironment and antitumor immunity of colorectal cancer and is closely related to the occurrence, development, treatment and prognosis of colorectal cancer. This review aimed to explore the molecular mechanism of pyroptosis and the role of pyroptosis in the occurrence, development, treatment and prognosis of colorectal cancer (CRC) and to provide ideas for the clinical diagnosis and treatment of CRC.

Effect of perioperative chemotherapy on resection of isolated pulmonary metastases from colorectal cancer: A single center experience.

BACKGROUND: Numerous studies have assessed surgical resection as a standard treatment option for patients with colorectal cancer (CRC) and resectable pulmonary metastases (PM). However, the role of perioperative chemotherapy after complete resection of isolated PM from patients with CRC patients remains controversial. We hypothesize that perioperative chemotherapy does not provide significant survival benefits for patients undergoing resection of PM from CRC. AIM: To determine whether perioperative chemotherapy affects survival after radical resection of isolated PM from CRC. METHODS: We retrospectively collected demographic, clinical, and pathologic data on patients who underwent radical surgery for isolated PM from CRC. Cancer-specific survival (CSS) and disease-free survival were calculated using Kaplan-Meier analysis. Inter-group differences were compared using the log-rank test. For multivariate analysis, Cox regression was utilized when indicated. RESULTS: This study included 120 patients with a median age of 61.6 years. The 5-year CSS rate was 78.2%, with 36.7% experiencing recurrence. Surgical resection for isolated PM resulted in a 5-year CSS rate of 50.0% for second metastases. Perioperative chemotherapy (P = 0.079) did not enhance survival post-resection. Factors associated with improved survival included fewer metastatic lesions [hazard ratio (HR): 2.51, P = 0.045], longer disease-free intervals (HR: 0.35, P = 0.016), and wedge lung resections (HR: 0.42, P = 0.035). Multiple PM predicted higher recurrence risk (HR: 2.22, P = 0.022). The log-rank test showed no significant difference in CSS between single and repeated metastasectomy (P = 0.92). CONCLUSION: Perioperative chemotherapy shows no survival benefit post-PM resection in CRC. Disease-free intervals and fewer metastatic lesions predict better survival. Repeated metastasectomy is warranted for eligible patients.

Olfactory neuroblastoma with orbital protrusion arising in the background of maxillary carcinoma.

An uncommon entity in the class of malignant neuroectodermal nasal tumors is the olfactory neuroblastoma, which originates in the roof of the nasal cavity from the olfactory epithelium. It is often mistaken by clinicians for a nasal polyp because it presents with indistinct features such as nasal obstruction and secondary sinus disease. Olfactory neuroblastoma has been observed to cause morbidity by distant metastasis, invasion through the cribriform plate, and secondary meningitis in most instances. It exhibits a range of biologic activities, from slow growth accompanied by long-term patient survival to a very aggressive malignancy with extensive metastases. We report the incidence of a rare case in which a patient, previously operated on and irradiated for squamous cell carcinoma of the maxilla, developed an olfactory neuroblastoma with orbital protrusion.

Unveiling the role of long non-coding RNA MALAT1: a comprehensive review on myocardial infarction.

Myocardial infarction (MI) stands at top global causes of death in developed countries, owing mostly to atherosclerotic plaque growth and endothelial injury-induced reduction in coronary blood flow. While early reperfusion techniques have improved outcomes, long-term treatment continues to be difficult. The function of lncRNAs extends to regulating gene expression in various conditions, both physiological and pathological, such as cardiovascular diseases. The objective of this research is to extensively evaluate the significance of the lncRNA called Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in the development and management of MI. According to research, MALAT1 is implicated in processes such as autophagy, apoptosis, cell proliferation, and inflammation in the cardiovascular system. This investigation examines recent research examining the effects of MALAT1 on heart function and its potential as a mean of diagnosis and treatment for post- MI complications and ischemic reperfusion injury.

Metastasis of breast cancer to the thyroid gland.

Metastases to the thyroid gland from nonthyroidal malignant tumors are rare but significant. They are often asymptomatic, indicating advanced-stage primary tumors and poor prognosis. Although infrequently, breast cancer (BC) can metastasize to the thyroid gland. We present the case of a 56-year-old woman with a history of BC who presented with a nodular goiter. Physical examination and imaging revealed a thyroid nodule and cervical lymph nodes with suspicious features. Fine-needle aspiration biopsy (FNAB) confirmed the presence of atypical epithelial cells in the thyroid nodule and lymph nodes. Further evaluation, including positron emission tomography, histological biopsy, and immunohistochemistry, supported the diagnosis of metastatic BC to the thyroid gland. Due to the local extent of the disease, total thyroidectomy was not feasible. The treatment with ribociclib and letrozole was initiated, but unfortunately, the patient had an unfavorable progression with the development of metastasis in the nervous system. Metastatic carcinoma to the thyroid gland is rare but has increased due to improved diagnostic techniques. BC can metastasize to the thyroid. Diagnosis involves imaging, FNAB, and immunohistochemistry. Treatment options include surgery, radiotherapy, and chemotherapy, but the prognosis is generally poor.

Las metástasis en la glándula tiroides a partir de tumores malignos no tiroideos son raras pero significativas. A menudo son asintomáticas, lo que indica tumores primarios en etapas avanzadas y un mal pronóstico. Aunque infrecuentemente, el cáncer de mama puede metastatizar en la glándula tiroides. Presentamos el caso de una mujer de 56 años con antecedente de cáncer de mama que consultó por bocio nodular. El examen físico y las imágenes revelaron un nódulo tiroideo y ganglios linfáticos cervicales con características sospechosas. La punción aspiración con aguja fina confirmó la presencia de células epiteliales atípicas en el nódulo tiroideo y los ganglios linfáticos. Una evaluación adicional, que incluyó tomografía por emisión de positrones, biopsia histológica e inmunohistoquímica, respaldó el diagnóstico de cáncer de mama metastásico en la glándula tiroides. Debido a la extensión local de la enfermedad, no fue factible realizar una tiroidectomía total. Se inició el tratamiento con ribociclib y letrozol, pero desafortunadamente la paciente tuvo una progresión desfavorable con el desarrollo de metástasis en el sistema nervioso. El carcinoma metastásico en la glándula tiroides es raro, pero ha aumentado debido a las técnicas de diagnóstico mejoradas. El cáncer de mama puede metastatizar en la tiroides. El diagnóstico implica imágenes, punción aspiración con aguja fina e inmunohistoquímica. Las opciones de tratamiento incluyen cirugía, radioterapia y quimioterapia, pero el pronóstico generalmente es desfavorable.

Intra-patient spatial comparison of non-metastatic and metastatic lymph nodes reveals a reduction in CD169+ macrophages within metastatic breast cancers.

BACKGROUND: Breast cancer cells suppress the host immune system to efficiently invade the lymph nodes; however, the underlying mechanism remains incompletely understood. Here, we aimed to comprehensively characterise the effects of breast cancers on immune cells in the lymph nodes. METHODS: We collected non-metastatic and metastatic lymph node samples from 6 patients with breast cancer with lymph node metastasis. We performed bulk transcriptomics, spatial transcriptomics, and imaging mass cytometry to analyse the obtained lymph nodes. Furthermore, we conducted histological analyses against a larger patient cohort (474 slices from 58 patients). FINDINGS: The comparison between paired lymph nodes with and without metastasis from the same patients demonstrated that the number of CD169+ lymph node sinus macrophages, an initiator of anti-cancer immunity, was reduced in metastatic lymph nodes (36.7 ± 21.1 vs 7.3 ± 7.0 cells/mm2, p = 0.0087), whereas the numbers of other major immune cell types were unaltered. We also detected that the infiltration of CD169+ macrophages into metastasised cancer tissues differed by section location within tumours, suggesting that CD169+ macrophages were gradually decreased after anti-cancer reactions. Furthermore, CD169+ macrophage elimination was prevalent in major breast cancer subtypes and correlated with breast cancer staging (p = 0.022). INTERPRETATION: We concluded that lymph nodes with breast cancer metastases have fewer CD169+ macrophages, which may be detrimental to the activity of anti-cancer immunity. FUNDING: JSPS KAKENHI (16H06279, 20H03451, 20H04842, 22H04925, 19K16770, and 21K15530, 24K02236), JSPS Fellows (JP22KJ1822), AMED (JP21ck0106698), JST FOREST (JPMJFR2062), Caravel, Co., Ltd, Japan Foundation for Applied Enzymology, and Sumitomo Pharma Co., Ltd. under SKIPS.

Unveiling the anticancer potential of Pestalotioprolide E, an unexplored macrolide: Targeting TRXR1-TRX1-ASK1-P38 signaling cascade in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is highly aggressive and metastatic in nature. Existing treatment modalities for TNBC are associated with severe side effects. Thioredoxin reductase (TRXR), the pivotal component of the thioredoxin system, remains overexpressed in various cancer cells including TNBC; promotes cell growth, proliferation, and metastasis, and inhibits apoptosis. Pestalotioprolide E is one of the potent macrolides, a class of secondary metabolites derived from an endophytic fungus Pestalotiopsis microspora with relatively unexplored biological activities. Our study revealed increased expression and activity of TRXR1 in MDA-MB-231 cells compared to the non-cancerous cells. In silico docking analysis and in vitro activity assay demonstrated that Pestalotioprolide E directly interacts with TRXR1 and inhibits its enzymatic activity. This inhibition induces apoptosis via TRX1/ASK1/P38MAPK death signaling cascade and retards metastasis through modulating VEGF, MMP-2, MMP-9, E-cadherin, N-cadherin in MDA-MB-231 cells. Taken together present study establishes TRXR1 as a molecular target for Pestalotioprolide E and its anticancer effect can be attributed to the inhibition of TRXR1 activity in MDA-MB-231.

ZNF8 promotes progression of gastrointestinal cancers via a p53-dependent mechanism.

p53 is a critical tumor suppressor, and the disruption of its normal function is often a prerequisite for the development or progression of tumors. Our previous works revealed that multiple members of Krüppel-associated box (KRAB) domain zinc-finger proteins (KZFPs) family regulate p53 transcriptional activity by interacting with it. But the tumor biology functions of these members have not been fully elucidated. Here, the pan-cancer analysis related to gastrointestinal cancers (GICs) revealed that ZNF8, a p53-interacting protein, is an unfavorable prognostic factor for patients with malignancies. ZNF8 interacts with p53 and further depresses its transcriptional activity in colon cancer cells. The knockdown of ZNF8 or the overexpression of ZNF8 inhibits or facilitates the in vitro colony formation, migration, invasion, and angiogenesis of p53+/+ colon cancer HCT116 cells, HepG2 cells and EC109 cells rather than p53-/- colon cancer HCT116 cells and p53-knockout HepG2 cells, respectively. Xenograft experiments conducted in vivo also showed that the knockdown of ZNF8 in p53+/+ but not in p53-/- HCT116 cells curbs the tumor growth and metastasis to lung, leading to an extended life span for tumor-bearing mice. Clinically, two independent immunohistochemistry cohorts of colon cancer and esophageal cancer also indicated that ZNF8 is higher expression in carcinoma tissues than adjacent tissues and this is associated with worse overall survival outcomes in patients without harboring p53 mutation. Together, our results provide insight into the p53-specific tumor oncogenic function of ZNF8. ZNF8 may prove to be a potential target for GICs treatment.

Metal complex lipid-based nanoparticles deliver metabolism-regulating lomitapide to overcome CTC immune evasion via activating STING pathway.

Activating the cGAS-STING pathway of circulating tumor cell clusters (CTC clusters) represents a promising strategy to mitigate metastases. To fully exploit the potential of cholesterol-regulating agents in activating CTCs' STING levels, we developed a nanoparticle (NP) composed of metal complex lipid (MCL). This design includes MCL-miriplatin to increase NP stiffness and loads lomitapide (lomi) modulating cholesterol levels, resulting in the creation of PLTs@Pt-lipid@lomi NPs. MCL-miriplatin not only enhances lomi's eliciting efficacy on STING pathway but also increases NPs' stiffness, thus a vital factor affecting the penetration into CTC clusters to further boost lomi's ability. Demonstrated by cy5 tracking experiments, PLTs@Pt-lipid@lomi NPs quickly attach to cancer cell via platelet membrane anchorage, penetrate deep into the spheres, and reach the subcellular endoplasmic reticulum where lomi regulates cholesterol. Additionally, these NPs have been shown to track CTCs in the bloodstream, a capability not demonstrated by the free drug. PLTs@Pt-lipid@lomi NPs more efficiently activate the STING pathway and reduce CTC stemness compared to free lomi. Ultimately, PLTs@Pt-lipid@lomi NPs reduce metastasis in a post-surgery animal model. While cholesterol-regulating agents are limited in efficacy when being repositioned as immunomodulatory agents, this MCL-composing NP strategy demonstrates the potential to effectively deliver these agents to target CTC clusters.

ALDH1A1 as a marker for metastasis initiating cells: a mechanistic insight.

Since metastasis accounts for the majority of cancer morbidity and mortality, attempts are focused to block metastasis and metastasis initiating cellular programs. It is generally believed that hypoxia, reactive oxygen species (ROS) and the dysregulated redox pathways regulate metastasis. Although induction of epithelial to mesenchymal transition (EMT) can initiate cell motility to different sites other than the primary site, the initiation of a secondary tumor at a distant site depends on self-renewal property of cancer stem cell (CSC) property. That subset of metastatic cells possessing CSC property are referred to as metastasis initiating cells (MICs). Among the different cellular intermediates regulating metastasis in response to hypoxia by inducing EMT and self-renewal property, ALDH1A1 is a critical molecule, which can be used as a marker for MICs in a wide variety of malignancies. The cytosolic ALDHs can irreversibly convert retinal to retinoic acid (RA), which initiates RA signaling, important for self-renewal and EMT. The metastasis permissive tumor microenvironment increases the expression of ALDH1A1, primarily through HIF1α, and leads to metabolic reprograming through OXPHOS regulation. The ALDH1A1 expression and its high activity can reprogram the cancer cells with the transcriptional upregulation of several genes, involved in EMT through RA signaling to manifest hybrid EMT or Hybrid E/M phenotype, which is important for acquiring the characteristics of MICs. Thus, the review on this topic highlights the use of ALDH1A1 as a marker for MICs, and reporters for the marker can be effectively used to trace the population in mouse models, and to screen drugs that target MICs.

DLCNBC-SA: a model for assessing axillary lymph node metastasis status in early breast cancer patients.

Background: Axillary lymph node (ALN) status is a crucial prognostic indicator for breast cancer metastasis, with manual interpretation of whole slide images (WSIs) being the current standard practice. However, this method is subjective and time-consuming. Recent advancements in deep learning-based methods for medical image analysis have shown promise in improving clinical diagnosis. This study aims to leverage these technological advancements to develop a deep learning model based on features extracted from primary tumor biopsies for preoperatively identifying ALN metastasis in early-stage breast cancer patients with negative nodes. Methods: We present DLCNBC-SA, a deep learning-based network specifically tailored for core needle biopsy and clinical data feature extraction, which integrates a self-attention mechanism (CNBC-SA). The proposed model consists of a feature extractor based on convolutional neural network (CNN) and an improved self-attention mechanism module, which can preserve the independence of features in WSIs for analysis and enhancement to provide rich feature representation. To validate the performance of the proposed model, we conducted comparative experiments and ablation studies using publicly available datasets, and verification was performed through quantitative analysis. Results: The comparative experiment illustrates the superior performance of the proposed model in the task of binary classification of ALNs, as compared to alternative methods. Our method achieved outstanding performance [area under the curve (AUC): 0.882] in this task, significantly surpassing the state-of-the-art (SOTA) method on the same dataset (AUC: 0.862). The ablation experiment reveals that incorporating RandomRotation data augmentation technology and utilizing Adadelta optimizer can effectively enhance the performance of the proposed model. Conclusions: The experimental results demonstrate that the model proposed in this paper outperforms the SOTA model on the same dataset, thereby establishing its reliability as an assistant for pathologists in analyzing WSIs of breast cancer. Consequently, it significantly enhances both the efficiency and accuracy of doctors during the diagnostic process.

Case report: Sclerosing encapsulating peritonitis in a cat with disseminated pancreatic adenocarcinoma of presumed ductal origin.

A 9-year-old, neutered male, domestic short-haired cat was referred for recurrent ascites of unknown etiology over a week. Physical examination revealed abdominal distension and ultrasonography revealed a large volume of ascites throughout the abdominal cavity; this was interpreted as modified transudate. The mesentery and abdominal fat were hyperechoic and edematous. Fat tissue was assessed using fine-needle aspiration cytology, and adipocytes, fat-phagocytizing macrophages, and neutrophils were identified. Computed tomography revealed a pancreatic mass connected to the left pancreatic leg. Exploratory laparoscopy confirmed nodular masses and organ adhesions, leading to a tentative diagnosis of sclerosing encapsulating peritonitis. The cat was administered prednisolone, vitamin E, and tamoxifen but died 22 days after the initial therapy. Necropsy revealed a multi-lobulated pancreatic tumor (10 × 10 cm) tightly attached to the stomach and intestine, with a large amount of ascites. The peritoneum, stomach, intestine, and mesentery were covered with numerous disseminated nodules of various sizes (1-5 mm diameter). Microscopically, the tumor consisted of extensive adipose tissue, locally extensive inflammatory infiltrates, fibrous connective tissue, and small invasive proliferative glands. Well-defined small irregular glands composed of single-layered epithelial cells that appear to be of ductal origin were surrounded by an abundant desmoplastic stroma. Neoplastic nodules were widespread in the liver, stomach, peritoneum, mesentery, mesenteric lymph nodes, lungs, and urinary bladder. Immunohistochemistry revealed that the neoplastic glands were positive for pan-cytokeratin, confirming the pancreatic epithelial origin of the tumor. This is the first report of sclerosing encapsulating peritonitis accompanied by aggressive pancreatic adenocarcinoma of presumed ductal origin and extensive metastasis in a cat.

Metastatic Pancreatic Adenocarcinoma Downstaged to T0N0 with Chemotherapy and Targeted Therapy, Confirmed by Surgical Pathology: A Case Report.

Introduction: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive human tumor that is typically diagnosed at a later stage when surgery is not possible. Case Presentation: We report the case of a 62-year-old woman who presented to the emergency department with abdominal pain. Computed tomography (CT) revealed a solitary hepatic lesion and a pancreatic body lesion. The pancreatic body lesion was biopsied endoscopically, and a tissue diagnosis was obtained to confirm the diagnosis of PDAC. She was then treated with 12 cycles of FOLFIRINOX with stable disease on CT. Due to the history of a hepatic lesion, she received 11 cycles of gemcitabine/Abraxane and a combination of a MEK inhibitor, Mekinist, and a BRAF inhibitor, BRAFTOVI. Subsequently, the patient underwent a liver biopsy. The biopsy result was negative, and the tumor was deemed resectable. The patient underwent a distal pancreatectomy. Surgical pathology demonstrated a 1.1-cm low-grade papillary mucinous neoplasm with negative margins and lymph nodes, staged T0N0. Adjuvant chemotherapy was not administered. Conclusion: To our knowledge, this is the first report of a patient with metastatic pancreatic adenocarcinoma who received prolonged IV and oral chemotherapy. At the time of the operation, the pathological stage was T0N0. The patient has recently been seen 9 months after surgery with no evidence cancer recurrence. Additionally, ctDNA remains negative.