The spleen is a very hostile environment for tumor cells due to its anatomic location, blood supply, and rich immunological property – which makes it one of the most unique organ to be involved in metastatic diseases.15 Splenic metastases from non-hematologic malignancies are rare ranging from 0.6 to 7.1% base on autopsy reports of cancer patients, and 1.1 to 3.4% base on review of splenectomy cases.14 Moreover, isolated splenic metastases are more infrequent with only 31 cases reported from 1969 to October 2015.16 A splenic abscess is an unusual formation and is usually caused by hematogenous spread from an infection. Such expected frequency varies in different autopsy studies between 0.14% and 0.7%.1 Albeit rare, abscess can also result from migration of gut flora brought about by direct invasion of tumor cells from a neighboring neoplasm.17 This is a case of a 36-year-old female who came in with a history of abdominal pain, chills and fever for seven months. CT scan of the whole abdomen revealed splenic abscess with suspicion of a splenic rupture. The patient underwent exploratory laparotomy with abscess evacuation, splenectomy and double barrel colostomy and given with intravenous antibiotics. Histopathology results showed metastatic adenocarcinoma in the spleen. Thorough deliberation of her case was done and she was eventually managed as a case of Colon Cancer Stage IV and underwent chemotherapy. Splenic abscess developing from splenic metastasis from a colonic adenocarcinoma is rare and with concomitant high mortality rate. More often than not, splenic metastasis is discovered in advanced stage together with metastatic tumor in other organs while isolated splenic metastasis is even more uncommon. A splenic abscess as an initial demonstration of a colon cancer is not a common daily encounter of physicians hence a high index of suspicion coupled with sensitive and specific imaging is necessary in order to provide prompt medical and surgical intervention.

Human ; Female ; Adult: 25-44 Yrs Old ; Abdomen ; Adenocarcinoma ; Autopsy ; Colostomy ; Gastrointestinal Microbiome ; Pain ; Research Report ; Infections ; History ; Splenic Rupture ; World Health Organization ; Neoplasms ; Disease ; Fever ; Hematologic Neoplasms

Abstract Ectopic hepatocellular carcinoma (EHCC) is an extremely rare neoplasm, especially in the mediastinum, which shares morphologic characteristics with intrahepatic hepatocellular carcinoma (HCC). Its clinical features remain unclear, posing significant diagnostic and therapeutic challenges. The prognosis is also unclear due to its rarity and potential variability. This study reports the first case of EHCC in the mediastinum with subsequent brain metastasis. A 50-year-old man presented with shoulder and chest discomfort persisting for 5 months, accompanied by progressive weight loss and fatigue over the preceding 2 years. Imaging showed a mediastinal mass initially suspected to be lymphoma due to its malignant characteristics. However, histopathological examination identified the lesion as HCC, supported by characteristic immunohistochemical markers, despite normal abdominal imaging. Two months later, the tumor progressed despite intensive radiotherapy, and the patient experienced recurrent seizures. Subsequent brain imaging confirmed multiple intracranial metastases. Unfortunately, the patient died 6 months after diagnosis. The ectopic liver is more susceptible to hepatocarcinogenesis than the main liver; this is attributed to its incomplete functional structure. EHCC can be considered as differential diagnosis of mediastinal masses, even when no intrahepatic HCC is found. The rarity of EHCC in the mediastinum poses difficulties in developing treatment protocols. This case emphasizes the diagnostic challenges and aggressive nature of ectopic HCC and the need for comprehensive management strategies. There are currently no definite guidelines regarding the diagnosis, treatment, and prognosis of EHCC.
ectopic hepatocellular carcinoma ; mediastinum ; metastasis

Introduction: Adrenocortical carcinoma (ACC) is an aggressive malignancy with high rates of recurrence even after surgical resection. Surgery remains the mainstay of treatment, while adjuvant options are limited. Mitotane is the only approved systemic therapy. Current guidelines recommend stereotactic body radiotherapy (SBRT) alongside adjuvant mitotane therapy in Rx, R1, R2 resections and in locally advanced disease. Case: We present a case of a 40-year-old female who presented with abdominal pain and was found to have a large heterogeneous left adrenal mass measuring 8.2 × 8.5 × 9.5 cm (Hounsfield Unit 63) on computed tomography (CT) imaging. Clinically, she was obese with a body mass index of 33.7 kg/m². No discriminatory feature of Cushing’s was present. Hormonal evaluation demonstrated autonomous cortisol secretion with failure of suppression on both overnight and low-dose dexamethasone suppression tests at 301 nmol/L and 313.6 nmol/L, respectively. DHEA, testosterone, and urinary metanephrine were within range. Hemoglobin A1c was 6.6%. She underwent open left adrenalectomy. Intra-operatively, a 12 × 10 cm adrenal tumor was identified with multiple areas of tumor rupture and spillage during mobilization. HPE confirmed high-grade ACC with high Weiss score of 8, Ki-67 index 60–80%, and mitotic count 54/50 hpf (pT2Nx). Post-operative CT imaging demonstrated a residual soft tissue lesion in the left adrenal bed (largest diameter 3.8 cm) with fluorodeoxyglucose avidity. We commenced adjuvant mitotane therapy, titrated to 2 g TDS with supraphysiological hydrocortisone replacement. Mitotane level was within therapeutic range (16 mcg/mL). She was deemed unsuitable for repeat surgery due to the proximity of the residual mass to the adjacent vessel and was planned for SBRT therapy after a multidisciplinary team discussion. Conclusion High-risk ACC with suspected residual disease remains a therapeutic challenge. While mitotane remains the cornerstone of adjuvant therapy, SBRT may represent a promising adjunctive local treatment modality in carefully selected patients. Further studies are required to define its role in improving local control and outcomes in ACC.
Adrenocortical Carcinoma ; Mitotane

Introduction: Cushing’s syndrome is a multisystem disorder with significant cardiovascular morbidity, yet presentation as acute heart failure is uncommon. When driven by adrenocortical carcinoma (ACC), the clinical course is often aggressive and rapidly fatal, with particularly poor out-comes in resourcelimited settings where access to therapy is constrained. Case: A 39-year-old previously well female presented with acute decompensated heart failure, newly diagnosed hypertension, type 2 diabetes mellitus, and obesity, preceded by a 3-year history of secondary amenorrhea and progressive weight gain. On admission, she exhibited florid Cushingoid features. Biochemical evaluation confirmed severe adrenocorticotropic hormone (ACTH)-independent hypercortisolism: morning serum cortisol 1,950 nmol/L, failure of suppression on overnight dexamethasone suppression test (post-ODST cortisol 2022.9 nmol/L), and elevated 24-hour urinary free cortisol (2,069 nmol/24 hours, 2.56 × upper limit of normal). Androgen excess was evident, with elevated dehydroepiandrosterone sulfate (DHEAS more than 27 µmol/L) and testosterone (9.91 nmol/L). ACTH was suppressed, supporting an adrenal source, while aldosterone was normal. Contrast-enhanced computed tomography demonstrated a large left adrenal mass (12 cm) with tumor thrombus extending into the inferior vena cava and renal veins, with extensive hepatic and pulmonary metastases, consistent with advanced ACC. Management was limited by disease severity and resource constraints. Ketoconazole was contraindicated due to transaminitis, and alternative steroidogenesis inhibitors were unavailable, leaving metyrapone as the only feasible option. Oncological therapy was deferred due to sepsis and clinical instability. Her course was fulminant, complicated by recurrent heart failure, sepsis, and metabolic derangements, culminating in refractory cardiopulmonary failure. She died within 1 month of diagnosis, prior to definitive oncological intervention. Conclusion Fulminant cortisol-secreting ACC may present catastrophically as acute heart failure and progress rapidly. Early recognition and timely access to multimodal cortisollowering therapy are critical, particularly in resourcelimited settings. In fulminant hypercortisolism, the challenge is not diagnosis—but timing.
Adrenocortical Carcinoma ; Hydrocortisone ; Heart Failure

Introduction: Adrenocortical carcinoma (ACC) is a rare and aggressive malignancy with a predilection for metastasis to the liver, lungs, and lymph nodes. Bone involvement is less common and typically occurs alongside widespread disease. Isolated skeletal progression without visceral involvement is unusual and not well characterized. Case: A 60-year-old female underwent left adrenalectomy in 2019 for an incidentally detected adrenal mass, which was reported as a benign adrenal cortical adenoma (Ki67 <3%). In 2022, she presented with persistent low back pain. Imaging demonstrated fluorodeoxyglucoseavid lesions involving the T12 vertebra and right ilium, without evidence of local recurrence or visceral metastases. Histopathological evaluation of a bone biopsy initially suggested a neuroendocrine neoplasm based on synaptophysin positivity. Following multiple expert reviews and integration of clinical, radiological, and immunohistochemical findings, a consensus diagnosis of metastatic ACC was established. She received palliative radiotherapy to symptomatic skeletal sites and subsequently completed six cycles of etoposide, doxorubicin, and cisplatin chemotherapy in 2023, achieving disease stabilization. Surveillance imaging in May 2025 demonstrated progression confined to the axial and appendicular skeleton, with no involvement of the adrenal bed or visceral organs. Mitotane therapy was initiated in December 2025. Ongoing management focuses on systemic disease control, symptom palliation, and multidisciplinary supportive care. Conclusion This case illustrates an uncommon pattern of ACC progression characterized by bone-dominant metastases in the absence of visceral disease. It also highlights the importance of reconsidering the initial histopathological diagnosis when clinical behavior is discordant. Vigilance for atypical metastatic patterns is warranted, even years after resection of an adrenal lesion initially classified as benign.
Adrenocortical Carcinoma

Introduction: Pancreatic neuroendocrine tumors (PNETs) are rare, comprising less than 3% of all pancreatic neoplasms. These tumors are broadly classified as functioning or nonfunctioning. Insulinoma is the most common functioning PNET. Non-functioning PNETs often present significant diagnostic issues and may be misdiagnosed as pancreatic adenocarcinoma, especially when immunohistochemical evaluation is omitted during histological examination. We describe a case of metastatic insulinoma that was misdiagnosed as a poorly differentiated pancreatic adenocarcinoma. Case: A 65-year-old female first presented to a private hospital in 2023 with obstructive jaundice and was found to have a pancreatic head lesion that was causing biliary obstruction. As a result, a biliary stent was placed. She underwent aortocaval lymph node biopsy, and the result showed poorly differentiated pancreatic adenocarcinoma. Nonetheless, she refused surgical and oncological intervention. Even so, she remained clinically stable and maintained good functional status for 2 years. In 2025, she presented to Hospital Canselor Tuanku Muhriz with recurrent hypoglycemia fulfilling Whipple’s triad. The unexpectedly indolent clinical course prompted reassessment of the initial diagnosis. Biochemical evaluation confirmed endogenous hyperinsulinemic hypoglycemia, with inappropriately elevated insulin (11.03 µIU/mL) and C-peptide levels (1,089 pmol/L). Computer tomography of the abdomen revealed multiple hepatic lesions and progressive lymphadenopathy, suggestive of metastatic disease. Re-evaluation of the initial histopathological specimen showed a well-differentiated neuroendocrine tumor (Grade 1, Ki-67 ~2%). Hence, the diagnosis was revised to metastatic insulinoma. She was referred to the hepatobiliary surgical team for surgical debulking, but the procedure was deemed highrisk and likely to have high mortality due to the extent of the disease. She was managed with diazoxide and longacting somatostatin analogues for glycemic control. Conclusion This case highlights the critical importance of diagnostic vigilance when evaluating pancreatic neoplasms. Persistent or unexplained clinical courses, especially when endocrine symptoms arise, should prompt thorough reassessment. Immunohistochemical confirmation is essential to avoid misdiagnosis and ensure optimal patient management.
Adenocarcinoma ; Insulinoma ; Pancreatic Neoplasms

Introduction: Müllerian tumors are rare in males, with serous tumors representing the most often subtype with only 50 cases documented. Excluding the benign/ borderline counterparts, only 29 are reported as primary malignant testicular masses and only 4 are reported in the elderly. Due to rarity, there is no exact consensus in the optimal grouping and management of these patients. Herein we report a case of serous cystadenocarcinoma of the paratestis in an elderly Filipino male. Case Description: A 66 y/o male presented with scrotal enlargement. He had previously undergone a Hartmann’s procedure for fecal impaction. An incidental finding of a complicated hydrocele was noted on CT scan done few months prior his scheduled colostomy takedown. He was subsequently referred to urology service for evaluation. Tumor markers (AFP and βHCG) were all normal. One month prior to admission, a marked increase in the size of the right scrotum was observed, prompting decision to proceed with surgery. Discussion: Orchiectomy specimen evaluation requires careful assessment of tumor appearance, location, and extent. In this case, the tumor arises in the paratestis without involvement of the testicular parenchyma, showing solid and cystic areas with papillary excrescences. The tumor showed enlarged, hyperchromatic nuclei with irregular contours, abundant cytoplasm, and psammoma bodies. IHC revealed negative for calretinin, glypican3, CDX2, SATB2, and CK20, but positive for CK7, Pax8, ER, and WT1. Paratesticular serous cystadenocarcinoma diagnosis was made after carefully ruling-out mesothelioma, YST and/or metastases. P53 staining was equivocal, with 5% of cells positive amid broad negativity. Molecular testing was advised for grading and prognosis. Conclusion Serous cancers are rare in males and must require IHC for diagnosis and radical surgery due to high resistance to other treatments. Hydrocele being a frequent finding can sometimes delay the diagnosis. Careful monitoring remains critical for detecting progression and metastasis.
Cystadenocarcinoma, Serous ; Orchiectomy

Introduction: Prostatic acinar adenocarcinoma is defined by loss of the basal cell marker p63, a feature routinely used to distinguish malignant glands from benign mimickers. Rarely, prostate carcinomas demonstrate aberrant nuclear p63 expression, representing a diagnostically challenging subtype reported in less than 1% of cases. Most described tumors exhibit lower Gleason grades and relatively indolent clinical behavior. We report a rare case of high-grade prostatic adenocarcinoma with aberrant p63 expression and aggressive clinical course. Case Description: A 77-year-old Filipino male presented with worsening hematuria and fever. PET-CT demonstrated multifocal Prostate-Specific Membrane Antigen (PSMA)-avid lesions in the left prostate with enlargement, irregular contour, intravesical extension, and PSMA-avid retroperitoneal and iliac lymph nodes suggestive of metastatic disease. The patient had a prior diagnosis of prostatic adenocarcinoma (Gleason 4+5=9) in 2022 and had been treated with androgen-targeted therapy. Due to persistent symptoms, transurethral resection was performed. Histology revealed complete effacement of prostatic architecture by malignant cells arranged in sheets with enlarged vesicular nuclei, prominent nucleoli, and frequent mitoses. Immunostaining showed diffuse CK, CAM5.2, and PSA positivity with aberrant patchy nuclear p63 expression and a Ki-67 index of 60%. Lymphoid, urothelial, and neuroendocrine markers were negative. The tumor was diagnosed as prostatic adenocarcinoma, Gleason score 5+5=10, with aberrant nuclear p63 expression. Discussion: Aberrant p63-positive prostatic adenocarcinoma is a rare molecular subtype characterized by a mixed basal–luminal immunophenotype. Most reported cases demonstrate lower Gleason scores and organ-confined disease with relatively favorable outcomes. In contrast, our case exhibited an exceptionally high Gleason score with radiologic evidence of metastasis and rapid clinical deterioration, suggesting a broader and potentially more aggressive spectrum of behavior. Conclusion Recognition of aberrant p63 expression is essential to avoid diagnostic misinterpretation. Despite ongoing therapy, the patient developed acute intracranial hemorrhage and ultimately succumbed to the disease. This case highlights an aggressive presentation of a rare immunophenotypic variant and underscores the importance of clinicopathologic correlation to better define its prognostic significance.
Adenocarcinoma

INTRODUCTION

Most cancer-related deaths globally are caused by lung cancer. The diagnosis is typically made following the evaluation of respiratory symptoms such as chronic cough or incidental finding of pulmonary lesions such as nodules and mass. Cardiac metastasis occurs in 2-18% of lung cancers, but cardiac tamponade complicating malignant pericardial effusion is an extremely rare and life-threatening initial presentation of non-small cell lung carcinoma.

CASE REPORT

A 59-year-old-male with a smoking history of 72 pack-year presented at the emergency room with severe dyspnea and was assessed to be in cardiac tamponade. The patient arrested for 16 minutes but returned to spontaneous circulation after 650mL of serosanguinous fluid was removed by pericardiocentesis. The work-up for infectious and immunologic causes was negative. Chest CT scan with contrast did not reveal any pulmonary mass. However, the pericardial fluid cytology immunohistochemical stains pointed to a primary lung adenocarcinoma. PET scan was requested which confirmed hypermetabolic focus in the left lung base. included patients admitted at East Avenue Medical Center for DFU. The primary endpoint was major amputation of the lower extremities. Data were analyzed using Receiver Operating Characteristic (ROC) analysis and logistic regression.

CONCLUSION

This case showed an extremely rare situation where life-threatening cardiac tamponade was the initial presentation of non-small cell lung adenocarcinoma, which highlights the need for vigilance in atypical presentation. Comprehensive diagnostic approach, including PET scans and cytologic analysis, must be done when standard imaging is inconclusive.

Human ; Male ; Middle Aged: 45-64 Yrs Old ; Cardiac Tamponade ; Adenocarcinoma Of Lung

Renal cell carcinoma (RCC) is notorious for its propensity to metastasize even after a prolonged period of remission following nephrectomy. The metastatic spread can occur months or even years after initial treatment, which necessitates a heightened level of clinical awareness and vigilance in patients with a history of renal malignancy, particularly who present with new or unexplained nasal symptoms. Although RCC most commonly metastasize to the lungs, bones and liver, its involvement in the nasal cavity is exceedingly rare, posing significant diagnostic challenges due to the non-specific nature of symptoms. We describe a case of metastatic renal cell clear cell carcinoma presenting with recurrent epistaxis and unilateral nasal obstruction. Immunohistochemistry studies play a crucial role in confirming the diagnosis and ruling out potential differential diagnoses, along with a comprehensive clinical history of the patient.

Human ; Male ; Middle Aged: 45-64 Yrs Old ; Clear Cell Renal Cell Carcinoma ; Carcinoma, Renal Cell ; Metastasis ; Neoplasm Metastasis ; Nasal Cavity ; Epistaxis