Metastatic seminoma and grade 1 follicular lymphoma presenting concurrently in a supraclavicular lymph node: a case report

An asymptomatic 67-year-old man presented with a left supraclavicular lymph node that enlarged over a 2-month period which was biopsied. Pathologic features were consistent with involvement by metastatic seminoma and follicular lymphoma, follicular pattern, grade 1 (of 3). Staging Positron Emission Tomography/Computed Tomography scans indicated several areas of enlarged lymph nodes. The patient completed chemotherapy with bleomycin, etoposide, and cisplatin chemotherapy. This is the first reported case of metastatic seminoma and follicular lymphoma occurring in the same lymph node. No obvious pathophysiologic link exists between these two malignancies and there are no shared common risk factors. Given the natural history of these two malignancies, if this patient develops recurrent lymphadenopathy, it will be difficult to identify whether the enlarged lymph nodes represent recurrent seminoma or follicular lymphoma without a biopsy of each pathologically enlarged node. Similarly, Fluorodeoxyglucose- Positron Emission Tomography is known to be active in both seminoma and follicular lymphoma, making this scan non-specific in this patient. Finally, this patient had no baseline elevation in any germ cell tumor marker. Thus, serum tumor markers cannot be relied upon as surrogates for response to chemotherapy or as identifiers of relapsed seminoma

Gastric hibernoma: a novel location and presentation of a rare tumor.

We present a case of gastric hibernoma, an unusual tumor with a location novel to the literature. A 39-year-old female presented with one year of upper gastrointestinal bleeding and dysphagia. Gastroenterology performed an esophagogastroduodenoscopy with ultrasound and identified a 6 cm mass within the muscularis propria of the antrum. Computed tomography demonstrated a 9.7 × 7.8 × 4.8 c

Pioglitazone, an Insulin Sensitizing Drug, Attenuates the Development of Kidney and Liver Disease in the PCK Rodent Model of Polycystic Kidney Disease

poster abstractPolycystic kidney disease is a genetic disorder characterized by growth of fluid-filled cysts predominately in kidney and liver. The only treatment currently available is the removal/aspiration of the largest cysts or organ transplantation. Promising pharmaceutical agents in clinical trials interfere with the action of hormones that increase cAMP thereby inhibiting secretion of Cl-, and compensatory fluid flux, into the cysts. Other treatments proposed include chemotherapeutic and immunosuppressive drugs that interfere with cellular proliferation as well as with signaling pathways for Cl- secretion. Long-term use of these agents will have multiple side effects. Based on a recent observation that peroxisome proliferator activated receptor γ agonists such as Actos (pioglitazone) and Avandia (rosiglitazone) decrease mRNA levels of a Cl- transport protein and the Cl- secretory response to vasopressin stimulation in cultured renal cells, it is hypothesized that PPARγ agonists will inhibit cyst growth. The current studies show that a 7 or 14 week feeding regimen of 20 mg/Kg BW pioglitazone inhibits renal and hepatic bile duct cyst growth in a rodent model orthologous to human PKD. In addition, the degree of renal cortical fibrosis was diminished in the pioglitazone-treated animals after 14 weeks. These results suggest that PPARγ agonists may be effective in controlling both renal and hepatic cyst growth and renal fibrotic development in polycystic kidney disease

Pioglitazone Attenuates Cystic Burden in the PCK Rodent Model of Polycystic Kidney Disease

Polycystic kidney disease (PKD) is a genetic disorder characterized by growth of fluid-filled cysts predominately in kidney tubules and liver bile ducts. Currently, the clinical management of PKD is limited to cyst aspiration, surgical resection or organ transplantation. Based on an observation that PPARγ agonists such as pioglitazone and rosiglitazone decrease mRNA levels of a Cl− transport protein, CFTR (cystic fibrosis transmembrane conductance regulator), and the Cl− secretory response to vasopressin in cultured renal cells, it is hypothesized that PPARγ agonists will inhibit cyst growth. The current studies show that a 7- or 14-week pioglitazone feeding regimen inhibits renal and hepatic bile duct cyst growth in the PCK rat, a rodent model orthologous to human PKD. These studies provide proof of concept for the mechanism of action of the PPARγ agonists and suggest that this class of drugs may be effective in controlling both renal and hepatic cyst growth and fibrosis in PKD

A 61-year-old woman with osteomalacia and a thoracic spine lesion

Phosphaturic mesenchymal tumor, mixed connective tissue variant (PMT-MCT) is a rare, largely benign, mesenchymal neoplasm almost invariably associated with oncogenic osteomalacia. It is generally found in the soft tissue and bone of the extremities. We report a case of a 61-year-old female with long-standing osteomalacia who was found to have PMT-MCT of the thoracic spine. There have been very few previously reported cases of PMT involving the spinal vertebrae and neuropathologists should be aware of this lesion. Recognition of PMT-MCT is critical for optimal patient care since complete surgical resection without additional therapy is curative

Histopathology and enhanced detection of tumor invasion of peritoneal membranes

<div><p>Tumor invasion of the peritoneal membrane may have an adverse prognostic significance, but its histopathologic features can be diagnostically difficult to recognize. We observed that local peritoneal injury associated with tumor invasion is characterized by activation and proliferation of serosal stromal cells that express cytokeratin, a characteristic property of injured serosal membranes that may have diagnostic utility. To explore this, we examined 120 primary tumors of the gastrointestinal tract and pancreaticobiliary system using cytokeratin and elastic stains to assess for tumor invasion of peritoneal membranes. Peritoneal invasion by tumor was associated with retraction, splaying, and destruction of the elastic lamina and proliferation of keratin-expressing stromal cells of serosal membranes. All 82 peritoneal invasive tumors were characterized by neoplastic cells that invaded the elastic lamina and the serosal connective tissue with neoplastic cells that abutted or were surrounded by keratin-positive stromal cells, whereas all 38 tumors limited to the subserosa showed none of these features. The diagnosis of tumor invasion of peritoneal membranes is enhanced by the combined use of cytokeratin and elastic stains, which in turn would enable better histopathologic correlation with patient treatment and outcome.</p></div

Histopathologic alteration of peritoneal membranes associated with tumor invasion (H&E and VVG).

<p>Tumor invasion of the peritoneal membrane is associated with localized inflammatory and desmoplastic reaction, resulting in hemorrhage and granulation tissue-like formation, surface fibrinous exudate, fibrosis, edema, and activation and proliferation of myofibroblast-like stromal cells (A, adenocarcinoma, colon, 40x). This is accompanied by retraction of the elastic lamina from the serosal surface toward the tumor (B, adenocarcinoma, colon, 20x) with splaying (C, adenocarcinoma, colon, 200x), attenuation, and fragmentation of its elastic fibers (D, adenocarcinoma, small intestine, 200x). Arrowheads: elastic lamina.</p

Tumor invasion of the peritoneal membrane is characterized by neoplastic cells that invade the elastic lamina and the peritoneal connective tissue with activation and proliferation of serosal stromal cells that express cytokeratin (H&E, VVG, and pan-keratin).

<p>Tumor invasion of the peritoneal membrane is associated with retraction, attenuation, and fragmentation of the elastic lamina and proliferation of serosal stromal cells that express cytokeratin, a unique feature not observed in stromal cells of extraperitoneal tissue. The keratin-positive stromal cells involve nearly the entire thickness of the expanded peritoneal membrane, forming a well-circumscribed population that is sharply delimited from the keratin-negative stromal cells of the subserosa by the elastic lamina. Neoplastic cells that invade the peritoneum abut or are surrounded by keratin-expressing stromal cells of the serosal membrane. (A-D, adenocarcinoma, small intestine, 40x, with higher magnification of boxed area in D, 200x; E-H, ductal adenocarcinoma, pancreas, 40x, with higher magnification of boxed area in H, 100x). Arrowheads: elastic lamina.</p

The degree of peritoneal injury correlates with the degree of stromal proliferation and cytokeratin expression, which is a reflection of the extent of tumor invasion, type of tumor, and magnitude of the tumor-associated fibroinflammatory reaction (H&E, VVG, and pan-keratin).

<p>Serosal membrane in the absence of injury, as in this adenocarcinoma of the stomach confined within lymphovascular channels subjacent to the mesothelium, lacked proliferation of peritoneal stromal cells and expression of cytokeratin (A and B, H&E and pan-keratin, 200x). This adenocarcinoma of the gallbladder focally invades the splayed elastic lamina of the peritoneum with only minimal serosal injury and mild proliferation of weakly keratin-expressing stromal cells (C-E, H&E, VVG, and pan-keratin, 200x). Poorly cohesive/signet ring cell carcinoma of the stomach extends close to the visceral serosal surface, but is associated with little inflammation, desmoplasia, and weak cytokeratin expression in a small population of peritoneal stromal cells (F-H, H&E, VVG, and pan-keratin, 200x). Arrowheads: elastic lamina.</p