Biomedical subjects

P Chandrasoma

Publications and source records attributed to P Chandrasoma.

At least 19 recordsLinked to original sources

PubMed2001

Retinoic acid receptor-alpha messenger RNA expression is increased and retinoic acid receptor-gamma expression is decreased in Barrett's intestinal metaplasia, dysplasia, adenocarcinoma sequence.

BACKGROUND: Expression levels of the retinoic acid receptors (RAR-alpha, RAR-beta, and RAR-gamma) are significantly different in neoplastic tissues compared with non-neoplastic tissues for some tumors. This study investigated whether retinoic acid receptor messenger RNA (mRNA) expression levels are altered in Barrett's esophagus and Barrett's adenocarcinoma tissues. METHODS: Relative mRNA expression levels of the RARs were quantified by using the ABI 7700 Sequence Detector (Taqman) system in Barrett's intestinal metaplasia (n = 15), dysplasia (n = 6), adenocarcinoma (n = 17), and matching normal esophagus tissues (n = 36). RESULTS: RAR-alpha expression was significantly increased, and RAR-gamma expression was significantly decreased, at higher stages in the Barrett's sequence. There was almost complete loss of RAR-gamma expression (relative expression level < or = 1) in a majority (70%) of the dysplasia and adenocarcinoma tissues. There were significant differences in RAR-alpha and RAR-gamma expression in histopathologically normal tissues in patients with cancer versus patients without cancer. RAR-beta expression levels were significantly elevated in adenocarcinoma versus normal esophagus tissues. The RAR expression profile was similar for cancers arising within the esophagus and for cancers arising at the gastroesophageal junction. CONCLUSIONS: RAR mRNA expression levels are significantly different in Barrett's tissues compared with normal esophagus tissues, and these levels are significantly different in Barrett's dysplasia and adenocarcinoma tissues compared with nondysplastic tissues. These results suggest that RAR mRNA levels may be useful biomarkers for this disease and that gastroesophageal junction adenocarcinomas are genetically similar to esophageal adenocarcinomas. These results also suggest that a cancer field is present in the esophagus in patients with cancer and that genetic alterations can precede histopathologic alterations in this disease.

Adenocarcinoma↗

PubMed2001

Carditis: a manifestation of gastroesophageal reflux disease.

This series consists of 141 patients in whom cardiac mucosa (CM) was present in biopsy samples from the gastroesophageal junctional region. Inflammation of CM, irrespective of its exact anatomic location, was defined as carditis and classified as acute or chronic based on the number of inflammatory cells present. In all cases, CM showed significant chronic inflammation. One hundred and eleven (79%) of the 141 patients with carditis showed no evidence of gastritis in biopsy samples from the gastric antrum and body. Helicobacter pylori was present in 20 of 141 (14%) patients; of these, 17 had evidence of a pangastritis, with 15 of these patients also showing H. pylori in CM. Patients with severe chronic inflammation in CM had a significantly higher acid exposure of the lower esophagus as quantitated by a 24-hour pH test than those with mild chronic inflammation in CM. Acute inflammation was uncommon in CM; it was present in only 26 of 141 (18.4%) patients. There was no significant difference in acid exposure of the lower esophagus between patients with and without acute inflammation in CM. The presence of acute inflammation in CM was significantly associated with distal gastritis and H. pylori infection. Men with carditis had quantitatively higher acid exposure of the lower esophagus than did women with this disorder. This difference was greatest in men with severe inflammation in CM who had no evidence of distal gastritis. These findings provide evidence that chronic inflammation in CM is strongly associated with acid reflux and that H. pylori is not a significant etiologic factor in carditis. They also show that in patients with CM in whom H. pylori gastritis develops, the infection frequently spreads to involve CM, resulting in acute inflammation with neutrophils that is superimposed on the chronic inflammation already present.

Adolescent↗

PubMed2000

Is adenocarcinoma following esophagoduodenostomy without carcinogen in the rat reflux-induced?

BACKGROUND: A widely used rat model for reflux-induced esophageal adenocarcinoma in the absence of carcinogens involves induction of duodenoesophageal reflux by performance of esophagoduodenostomy. The aim of this study was to test the hypothesis that acid reflux reduces the incidence of adenocarcinoma in this animal model. METHODS: One hundred ninety 8-week-old male Sprague-Dawley rats were studied. The animals were randomly divided into four groups with a different type of reflux established in each group. Group 1 had an esophagoduodenostomy for duodenogastroesophageal reflux (n = 59), group 2 had an esophagoduodenostomy and a total gastrectomy for duodenoesophageal reflux (n = 54), group 3 had an esophagoduodenostomy and a total gastrectomy with acid supplementation with acidified water to control for the effect of the gastrectomy (n = 50), and group 4 had a total gastrectomy with Roux-en-Y reconstruction to eliminate all reflux (n = 25). One hundred eighty-eight surviving animals were sacrificed at 36 weeks of age and the resected esophagi were examined. RESULTS: All animals except the no reflux control group had severe reflux esophagitis. The frequency of tumor development was similar in all study groups. All of the tumors were well-differentiated adenocarcinomas that were located on the external surface of the bowel either at or immediately distal to the esophagoenteric anastomosis. The tumors appeared to arise from the submucosa and did not involve the overlying mucosa. There was no definite evidence of columnar lining of the esophagus but an admixture of squamous and columnar epithelium was found microscopically in all groups. This finding was unrelated to the presence and composition of reflux. CONCLUSIONS: Adenocarcinomas in this animal model are not reflux-induced and do not arise from the mucosa. Despite previous reports to the contrary, we suggest that this model may not be valid for the study of reflux-induced esophageal adenocarcinoma.

Adenocarcinoma, Mucinous↗

PubMed2000

Clinical significance of p53 mutations in adenocarcinoma of the esophagus and cardia.

OBJECTIVE: To compare the frequency and spectrum of p53 gene mutations in adenocarcinomas of the esophagus and cardia and to compare clinical and pathologic features in patients with p53 mutant and nonmutant cancers. SUMMARY BACKGROUND DATA: The p53 gene is commonly mutated in human cancers, and a p53 mutation is reported to be present in more than 50% of esophageal adenocarcinomas. Although many studies have investigated the frequency of p53 protein overexpression in adenocarcinomas of the esophagus or esophagogastric junction, few studies have assessed the frequency and clinical significance of p53 mutations in these tumors. In particular, the prognostic importance of p53 mutation is uncertain. Adenocarcinomas of the esophagus and cardia share many epidemiologic and pathologic features, but it is controversial whether they represent the same tumor. A comparison of the frequency and spectrum of mutations in adenocarcinomas of the esophagus and cardia would test whether these tumors are also similar at the molecular level. METHODS: DNA was isolated from microdissected paraffin-embedded tumor tissues of patients who underwent esophagogastrectomy for adenocarcinoma of the esophagus (n = 19), cardia (esophagogastric junction, n = 12), or subcardia (n = 6). Exons 5 to 8 of the p53 gene were analyzed for the presence of mutations using the polymerase chain reaction with single-strand conformation polymorphism and DNA sequencing of bands showing abnormal mobility. The presence of mutation was confirmed by selective hybridization of a mutant-specific oligonucleotide to DNA isolated from the tumor. RESULTS: p53 mutations were identified in 18 of 37 (48.6%) tumors. Patients with p53 mutant tumors were significantly younger and had a significantly poorer prognosis. There was a similar prevalence of p53 mutations in adenocarcinomas of the esophagus (53%) and cardia (58%). In contrast, mutations were relatively uncommon in subcardia adenocarcinomas (one mutant tumor [17%]). The types of mutations found in the esophageal and the cardia cancers were also similar. CONCLUSIONS: Adenocarcinomas of the esophagus and cardia have a similar frequency and spectrum of p53 gene mutations, suggesting that these tumors have a common pathogenesis. Patients with mutations are younger, have signs of more advanced disease, and have a poorer prognosis than patients without mutations.

Adenocarcinoma↗

PubMed1999

Loss of function of Trp53, but not Apc, leads to the development of esophageal adenocarcinoma in mice with jejunoesophageal reflux.

INTRODUCTION: APC and TP53 are tumor suppressor genes known to be altered frequently in human esophageal adenocarcinoma (EAC), which arises as a complication of reflux disease. To determine the functional role of these genes in the development of EAC, we have created reflux in mice gene-targeted for either Trp53 or Apc. METHODS: Wild-type (WT), p53-knockout (Trp53-/-), or Apc-mutated (ApcMin/+) mice were generated in our breeding colony. Total gastrectomy with esophagojejunostomy was performed at 6 weeks of age, creating jejunoesophageal reflux. Unoperated control mice were maintained under identical conditions. Mice were sacrificed at 30 weeks of age. Histology of the esophagus and jejunal anastamosis or gastroesophageal junction was reviewed by a single pathologist blinded to the genotype of the animal. RESULTS: The esophagus was normal in all of the unoperated mice (6 ApcMin/+, 6 WT, and 6 Trp53-/-). All operated mice (6 ApcMin/+, 12 WT, and 4 Trp53-/-) had esophagitis, with squamous hyperplasia and early focal ulceration. Barrett's metaplasia was identified in 33% of the operated ApcMin/+ (2/6) and 25% of the Trp53-/- (1/4) mice, but not in the WT mice. Of 4 operated Trp53-/- mice, all developed severe dysplasia of the squamous epithelium and 2 (50%) had EAC on histology, although no gross tumors were seen. No severe dysplasia or carcinoma was identified in any of the ApcMin/+ or WT mice. CONCLUSIONS: Loss of either Trp53 or Apc leads to the development of columnar metaplasia, whereas loss of Trp53, but not Apc, leads to development of cancer in mice with jejunoesophageal reflux.

Adenocarcinoma↗

PubMed1999

Biology of gastroesophageal reflux disease: pathophysiology relating to medical and surgical treatment.

This chapter reviews the biology of gastroesophageal reflux disease, relating pathophysiology to medical and surgical therapy. Various definitions of the disease are presented and workable criteria are developed to identify patients with the disease. The central importance of the lower esophageal high-pressure zone as a barrier to reflux is emphasized, along with an analysis of its biomechanical alteration in disease. The composition of the refluxed gastric juice is characterized in regard to its potential for mucosal injury. Evidence is provided that cardiac-type mucosa is an acquired sequel to acid-induced squamous mucosal injury in the terminal esophagus. A hypothesis regarding the process of intestinalization of cardiac-type mucosa to form Barrett's esophagus is presented. An integrated concept of the pathophysiology of gastroesophageal reflux disease is constructed. Practical concepts regarding the treatment of gastroesophageal reflux disease are developed, based on a review of studies on the natural history of the disease and the long-term outcome of therapy.

Barrett Esophagus↗

PubMed1998

Ultrasonic epithelial ablation of the lower esophagus without stricture formation. A new technique for Barrett's ablation.

BACKGROUND: The premalignant potential of Barrett's esophagus has stimulated efforts to find a way to ablate the columnar epithelium in order to reheal the area with squamous epithelium, thus obviating the cancer risk. This study describes and evaluates a new technique using ultrasonic energy to ablate the epithelium of the lower esophagus in a porcine model. METHODS: Eight young farm pigs were used to develop the technique of applying a laparoscopic Cavitron Ultrasonic Surgical Aspirator (CUSA) to the lower esophageal mucosa through an operating gastrostomy. A further 11 Yakutan minipigs then underwent CUSA epithelial ablation, followed by a laparoscopic Nissen fundoplication or postoperative acid suppression therapy. We then assessed the healing response in these subjects. RESULTS: Optimal CUSA energy settings enabled complete ablation of the squamous epithelium with preservation of the muscularis mucosa and submucosa. The integrity of the aspirated cells was sufficient for cytological analysis. Healing occurred by squamous regeneration without stricture formation. CONCLUSION: The CUSA technique holds promise for complete ablation of the Barrett's epithelium in a single setting. The unique tissue-selective nature of the ablative process allows complete mucosal reepithelialization without stricture formation.

Animals↗

PubMed1997

Inflammation and specialized intestinal metaplasia of cardiac mucosa is a manifestation of gastroesophageal reflux disease.

OBJECTIVE: The purpose of the study was to test the hypothesis that cardiac mucosa, carditis, and specialized intestinal metaplasia at an endoscopically normal-appearing cardia are manifestations of gastroesophageal reflux disease. SUMMARY BACKGROUND DATA: In the absence of esophageal mucosal injury, the diagnosis of gastroesophageal reflux disease currently rests on 24-hour pH monitoring. Histologic examination of the esophagus is not useful. The recent identification of specialized intestinal metaplasia at the cardia, along with the observation that it occurs in inflamed cardiac mucosa, led the authors to focus on the type and condition of the mucosa at the gastroesophageal junction and its relation to gastroesophageal reflux disease. METHODS: Three hundred thirty-four consecutive patients with symptoms of foregut disease, no evidence of columnar-lined esophagus, and no history of gastric or esophageal surgery were evaluated by 1) endoscopic biopsies above, at, and below the gastroesophageal junction; 2) esophageal motility; and 3) 24-hour esophageal pH monitoring. The patients were divided into groups depending on the histologic presence of cardiac epithelium with and without inflammation or associated intestinal metaplasia. Markers of gastroesophageal reflux disease were compared between groups (i.e., lower esophageal sphincter characteristics, esophageal acid exposure, the presence of endoscopic erosive esophagitis, and hiatal hernia). RESULTS: When cardiac epithelium was found, it was inflamed in 96% of the patients. The presence of cardiac epithelium and carditis was associated with deterioration of lower esophageal sphincter characteristics and increased esophageal acid exposure. Esophagitis occurred more commonly in patients with carditis whose sphincter, on manometry, was structurally defective. Specialized intestinal metaplasia at the cardia was only seen in inflamed cardiac mucosa, and its prevalence increased both with increasing acid exposure and with the presence of esophagitis. CONCLUSION: The findings of cardiac mucosa, carditis, and intestinal metaplasia in an endoscopically normal-appearing gastroesophageal junction are histologic indicators of gastroesophageal reflux disease. These findings may be among the earliest signs of gastroesophageal reflux and contribute to the authors understanding of the pathophysiology of the disease process.

Adolescent↗

PubMed1997

Prolonged survival after massive pulmonary embolism in a patient with atrial septal defect and mass in the right ventricle.

Unless thrombolytic or surgical therapy is rapidly available, massive pulmonary embolism in both pulmonary arteries invariably results in instantaneous death. A patient is presented with congenital atrial septal defect and right ventricular thrombus who developed extensive bilateral pulmonary embolism with an apparently prolonged survival. The ante- and postmortem findings represent the unusual and interesting aspects of this particular case.

Acute Disease↗

PubMed1997

Pathophysiology of Barrett's esophagus.

A novel pathophysiology of Barrett's esophagus and a new method of assessing biopsy specimens in patients with gastroesophageal reflux disease (GERD) are presented. This is based on the observation in autopsy studies of patients without GERD that the squamous epithelium of the esophagus transitions directly to fundic mucosa in many people and that the cardiac mucosa is of very short length in others. Available evidence suggests that what is termed gastric cardiac mucosa is in reality an abnormal mucosa resulting from metaplasia of the squamous epithelium of the esophagus as a result of GERD. The severity of GERD correlates with the length of metaplastic cardiac mucosa and further changes occurring in it, permitting development of a system that provides good correlation between biopsy histology and severity of GERD. Intestinal metaplasia ("Barrett's esophagus") always occurs in this metaplastic cardiac mucosa. The recognition of this new pathophysiology of Barrett's esophagus permits identification of the entire sequence whereby GERD leads to adenocarcinoma: GERD-->cardiac metaplasia of squamous epithelium-->reflux carditis-->intestinal metaplasia-->dysplasia-->adenocarcinoma. This article also attempts to develop a terminology that avoids use of the confusing term "Barrett's esophagus," which should be discarded.

Barrett Esophagus↗

PubMed1996

The influence of size or number of biopsies on rapid urease test results: a prospective evaluation.

BACKGROUND: The optimal number or size of endoscopic biopsies for use in rapid urease testing has not been established. Postulating that increasing the amount of tissue sampled would improve diagnostic yield and hasten development of a positive test, we compared urease testing with one regular biopsy, two regular biopsies, and one "jumbo" forceps biopsy. METHODS: One hundred fifty patients undergoing endoscopy had three sets of prepyloric biopsies placed in a CLOtest: one regular forceps biopsy, two regular forceps biopsy, and one large-channel jumbo forceps biopsy. Biopsies were then taken for two independent histologic examinations. Disagreements were resolved by another examiner. RESULTS: Eighty-nine patients (59%) had Helicobacter pylori infection by histology; interobserver agreement was 90% with kappa = 0.78. The mean time to a positive test was 5.3 +/- 0.9 hours for one regular biopsy, 3.2 +/- 0.7 hours for two regular biopsies, and 3.8 +/- 0.8 hours for one jumbo biopsy (p < 0.01 for two regular, one jumbo vs. one regular biopsy). Compared to one regular biopsy, the urease test was positive at least 30 minutes earlier in 56% of the patients with two regular biopsies and 54% with one jumbo biopsy. Sensitivities for one regular versus two regular biopsies were 1 hour, 19% versus 33% (p = 0.059); 2 hours, 38% versus 49% (p = 0.17); 3 hours, 48% versus 60% (p = 0.18); and 24 hours, 75% versus 79% (p > 0.20). CONCLUSIONS: Doubling the amount of tissue in the CLOtest hastens the development of a positive test by approximately 1 1/2 to 2 hours; tests become positive at least 30 minutes earlier in over 50% of the patients. Low cost, ease, and excellent specificity make the rapid urease test a valuable diagnostic tool. Nevertheless, if used as a "rapid" diagnostic test (read within 3 hours of biopsy), it is associated with a false negative rate of approximately 40%.

Adult↗

PubMed1996

Pseudotumor associated with CNS lymphoma.

A 42-year-old immune-competent woman with orbital pseudotumor and presumed intracranial extension into the temporal lobe responded well clinically and radiologically to high-doses of corticosteroids. Five months later, she developed worsening headaches and recurrence of the temporal lobe lesion. Biopsy revealed a central nervous system (CNS) lymphoma with severe reactive gliosis abutting an area of subarachnoid lymphocytic infiltrate.

Adult↗

PubMed1995

High-frequency ultrasound: determination of the lowest frequency required for cellular imaging and detection of myocardial disease.

We have previously demonstrated that a 600 MHz transducer enables the visualization of cellular detail in specimens of myocardium. However, lower-frequency transducers are more practical and provide better tissue penetration for possible in vivo application of this technique. This study was designed to ascertain the lowest frequency at which cellular detail can be imaged. We performed ultrasound imaging of 5 microns sections of 14 samples of myocardium. Each specimen was examined serially with 600 MHz, 400 MHz, 200 MHz, and 100 MHz transducers. Normal cardiac myocytes and pathologic phenomena such as fibrosis, cell fallout, and round cell infiltration were clearly identified with a 600 MHz transducer. Although there was a slight decrease in resolution, normal and pathologic phenomena were also identified with 400 and 200 MHz transducers. However, cellular detail could not be adequately identified with a 100 MHz transducer. In conclusion, transducer frequencies of 600 to 200 MHz enable visualization of cell detail and detection of pathologic changes in the myocardium. A transducer frequency of at least 200 MHz is probably required for possible in vivo application of this technique.

Cardiomyopathies↗

PubMed1995

Third ventricular cysticercal cyst mimicking a colloid cyst: case report.

We describe a case of a 28-year-old Latino man who presented with signs and symptoms of raised intracranial pressure and radiographic evidence of a third ventricular cystic lesion. The cyst was removed via a transcallosal approach; the histology was noted to be a cysticercal lesion. The radiographic and histological features of this interesting case are discussed.

Adult↗

PubMed1994

Fulminant amebic colitis. A morphologic study of four cases.

PURPOSE: The morphologic features of fulminant amebic colitis are poorly documented. In this report, we describe the clinical and pathologic findings in four of these cases. METHODS: The surgical pathology reports and accompanying histologic slides were examined from four patients who underwent surgical resections for fulminant amebic colitis. Clinical information was obtained from the patients' medical records. RESULTS: Large, geographic mucosal ulcers were typically present and were accompanied by yellow-green pseudomembranes. The muscularis externa was usually attenuated and necrotic, imparting a "wet blotting paper" consistency. Large numbers of amebic trophozoites were present within the inflammatory exudates. The mucosa adjacent to and undermined by the ulcers was often hemorrhagic or inflamed, resembling ischemic colitis or idiopathic inflammatory bowel disease, respectively. Two patients died within four weeks of their surgery. A third patient died one year later as a result of AIDS-related complications. The remaining patient has been lost to follow-up. CONCLUSION: An uncommon but life-threatening manifestation of intestinal amebiasis is a fulminant colitis. Early surgical intervention and intensive antiamebic chemotherapy are essential for efficacious management.

AIDS-Related Opportunistic Infections↗

PubMed1994

Isolated cerebral mucormycosis: case report and therapeutic considerations.

Cerebral mucormycosis (without associated involvement of and invasion from the nasal sinuses and turbinates) is an extremely rare opportunistic infection of the central nervous system. We report the case of an intravenous drug abuser (who was negative for the human immunodeficiency virus) who presented with hemiparesis on the right side, slurred speech, altered mental status, and an unsteady gait. Imaging studies revealed a large left-side basal ganglia lesion. A stereotactic biopsy obtained a tissue sample that revealed wide, nonseptated hyphal fragments with granulomatous inflammation. The patient was treated with 3 gm of amphotericin B during a 5-month period. The patient had no residual neurological dysfunction after treatment. Open surgical resection was not employed. This case suggests that stereotactic biopsy followed by long-term amphotericin B therapy, in lieu of open surgical resection, represents a viable treatment option for this rare disorder.

Adult↗

PubMed1994

Outcome of adenocarcinoma arising in Barrett's esophagus in endoscopically surveyed and nonsurveyed patients.

The value of endoscopic surveillance of Barrett's esophagus and the appropriate management of high-grade dysplasia remain unclear. Seventeen patients who were referred from endoscopic surveillance programs for management of high-grade dysplasia or adenocarcinoma developing in Barrett's esophagus were compared with 35 patients who had a newly recognized Barrett's adenocarcinoma, who had not been in a surveillance program. The referral diagnosis in the surveyed group was adenocarcinoma in six and high-grade dysplasia in 11. After repeat endoscopy with aggressive biopsy, two additional patients with adenocarcinoma were identified. Of the nine patients who underwent esophagectomy for high-grade dysplasia, five had invasive adenocarcinoma in the esophagectomy specimen, which had been missed before the operation, despite the fact that the median number of biopsy specimens obtained per 2 cm of Barrett's mucosa was 7.8 (range 1.5 to 15.0). Overall, 13 patients in the surveyed group had adenocarcinoma, 12 staged early and one staged intermediate by the WNM classification. Surveyed patients were operated on at an earlier stage than the nonsurveyed patients (10 early, 14 intermediate, and 11 late stage tumors; chi 2 = 15.6, p < 0.01). Despite the presence of adenocarcinoma in 13 of the 17 surveyed patients, their survival was significantly better than that of the nonsurveyed group (chi 2 = 5.8, p < 0.05). Patients referred from surveillance programs for Barrett's esophagus have a better outcome and earlier stage tumors than nonsurveyed patients. Inasmuch as multiple biopsy procedures do not exclude the presence of adenocarcinoma, continued surveillance of high-grade dysplasia is dangerous and potentially destructive to surveillance efforts.

Adenocarcinoma↗

PubMed1994

Oncostatin-M is an autocrine growth factor in Kaposi's sarcoma.

Oncostatin-M is a cytokine produced by macrophages and activated T lymphocytes that has recently been shown to be a mitogen for AIDS-related Kaposi's sarcoma (KS)-derived spindle cells. The significance of oncostatin-M production in AIDS-related KS in vivo, however, remains unknown. In this study we wanted to determine whether oncostatin-M is expressed in vivo in patients with HIV-I-related KS, define the cell types that express this cytokine, and compared with the control tissues from HIV-I-negative individuals. A second objective of our study was to define the expression of oncostatin-M in AIDS-KS-derived spindle cell isolates cultured in vitro and to determine whether oncostatin-M is an autocrine growth factor for these KS cells. We have determined that oncostatin-M is not expressed in any of the several organs examined in control cases, whereas the tumor tissue obtained from the skin biopsies of HIV-I-infected cases with KS displayed oncostatin-M expression in the spindle cell components of the tumor, as well as the cells lining the vascular structures, smooth muscle cells lining the eccrine sweat glands, and the epidermal layers of the skin. Furthermore, uninvolved skin of patients with HIV-related KS express oncostatin-M in the cells lining normal vessels. The mRNA polymerase chain reaction analysis confirmed findings in the primary tissues and showed expression in all of the AIDS-KS-derived spindle cell isolates examined. We have also shown with the use of oncostatin-M-specific antisense oligodeoxynucleotides that KS cell proliferation is inhibited, which correlated with a more precipitous decline in the production of interleukin-6 by these cells. We conclude that oncostatin-M is only expressed in the skin and KS tumor of HIV-I-infected individuals. Furthermore, we provide evidence that oncostatin-M is an autocrine growth factor for KS.

Acquired Immunodeficiency Syndrome↗