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Dongfeng Tan

Publications and source records attributed to Dongfeng Tan.

43 records · Page 3Linked to original sources
PubMed2002

Loss of heterozygosity in primary lung cancer using laser capture microdissection and WAVE DNA fragment analysis techniques.

BACKGROUND: A number of molecular changes observed by varied conventional methods, including loss of heterozygosity (LOH) on chromosome 3, have been associated with primary lung cancer. To further define the locus of chromosome 3p allele loss in lung cancer, we performed LOH study by using innovative laser capture microdissection and WAVE DNA Fragment Analysis. MATERIAL/METHODS: Thirty-eight paired specimens from patients with adenocarcinoma of the lung were used for this study. Formalin-fixed, paraffin-embedded tissue from normal stromal cells or lymphocytes and adenocarcinoma were collected using laser capture microdissection. DNA was extracted and amplified by PCR using six polymorphic DNA markers for chromosome 3. PCR products were analyzed by both gel electrophoresis and WAVE DNA Fragment Analysis. RESULTS: LOH at 3p22-24 was found in tumor cells from twelve out of thirty-eight patients (32%) when analyzed by WAVE DNA Fragment Analysis and LOH was found in tumor cells from nine out of thirty-eight patients (23%) when analyzed by gel electrophoresis. LOH was found in normal control from one out of thirty-eight patients. CONCLUSIONS: 1. Our results suggest putative tumor suppressor gene(s) is present in a region at 3p22-24, which may play a role in carcinogenesis of lung cancer. 2. Laser capture microdissection is essential tool for defined LOH studies. 3. WAVE DNA Fragment Analysis is an accurate, sensitive and automated tool for analysis of DNA fragments.

Adenocarcinoma↗
PubMedDate not supplied

Malignant hypercalcemia associated with a parathyroid macrocyst and the early genesis of a giant cell tumor.

Parathyroid cysts rarely cause primary hyperparathyroidism. In most cases, the resultant hypercalcemia is mild and detected before any significant skeletal disease develops. We report a patient with severe hypercalcemia, a synchronous brown tumor (osteitis fibrosa cystica) of the maxilla, and a large benign functional parathyroid cyst. The unusual patient presentation and management are described and illustrated. The pertinent literature is reviewed.

Biopsy, Needle↗
PubMedDate not supplied

Tissue eosinophilic infiltration: a useful marker for assessing stromal invasion, survival and locoregional recurrence in head and neck squamous neoplasia.

UNLABELLED: The assessment of stromal invasion in aerodigestive neoplastic squamous proliferation often poses diagnostic and therapeutic challenges. Eosinophilic infiltration is thought to be an adjunctive histologic criterion in determining tumor aggressiveness and invasion. We investigated whether an eosinophilic infiltration in head and neck squamous cell carcinoma measured in biopsies would aid in predicting tumor invasion, response to treatment, locoregional recurrence, and survival. METHODS: Eighty-seven patients with in situ and invasive squamous cell carcinoma of the head and neck region were evaluated and treated according to their staging. The number of eosinophils per high-power field (eosinophil/HPF), and per 10 high-power fields (eosinophil/10 HPF) at the tumor interface and in tumor tissue, was counted and classified as focally or diffusely present. Each sample was assigned an eosinophilic index of 1-4 based on the number of eosinophils/HPF or 10 HPF. Of 87 patients, 20 patients were followed up after appropriate treatment for locoregional recurrence, distant metastasis, and disease-free survival. RESULTS: Eosinophilic counts were elevated focally and/or diffusely more frequently in invasive squamous cell carcinoma than in noninvasive tumors. The increased eosinophilic counts, specifically > 10/HPF and > 20/10 HPF, were both significantly associated with stromal invasion. Greater than 10 eosinophils/HPF and/or > 20 eosinophils/10 HPF had the highest predictive power for invasion, with sensitivity, specificity, and positive predictive values of 66%, 94%, 96% and 61%, 100%, and 100%, respectively. Eosinophilic counts greater than 20 eosinophils/10 HPF and eosinophilic indices > 2 were virtually diagnostic for tumor invasion. Patients' biopsies with eosinophilic indices < 2 had a better survival (P = 0.0156). Using Cox regression analysis, we found that most patients' biopsies that had eosinophilic indices > 2 recurred locally or regionally. CONCLUSIONS: The elevated eosinophilic counts in biopsies and eosinophilic indices in specimens of squamous cell carcinoma of the aerodigestive tract are a histopathologic marker associated with tumor invasion and a clinical predictor for aggressive tumor biology. Similarly, the presence of eosinophils meeting these thresholds in an excisional specimen should indicate the need for additional therapeutic measures and close surveillance to detect earlier locoregional recurrence and possible distant metastasis.

Adult↗
PubMedDate not supplied

Photodynamic therapy for sarcoma pulmonary metastases: a preclinical toxicity study.

BACKGROUND: Intraoperative pleural and interstitial PDT accompanying resection may reduce peripheral micrometastatic foci and preclude lobectomy when applied to hilar lesions. MATERIALS AND METHODS: Fourteen beagles were used to determine the safety and histologic changes resulting from PDT. Photosensitizers HPPH (0.3 mg/kg) or Photofrin (2.0 mg/kg) were administered i.v. 48 hours prior to thoracotomy and light delivery. At thoracotomy interstitial or pleural light was given. They underwent necropsy at eight and 30 days. RESULTS: The significant toxicitities occurred with pleural PDT using high dose HPPH (15 & 30 J/cm2) including pyrexia, elevated WBC and CPK, and respiratory distress. However, using single beam pleural surface treatment all light doses for HPPH and Photofrin (5-40 J/cm2) were tolerated with depths of treatment effect up to 10 mm with HPPH. CONCLUSION: Histologic and clinical changes associated with interstitial and pleural PDT were acceptable after dosimetry was adjusted. PDT holds promise as an adjuvant treatment for sarcoma pulmonary metastases.

Animals↗
PubMedDate not supplied

Nuclear survivin expression predicts poor outcome in cholangiocarcinoma.

BACKGROUND/AIMS: Survivin is an anti-apoptotic protein expressed in cancer and may have prognostic value. Our study examined the prognostic role of survivin in biliary cancer. METHODOLOGY: Twenty-four consecutive cases of cholangiocarcinoma were studied. Immunohistochemistry was performed using a monoclonal antibody to survivin. Survivin expression was described as absent or weak and strong. RESULTS: Median age was 68 years (range 40 to 77). There were 16 females and 8 males. SEER (Surveillance, Epidemiology and End Results) staging was local in 2, regional in 15 and distant in 7. Treatments included chemotherapy (n=3), surgery (n=9), combined modality (n=10) or no therapy (n=2). Cytoplasmic and nuclear survivin expression was seen in 13 and 11 patients respectively. Strong cytoplasmic survivin expression was seen in 6 cases and strong nuclear survivin in 4. Patients with strong nuclear survivin had a median survival of 11 months, significantly lower than for patients with weak nuclear survivin expression (20 months, p=0.033). Multivariate analysis using the Cox-proportional hazards model identified 4 important prognostic predictors: nuclear survivin (P=0.022), presence of metastasis (P=0.025), age (P=0.019) and use of combined modality therapy (P=0.006). CONCLUSIONS: Nuclear survivin expression in cholangiocarcinoma may identify those with a poor prognosis.

Adult↗
PubMedDate not supplied

Aberrant crypt foci.

Colon cancer evolves through epithelial cell deregulation and inappropriate proliferation. These histopathological characteristics are exemplified in the biochemical, immunohistochemical, genetic and epigenetic elements detected within colonic mucosa. Early detection is paramount for the prevention of colon cancer deaths. Aberrant crypt foci (ACF) are thought to be the earliest identifiable neoplastic lesions in the colon carcinogenetic model. The progression of ACF to polyp and, subsequently, to cancer parallels the accumulation of several biochemical alterations and mutations whereby a small fraction of ACF evolve to colon cancer. Recent data indicate that, not uncommonly, some ACF bypass the polyp stage in their carcinogenesis thus reinforcing the importance of their early detection and our understanding of their pathogenesis. Since ACF were first detected in carcinogen-treated mice, research efforts have focused on these microscopically visible lesions both in animal and human models. ACF show variable histological features, characterized by Kudo (20) and, therefore, can be grouped into differing categories by in vivo examination with high-magnification-chromoscopic-colonoscopy (HMCC). As expected, ACF are more frequently detected in distal animal and human colons coinciding with the geographic distribution of colorectal cancer (CRC). Various proteomic (Prot) markers may be altered within ACF suggesting possible prospective pathological changes. These markers include Calreticulin, Transgelin, Serotransferrin, Triphosphate isomerase and Carbonic anhydrase II. Other markers of importance include carcinoembryonic antigen (CEA), B-catenin, placental cadherin (P-cadherin), epithelial cadherin (E-cadherin), inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2) and P16INK4a. Genetic mutations of K-ras, B-Raf APC and p53 have been demonstrated in ACF as well as the epigenetic alterations of CpG island methylation. Genomic instabilities (GI), illustrated by a higher GI Index (GII), microsatellite instability (MSI), loss of heterozygosity (LOH) and defects in mismatch repair (MMR) systems, are also expressed. These transformations may lead to the identification of the earliest pathological features initiating colon tumorigenesis. In this review, the advances in ACF research as precursors of CRCs are highlighted.

Animals↗