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David M Jablons

Publications and source records attributed to David M Jablons.

51 records · Page 3Linked to original sources

1st International Lung Cancer Conference in Beijing, October 27-30, 2002.

The 1st International Lung Cancer Conference was held on October 27-30, 2002 in Beijing, China. Leaders in the field of lung cancer came from Europe, Asia, and North America to speak at the event. Over 150 Asian physicians and scientists attended as well as attendees from both Europe and the US. Topics included Primary Prevention and Tobacco Control, Screening and Early Detection, Chemotherapy and Molecular Targeted Therapies, Chemoprevention, Molecular Biology/Pathology, Radiotherapy and Surgery. This paper is a comprehensive review of the data presented at the meeting.

China↗

Intraoperative radiation therapy in the multimodality approach to upper aerodigestive tract cancer.

The cure rate of operable lung cancer and locally advanced head and neck cancer remains suboptimal, with a limited rate of local control despite improvements in the surgical removal of primary tumors and in methods for mediastinal lymph node dissection, in particular. The efficacy of adjuvant therapy, such as EBRT, has improved, and the immediate efficacy of new chemotherapeutic drugs is increasingly significant, although local recurrences remain frequent. Locoregional failure is not uncommon in upper aerodigestive tract cancers. Factors limiting radiocurability for locally advanced (stage III) lung cancer include mediastinal intolerance of irradiation (high risk of mediastinal fibrosis, which increases exponentially when levels of much more than 50 Gy are administered to the whole mediastinum) and the very high radiosensitivity of the healthy lung, which can develop fibrosis with relatively small or moderate doses starting at 18 to 20 Gy, and even more frequently when larger volumes are irradiated. Head and neck neoplasms are less difficult sites in which to administer doses of up to 70 Gy of external beam radiotherapy initially, but, like locoregionally recurrent lung cancers, they are not easily reirradiated with tumoricidal doses of EBRT. For these reasons, IORT seems to be a good option for increasing local control, because areas of [figure: see text] residual microscopic disease may be irradiated using IOERT approaches without affecting critical organs to the same extent. In addition, careful patient selection is paramount. Combined modality treatment regimens incorporating IORT may benefit patients with locally advanced disease. The ability of IORT to sterilize microscopic residual disease can enhance the "completeness" of resection and thus, theoretically, improve local control. Although distant disease dissemination remains by far the overriding issue, as newer effective agents emerge, local failure will continue to be a problem. Preliminary studies have demonstrated that IORT can be administered to patients who have locally advanced NSCLC and head and neck cancer, in the context of aggressive combined modality therapy, and is generally well tolerated. Long-term efficacy and benefit can only be determined in the setting of carefully designed clinical trials. (See the article by Thomas and Merrick elsewhere in this issue for further discussion of this topic.) Several relatively small, single-institution pilot studies exploring the utility and benefit of IORT for locally advanced upper aerodigestive tract cancers have been conducted. Clear conclusions have been difficult to determine because of the mixing of disease stages, varying degrees and completeness of surgical resection, varying radiation doses, different schemas, and other factors. Yet, given the major morbidity and mortality associated with locally recurrent lung cancer, methods of improving local control need to be pursued and refined. Encouraging preliminary data suggest that IOERT can be safely administered and may benefit local control. Based on several centers' expertise in the combined modality treatment of locally advanced lung cancer and familiarity with IORT, the UCSF Thoracic Oncology Program has proposed a multicenter phase 2 study incorporating IORT in a combined multimodality treatment schema for patients who have completely resected locally advanced stage IIIA and IIIB NSCLC (nonpleural effusion, non-N3) (Fig. 1). It is hoped that this study will commence in the upcoming year.

Combined Modality Therapy↗

Potential of mobile intraoperative radiotherapy technology.

Mobile IORT units have the potential to change the way patients who have cancer are treated. The integration of IORT into cancer treatment programs, made possible by the new technologies of mobile linear accelerators that can be used in unshielded operating rooms, makes IORT significantly less time-consuming, less costly, and less risky to administer. It is now practical for IORT to be used in early-stage disease, in addition to advanced disease, and in sites for which patient transportation in the middle of surgery is considered too risky. Preliminary results of trials for early-stage breast and rectal cancer indicate benefits of IORT. Pediatric patients and patients who have lung cancer, previously underserved by IORT therapies, can be offered potential gains when patient transport issues do not limit IORT. Furthermore, because many of these mobile systems require no shielding, it is now practical for mobile units to be shared between hospitals, making this new mobile technology much more widely available.

Adult↗

c-Kit is not expressed in malignant mesothelioma.

Overexpression of KIT protein (CD117), the product of the c-kit gene, has been shown to have important prognostic and therapeutic implications for a number of malignant neoplasms. Previous studies have shown conflicting results regarding the expression of c-kit in malignant mesothelioma. To determine whether malignant mesothelioma expresses KIT, immunohistochemistry and RT-PCR were used to analyze archived tissue from 37 cases of mesothelioma. Although a subset of mesotheliomas demonstrated specific staining with the DAKO anti-KIT antibody, in each case staining was nuclear. We could not detect c-kit mRNA by a sensitive RT-PCR assay, even in cases with strong nuclear staining. Furthermore, a second anti-KIT antibody (Cell-Marque) only demonstrated staining in a single mesothelioma case and in none of the cases that demonstrated nuclear staining. We conclude that immunoreactivity for KIT in mesothelioma does not represent expression of the c-kit gene and may represent antibody cross-reaction with nuclear proteins. Our results raise doubt about previously reported expression of KIT in mesothelioma and consequently, the applicability of therapeutic agents that target the kinase activity of KIT.

Biomarkers, Tumor↗

Malignant mesothelioma does not demonstrate overexpression or gene amplification despite cytoplasmic immunohistochemical staining for c-Erb-B2.

BACKGROUND: Previous studies have shown conflicting results regarding the expression of c-Erb-B2 in malignant mesothelioma. Overexpression of the c-erb-B2 gene product in a subset of mesothelioma may have prognostic or therapeutic implications. OBJECTIVE: To determine whether malignant mesothelioma demonstrates c-Erb-B2 overexpression and, if so, whether such overexpression correlates with gene amplification. METHODS: Immunohistochemistry, reverse transcription-polymerase chain reaction, and fluorescent in situ hybridization were used to analyze archived tissue from 37 cases of malignant mesothelioma. RESULTS: Although immunohistochemical staining for c-Erb-B2 was detected in most mesotheliomas, the staining was cytoplasmic and was not consistent between the 2 different primary antibodies used. Moreover, even cases with strong cytoplasmic staining for c-Erb-B2 did not demonstrate increased messenger RNA levels or gene copy numbers compared to cases that demonstrated no staining. CONCLUSIONS: Cytoplasmic immunoreactivity for c-Erb-B2 in mesothelioma does not represent gene overexpression or amplification and may be an immunohistochemical artifact.

Antibodies, Monoclonal↗

Emergent surgery for massive pulmonary embolism on the basis of clinical diagnosis.

We treated a 52-year-old man for a large pleural effusion that had occurred after he fell from a ladder. Upon discharge from the hospital, the patient collapsed and was nonresponsive and hypotensive. We suspected the cause to be pulmonary embolism. When it became evident that this patient would die without emergent intervention, he was taken to surgery. A massive clot was removed from the left pulmonary artery, and multiple smaller clots were removed from both pulmonary arteries. The patient recovered and was discharged from the hospital on the 11th postoperative day. To our knowledge, this is the 1st report of pulmonary embolectomy being performed on the basis of clinical diagnosis alone.

Accidental Falls↗

Genomic copy number analysis of non-small cell lung cancer using array comparative genomic hybridization: implications of the phosphatidylinositol 3-kinase pathway.

Genomic abnormalities at 348 loci encoding genes that may contribute to lung cancer transformation and progression were assessed using array comparative genomic hybridization in 21 squamous carcinomas (SqCas) and 16 adenocarcinomas (AdCas). Hierarchical clustering showed a clear pattern of gains and losses for the SqCas, whereas the pattern for AdCas was less distinct. Cross-validated classification using a K-nearest-neighbor assigned, on average, 32 of 37 samples to their proper histological subtype. The most noticeable differences between SqCas and AdCas were gain of chromosome 3q22-q26 and loss of chromosome 3p. These occurred almost exclusively in SqCas. The region of recurrent increase is approximately 30 Mb in extent, ranging from EVI1 to TFRC. PIK3CA, the alpha catalytic subunit of phosphatidylinositol 3-kinase (PI3K), is in this region. The PIK3CA copy number increase was validated using fluorescence in situ hybridization to lung cancer tissue microarrays. Activity of the downstream PI3K effector protein kinase B (PKB) was higher in SqCas than in AdCas and was correlated with PIK3CA copy number (r = 0.75), suggesting that these copy number increases contribute to activation of PI3K signaling in SqCas of the lung.

Adenocarcinoma↗

Radical pleurectomy/decortication and intraoperative radiotherapy followed by conformal radiation with or without chemotherapy for malignant pleural mesothelioma.

OBJECTIVES: We performed a retrospective review of the efficacy and morbidity of radical pleurectomy/decortication and intraoperative radiotherapy followed by external beam radiation therapy with or without chemotherapy for diffuse malignant pleural mesothelioma. METHODS: A total of 32 patients with diffuse malignant pleural mesothelioma were initially evaluated between January 1995 and September 2000. Three patients were excluded from analysis because of unresectable disease. Two patients died postoperatively, and one patient had recurrent disease previously treated at an outside institution. Of the remaining 26 patients included in the analysis, 24 received intraoperative radiotherapy. External beam radiation therapy was generally started 1 to 2 months after resection and delivered by means of 3-dimensional conformal radiation therapy or with inverse treatment planning intensity-modulated radiation therapy. When given, chemotherapy consisted of 2 to 3 cycles of cyclophosphamide, doxorubicin (Adriamycin), and cisplatin initiated 1 to 2 months after completion of radiation. RESULTS: At the time of data analysis, 5 of 26 patients were alive. The median follow-up was 9.7 months (range, 2-67.6 months). The median overall survival and progression-free interval from the time of the operation were 18.1 and 12.2 months, respectively. The Kaplan-Meier estimates of overall survival and freedom from progression at 1 year were 64% and 50%, respectively. The site of failure was mostly locoregional. However, there were 4 abdominal failures and 1 contralateral lung failure. CONCLUSIONS: Radical pleurectomy/decortication with aggressive radiotherapy with or without chemotherapy might offer an alternative treatment option to those who cannot tolerate extrapleural pneumonectomy.

Aged↗

Induction of apoptosis in mesothelioma cells by antisurvivin oligonucleotides.

Malignant pleural mesothelioma is a rare and aggressive tumor characterized by rapid progression, late metastases, and poor prognosis. In this study, we investigated the expression of survivin, a member of the inhibitors of apoptosis protein gene family, in mesothelioma and an antisense oligonucleotide-based gene therapy for mesothelioma using survivin as a target. Initially, we documented the expression of survivin in human mesothelioma cell lines and fresh tissues using reverse transcription-PCR and Western blot analysis. Our results showed that survivin was overexpressed in 7 of 8 (87.5%) mesothelioma cell lines assayed and in all (12 of 12; 100%) freshly resected mesothelioma tissues analyzed. To investigate the use of survivin as a therapeutic target on mesothelioma, we carried out transfections with antisurvivin oligonucleotides to induce apoptosis in mesothelioma cell lines MS-1 and H28. Results from cellular transfection and subsequent analysis using the flow cytometry demonstrated that antisurvivin oligonucleotides induced significantly greater apoptosis rates in the survivin-positive mesothelioma cell line H28 (42.5%) as compared with the control oligonucleotides (16.2%; P < 0.001). The survivin-negative cell line LRK1A (survivin-/-) did not apoptose with antisense oligonucleotides. Furthermore, time course evaluation by Western blot analysis showed that survivin was inhibited by antisurvivin oligonucleotides within 12 h after transfection. Our results show, for the first time, that survivin, an inhibitors of apoptosis protein family gene member, is highly overexpressed in malignant pleural mesothelioma. Down-regulation of survivin by a targeted antisense oligonucleotide appears to be an effective gene therapy approach to the treatment of mesothelioma.

Annexin A5↗

A monoclonal antibody against Wnt-1 induces apoptosis in human cancer cells.

Aberrant activation of the Wingless-type (Wnt)/beta-catenin signaling pathway is associated with a variety of human cancers. Little is known regarding the role that Wnt ligands play in human carcinogenesis. To test whether a Wnt-1 signal is a survival factor in human cancer cells and thus may serve as a potential cancer therapeutic target, we investigated the effect of inhibition of Wnt-1 signaling in a variety of human cancer cell lines, including non small cell lung cancer, breast cancer, mesothelioma, and sarcoma. Both monoclonal antibody and RNA interference (RNAi) were used to inhibit Wnt-1 signaling. We found that incubation of a monoclonal anti-Wnt-1 antibody induced apoptosis and caused downstream protein changes in cancer cells overexpressing Wnt-1. In contrast, apoptosis was not detected in cells lacking or having minimal Wnt-1 expression after the antibody incubation. RNAi targeting of Wnt-1 in cancer cells overexpressing Wnt-1 demonstrated similar downstream protein changes and induction of apoptosis. The antibody also suppressed tumor growth in vivo. Our results indicate that both monoclonal anti-Wnt-1 antibody and Wnt-1 siRNA inhibit Wnt-1 signaling and can induce apoptosis in human cancer cells. These findings hold promise as a novel therapeutic strategy for cancer.

Antibodies, Monoclonal↗

Malignant pleural mesothelioma: evaluation with CT, MR imaging, and PET.

Imaging plays an essential role in the evaluation of malignant pleural mesothelioma (MPM). Computed tomography is the primary imaging modality used for the diagnosis and staging of MPM. Magnetic resonance (MR) imaging and, more recently, positron emission tomography (PET) have emerged as modalities that can provide additional important diagnostic and prognostic information to help further delineate the extent of disease, especially in surgical candidates. Use of MR imaging performed with different pulse sequences and gadolinium-based contrast material can improve the detection of tumor extension, especially to the chest wall and diaphragm. PET can provide both anatomic and metabolic information, especially in cases of extrathoracic and mediastinal nodal metastasis. Each imaging modality has its advantages and limitations, but their combined use is crucial in determining the most appropriate treatment options for patients with MPM.

Aged↗

Wnt-1 signal as a potential cancer therapeutic target.

Wnt-1 was first identified as a proto-oncogene activated in mouse mammary tumors induced by mouse mammary tumor virus in 1982. Wnt-1 signal is a secreted glycoprotein that plays important roles in embryonic development and carcinogenesis. In a conditional Wnt-1 transgenic mouse tumor model, reduction of Wnt-1 signaling results in the regression of the Wnt-1 initiated primary mammary tumors and lung metastasis. Aberrant activation of the Wnt pathway has been strongly linked to the development of human cancers. Increased Wnt-1 signal has been found in a variety of human cancers. Our group has shown that blockade of Wnt-1 signaling, by either Wnt-1 small interference RNA or anti-Wnt-1 antibody induces apoptosis in human cancer cells and inhibits tumor growth in vivo. This review summarizes the recent significant findings and the potentials of Wnt-1 signal as a new therapeutic target for cancer.

Animals↗

A comparison analysis of anti-tumor efficacy of adenoviral gene replacement therapy (p14ARF and p16INK4A) in human mesothelioma cells.

BACKGROUND: Tumor suppressor genes encode critical cell cycle regulatory proteins that are frequently mutated or deleted in cancer and, therefore, are important candidates for cancer treatment based on gene replacement strategies. MATERIALS AND METHODS: We evaluated and compared the relative potential therapeutic efficacy of p14ARF and p16INK4A expressed in adenoviral vectors (Adp14ARF and Adp16INK4A, respectively) in three human mesothelioma cell lines. RESULTS: The cytotoxic effects of expressed p16INK4A were significantly greater than that of p14ARF in both H28 and H2052 cells. Cell cycle G1 arrest occurred earlier with Adp16INK4A treatment than Adp14ARF (24 hours vs. 48 hours, respectively). Although both Adp14ARF and Adp16INK4A inhibited cell proliferation significantly and were potentiated by chemotherapy, Adp16INK4A appeared more potent. CONCLUSION: Our results suggest that adenoviral gene-based therapy, especially using Adp16INK4A-based strategy, may be effective in the treatment of human mesothelioma.

Adenoviridae↗

Genomic alterations in human mesothelioma including high resolution mapping of common regions of DNA loss in chromosome arm 6q.

BACKGROUND: Molecular genetic analysis of 14 freshly resected human mesotheliomas was used to identify regions in the tumor genomes that display DNA copy number alterations, especially the regions that may harbor tumor suppressor genes. MATERIALS AND METHODS: Three methods for molecular analysis were used, comparative genomic hybridization (CGH), loss of heterozygosity (LOH) and a new method, quantitative microsatellite analysis (QuMA). RESULTS: The most frequent alteration detected by CGH and LOH was deletion in chromosome 6q, for which QuMA was performed at 30 different loci so as to define the region(s) of common deletion(s). Our data indicates that there are three independent regions of common deletion, one of size 8.4 Mb located at 6q14, a second of size 15.9 Mb at 6q22 and a third of size 12.0 Mb at 6q24. CONCLUSION: This suggests that at least 3 tumor suppressor genes mapped to chromosome 6q are commonly involved in the pathogenesis of mesothelioma.

Aged↗