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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lung cancers invading the chest wall and spinal column are often considered unresectable, and consequently there are few reports describing resection of invasive vertebral lesions. The authors developed a new anterior approach procedure for the en bloc resection of primary lung adenocarcinoma invading the thoracic spine and chest wall, in which the primary tumor does not need to be separated from the vertebrae. The authors describe a total spondylectomy for the en bloc resection of lung cancer invading the spine. A combination of surgical techniques was required, including resection of the osseous elements T-2 and T-3 (the pedicles were excised using a thread saw), anterolateral thoracotomy, apical lobectomy, chest wall resection, vertebrectomy, anterior spinal column reconstruction with a titanium mesh cage containing bioactive glass ceramic, and placement of anterior and posterior spinal instrumentation. At 46 months after surgery, there is no evidence of local recurrence or distant metastasis, and the patient continues to improve. This new procedure allows for the en bloc resection of primary lung tumors and adherent vertebral invasion without separation of the lesion from the vertebra. Thus, surgical management by complete excision of Pancoast tumors can achieve longer-term survival rates without sequelae.
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PMID:Total spondylectomy for en bloc resection of lung cancer invading the chest wall and thoracic spine. Case report. 1507 Jan 43

Hemostatic mechanisms play a role not only in cancer associated thrombotic diathesis, but also in tumor growth and dissemination. Hence, inhibition of fibrin formation has been considered a possible tool against the progression of malignant disease. An antineoplastic effect of antithrombotic agents in various experimental models (i.e. tumor cell in culture, experimental animals, and cancer patients) has often been suggested. Anticoagulant drugs such as heparins and vitamin K antagonists have been repeatedly tested in this context. However, heparins have been more extensively studied. Several reports in animal models demonstrate that heparin can reduce the primary tumor growth or its metastatic spread. Clinical studies of thrombosis in cancer patients show that, besides their role as antithrombotics, heparins may have beneficial effects on survival in these patients, with a major role for low molecular-weight heparin (LMWHs) compared to unfractionated heparin (UFH). More recently a number of prospective randomized clinical trials of LMWH for survival as a primary end-point in cancer patients have been conducted, showing favourable results.
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PMID:Biological and clinical aspects of anticancer effects of antithrombotics. 1569 49

This manuscript reviews the theories behind the propensity of prostate cancer to cause bone metastases and skeletal implications of the prostate cancer biology and treatment modalities. The escape of tumor cells from the primary tumor in the prostate to secondary tumor sites in the axial skeleton probably occurs before the primary tumor is detected. Several theories offer explanations for the observed proclivity of prostate tumors to selectively colonize the axial skeleton. The interaction between the tumor cells and cells that populate bone marrow, in particular osteoblasts and osteoclasts, is important for creating a 'fertile' environment where tumor cells can establish and grow. Prostate cancer cells are capable of producing growth factors that can affect both osteoblasts, resulting in osteoblastic bone formation, and osteoclasts, resulting in excessive bone resorption. In addition to the capability to progress from testosterone-dependent to testosterone-independent phenotype, the hallmark of metastatic prostate cancer is osteosclerosis similar to one induced experimentally in nude rats using CWR22 human prostate cancer cell line. Metastatic bone disease caused by excessive bone formation and bone resorption is the major cause of morbidity in patients with prostate cancer. The most common symptoms include pain, pathological fractures, spinal cord compression, cranial nerve palsies, bone marrow suppression and hypercalcemia. The introduction of prostate-specific antigen in clinical practice created a shift to where more prostate cancer patients with early disease receive androgen ablation treatment, which in return causes more bone loss and cancer-associated osteoporosis. Introduction of third generation bisphosphonates to treat skeletal consequences of malignancy further stressed the important interaction between the bone marrow stroma and cancer cells. Nevertheless, animal models and human prostate tumor cell lines that mimic all aspects of skeletal conditions in prostate cancer patients including osteoblastic bone response are needed to develop and screen for novel therapeutic and diagnostic modalities.
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PMID:Skeletal implications of prostate cancer. 1575 51

The epidermal growth factor receptor (EGFR) gene has recently been reported to be mutated in a subset of non-small cell lung cancers (NSCLC), with the mutations being correlated with the patients' drug sensitivity to gefitinib, an EGFR kinase inhibitor. In this study, we searched for EGFR mutations in patients with lung cancer using primary tumor specimens obtained at initial surgery and examined whether their recurrent tumors showed a response to gefitinib depending on the presence of the activating mutation. Among 12 lung cancers that were treated with gefitinib after recurrence, we found that all four tumors which showed a response to gefitinib had an activating mutation in EGFR, whereas none of the remaining eight tumors had a mutation. Southern blot analysis showed that two of the four responsive tumors had the EGFR gene amplification. We also examined another 73 NSCLC specimens (47 males and 26 females; 53 adenocarcinomas and 20 non-adenocarcinomas) which were not treated with gefitinib to determine whether NSCLCs with an EGFR mutation have different clinicopathological properties and/or unique genetic alterations of the other cancer-associated genes. We found that 13 (18%) of 73 tumors had a mutation of the EGFR gene, with the most being detected in female adenocarcinomas. Comparing the alterations in KRAS and P53 with the EGFR mutation, we found that 10 tumors with the KRAS mutation did not have an EGFR mutation, suggesting that each mutation occurs exclusively during the development of lung cancer. These results suggest that the mutation analysis of the EGFR gene using the specimens obtained at surgery might be useful in selecting the appropriate treatment(s) for recurrent lung cancer patients.
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PMID:Mutations of epidermal growth factor receptor of non-small cell lung cancer were associated with sensitivity to gefitinib in recurrence after surgery. 1614 Apr 20

Patients with gallbadder cancer associated with remarkable lymph node involvement along the para-aortic region are usually excluded from therapeutic plans because of their oppressive outlook. We experienced two patients with Stage IV gallbadder cancer who had undergone intra-aortic infusion chemotherapy and experienced its tumoricidal effects. By keeping the tip of the catheter in the aorta at the Th 9-10 level, we intended to improve the efficiency of drug delivery to both primary lesion and para-aortic metastatic lymph nodes. The anti-cancer drugs employed were gemcitabine (day 3, 9, 1,000 mg/m2/30 min) and low-dose CDDP (day 1-5, day 8-12, 5 mg/30 min) combined with 5-FU (day 1-5, day 8-12, 250 mg/24 h). Day 15-21 was the treatment-free time for recovery from drug toxicities. Since this regimen was well tolerated, the patients could undergo this plan repeatedly. The evidence on CT scans or cholangiography revealed remarkable regression of both primary tumor and metastatic lymph nodes, or resolution of the biliary obstruction. The survival periods from the induction of the treatment were 12 and 14 months, respectively. Thus intra-aortic infusion chemotherapy may be beneficial for the treatment of gallbladder cancer associated with para-aortic lymph node involvement.
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PMID:[Two cases of advanced gallbadder cancer with para-aortic lymph node metastasis responding to intra-aortic infusion of gemcitabine and low-dose CDDP/5-FU]. 1618 39

Cancer metastases (spread to distant organs from the primary tumor site) signify systemic, progressive, and essentially incurable malignant disease. Anorexia and wasting develop continuously throughout the course of incurable cancer. Overall, in Westernized countries nearly exactly half of current cancer diagnoses end in cure and the other half end in death; thus, cancer-associated cachexia has a high prevalence. The pathophysiology of cancer-associated cachexia has two principal components: a failure of food intake and a systemic hypermetabolism/hypercatabolism syndrome. The superimposed metabolic changes result in a rate of depletion of physiological reserves of energy and protein that is greater than would be expected based on the prevailing level of food intake. These features indicate a need for nutritional support, metabolic management, and a clear appreciation of the context of life-limiting illness.
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PMID:Cancer-associated cachexia and underlying biological mechanisms. 1660 32

Paraneoplastic syndromes represent the clinical manifestations of the indirect and remote effects produced by tumor metabolites or other products. The clinical spectrum of the various paraneoplastic syndromes related to primary malignancies of the head and neck region is presented. A review of the literature on paraneoplastic syndromes in patients with primary head and neck cancer was carried out. Paraneoplastic syndromes related to primary malignancies of the head and neck region can be categorized as: endocrine, cutaneous or dermatologic, hematologic, neurologic, osteoarticular or rheumatologic, ocular syndromes. Sometimes, paraneoplastic syndromes can be more serious than the consequences of the primary tumor itself and can precede, follow or be concurrent to the diagnosis of a malignancy; moreover, they can dominate the clinical picture and thus lead to errors with respect to the origin and type of the primary tumor. Physicians who deal with cancer-associated syndromes should be able to differentiate the paraneoplastic syndromes from the benign disorders that mimic them. Patients with a suspected paraneoplastic disorder should undergo a complete panel of laboratory studies, in addition to imaging studies and endoscopy. Identification of paraneoplastic syndromes allow the clinician to make an early diagnosis and to provide adequate treatment of tumors, with a favorable oncologic outcome and improved life expectancy for the patient. These syndromes can follow the clinical course of the tumor and thus be useful for monitoring its evolution.
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PMID:Paraneoplastic syndromes in patients with primary head and neck cancer. 1720 3

Ovarian cancer presents as disseminated disease in the majority of cases. Tumor metastasis to the peritoneal and/or pleural cavity is evident in two-thirds of cases at diagnosis and relapse is most often detected at this anatomic site. Despite the fact that the primary tumor is amenable to surgical removal in the majority of cases, ovarian cancer research, including the evaluation of therapeutic targets, has concentrated on primary disease. In recent years, we analyzed the site-dependent expression of cancer-associated and regulatory molecules in primary tumors, effusions and solid metastases. Our data show that some molecules (e.g., Ets transcription factors) are expressed at all anatomic sites in ovarian carcinoma and that their expression in primary and metastatic disease is associated with poor prognosis. However, the majority of molecules (e.g., cadherins, integrins, and nerve growth factor receptors) are differentially expressed along tumor progression and have different prognostic value depending on the organ sampled. Specifically, cancer-associated molecules with a well-characterized clinical significance in solid tumors (e.g., matrix metalloproteinases) have no such role in effusions. Finally, a growing number of molecules are differentially expressed in primary diagnosis (pre-chemotherapy) and disease recurrence (post-chemotherapy) specimens, reflecting the effect of disease progression and chemotherapy. This review will present the current knowledge in this area.
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PMID:Anatomic site-related expression of cancer-associated molecules in ovarian carcinoma. 1730 82

Coagulation activation by tissue factor (TF) is implicated in cancer progression, cancer-associated thrombosis and metastasis. The role of direct TF signaling pathways in cancer, however, remains incompletely understood. Here we address how TF contributes to primary tumor growth by using a unique pair of isotype-matched antibodies that inhibit either coagulation (monoclonal antibody [Mab]-5G9) or direct signaling (Mab-10H10). We demonstrate that the inhibitory antibody of direct TF-VIIa signaling not only blocks TF-VIIa mediated activation of PAR2, but also disrupts the interaction of TF with integrins. In epithelial and TF-expressing endothelial cells, association of TF with beta1 integrins is regulated by TF extracellular ligand binding and independent of PAR2 signaling or proteolytic activity of VIIa. In contrast, alpha3beta1 integrin association of TF is constitutive in breast cancer cells and blocked by Mab-10H10 but not by Mab-5G9. Mab-5G9 has antitumor activity in vivo, but we show here that Mab-10H10 is at least as effective in suppressing human xenograft tumors in 2 different models. Breast tumor growth was also attenuated by blocking PAR2 signaling. These results show that tumor cell TF-PAR2 signaling is crucial for tumor growth and suggest that anti-TF strategies can be applied in cancer therapy with minor impairment of TF-dependent hemostatic pathways.
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PMID:Inhibition of tissue factor signaling suppresses tumor growth. 1790 Dec 45

Background. Spine is the most common place of metastatic tumors in the skeletal system. Due to diagnostic problems and the risk of quickly increasing neurological defects, the treatment of metastatic spine tumors is a significant clinical problem. The goal of surgical treatment is decreasing pain, neurological improvement and achieving full spinal stability. <br /> Material and methods. Material consists of 31 patients with metastases in spine, who underwent spine surgery. Tumors were placed in thoracic spine at 48% patients, at lumbar spine - 42% patients, and at cervical spine in 10% patients; one level was involved in 56% cases, two or more levels - in 44 % cases. Qualification for surgery contained: the type of primary tumor, the amount of metastases to the spine impairment of spinal biomechanics and overall patient's condition of the. Corporectomy with anterior stabilization (intervertebral cage) was performed at 13 patients, and with additional anterior implants at 2 cases. At 8 patients, with destabilization of posterior spinal column, in spite of corporectomy, posterior stabilization was done. Surgery from posterior approach was performed in 3 cases. <br /> Results. After operation, we noted pain relief at 34% of patients, while in 14% of them transient increase of pain occurred. Neurological status worsened after surgery at 1 patient. We achieved proper spine stabilization, without the need of use of external orthoses at 30 patients. At one patients, reoperation with change of implants and the range of stabilization was necessary. The amount of complications correlated with patient's general condition at the time of surgery.<br /> Conclusions. 1. The main condition of success in operative treatment of spinal metastatic tumors is individual patient's qualification for surgery, including the extent of disease and general patient's condition. 2. Good stabilization with use of implants is a necessary element of surgery of spinal metastases from both anterior and posterior approach.
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PMID:Indications and range of surgery in the treatment of spine metastatic tumours. 1803 1


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