Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cystic neck masses are varied in their histology and embryogenesis. Because neural, vascular, and lipomatous lesions may all appear cystic, a multimodality imaging approach can help identify these potential mimics. Developmental neck cysts include thyroglossal duct, thymic, and branchial cleft cysts, and teratomatous lesions or lymphangiomas. Although laryngoceles are acquired lesions, congenital anomalies (e.g., abnormally long saccules) may play a role in their formation. Lesion location is at least as important a determinant as morphology in formulating the differential diagnosis of a cystic neck mass. Midline cystic lesions are most commonly thyroglossal duct cysts, although dermoid tumors are also frequently midline. Squamous cell carcinoma metastatic to anterior triangle lymph nodes (Fig. 17), and cystic, necrotic schwanommas, can mimic the typical appearance of an infected second branchial cleft cyst. Posterior triangle lymphadenopathy and lipomatous lesions may resemble cystic hygromas. Cystic-appearing masses in the carotid space include neurogenic tumors, vascular thromboses, and carotid chain lymphadenopathy. Neural-based lesions typically occur posterolateral to the carotid artery. Necrotic lymphadenopathy may be suggested by lesion multiplicity, or by the presence of ancillary features, such as systemic symptoms, or the existence of a primary tumor. It must be emphasized that the primary role of the radiologist in head and neck imaging is to help stage disease and guide surgery. Despite clinical and radiographic analysis, the diagnosis of many lesions ultimately depends on image-guided or excisional biopsy.
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PMID:Imaging of cystic lesions. 1105 66

Atrial myxoma is the most common benign primary tumor of the heart most commonly in the left atrium (LA). Cystic or cavitated intracardiac masses are rare. We report the case of a 43-year-old male patient admitted with chest infection, hemoptysis, and severe respiratory distress, who had to be ventilated. Chest computed tomography showed bilateral lung consolidation with large mass occupying the region of the LA. Transthoracic echocardiography and transesophageal echocardiography showed a large intracavitary left atrial cystic mobile mass. Open-heart surgical exploration did not show any mass inside the LA. A posterior left atrial wall hematoma was found and evacuated. Biopsies confirmed the presence of blood clots. Posterior left atrial wall hematoma may appear as left atrial intracavitary cystic mass and should be included in the differential diagnosis of cystic left atrial mass.
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PMID:Posterior left atrial wall hematoma mimicking cystic intracavitary atrial mass. 2049 60

The purpose of this work is to retrospectively analyze the effect of the inhomogeneity correction using clinically treated plan of stage III non-small-cell lung cancer within multiple institutions in Japan. Twenty-five patients among five facilities of radiation therapy were registered for this study. The isocenter dose or D(95) of PTV or other important values were compared with and without an inhomogeneity correction using model-based algorithm. The differences in isocenter dose were 4% average and 10% maximum for the first Anterior-Posterior opposed field plan to 40 Gy and 6% average and 11% maximum for the off-cord boost oblique field plan of 20 Gy. The differences in D(95) dose were 1% average and 9% maximum for the first plan and 1% average and 6% maximum for the boost plan. D(95) prescription seemed to be a superior method; however, its reliability depends on each clinical case. Additionally, maximum dose, minimum dose and mean dose for both the primary tumor and the metastatic lymph node were analyzed, and the minimum dose had the most impressive results. In some cases, the target volume had unintended underdose of more than 10%. Finally, an analysis of the organ at risk was added, and this showed no meaningful differences for the V(20) of the lung and the maximum dose of the spinal cord. These results provide a standard for the effects of the inhomogeneity correction.
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PMID:Multi-institutional retrospective analysis of the inhomogeneity correction for radiation therapy of lung cancer. 2118 64

The establishment of a functional, integrated vascular system is instrumental for tissue growth and homeostasis. Without blood vessels no adequate nutrition and oxygen would be provided to cells, nor could the undesired waste products be efficiently removed. Blood vessels constitute therefore one of the largest and most complex body network whose assembly depends on the precise balance of growth factors acting in a complementary and coordinated manner with cells of several identities. However, the vessels that are crucial for life can also foster death, given their involvement in cancer progression towards malignancy and metastasis. Targeting tumor vasculature has thus arisen as an appealing anti-cancer therapeutic approach. Since the milestone achievements that vascular endothelial growth factor (VEGF) blockade suppressed angiogenesis and tumor growth in mice and prolonged the survival of cancer patients when administered in combination with chemotherapy, the clinical development of anti-VEGF(R) drugs has accelerated remarkably. FDA has approved the use of bevacizumab - a humanized monoclonal antibody against VEGF - in colorectal, lung and metastatic breast cancers in combination with standard chemotherapy. Additional broad-spectrum VEGF receptor tyrosine kinase inhibitors, such as sunitinib and sorafenib, are used in monotherapy for metastatic renal carcinoma, while sunitinib is also approved for imatinib resistant gastrointestinal stromal tumors and sorafenib for advanced stage hepatocellular carcinoma. Nevertheless, the survival benefit offered by VEGF(R) blockers, either as single agents or in combination with chemotherapy, is calculated merely in the order of months. Posterior studies in preclinical models have reported that despite reducing primary tumor growth, the inhibition of VEGF increased tumor invasiveness and metastasis. The clinical implications of these findings urge the need to reconcile these conflicting results. Anti-angiogenic therapy represents a significant step forth in cancer therapy and in our understanding of cancer biology, but it is also clear that we need to learn how to use it. What is the biological consequence of VEGF-blockade? Does VEGF inhibition starve the tumor to death - as initially postulated - or does it rather foster malignancy? Can anti-VEGF(R) therapy favor tumor vessel formation by VEGF-independent means? Tumors are very diverse and plastic entities, able to adapt to the harshest conditions; this is also reflected by the tumor vasculature. Lessons from the bench to the bedside and vice versa have taught us that the diversity of signals underlying tumor vessel growth will likely be responsive (or resistant) to distinct therapeutic approaches. In this review, we propose a reflection of the different strategies tumors use to grow blood vessels and how these can have impact on the (un)success of current anti-angiogenic therapies.
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PMID:Growing tumor vessels: more than one way to skin a cat - implications for angiogenesis targeted cancer therapies. 2154 50