Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After radiosurgery of malignant tumors, it can be difficult to discriminate between transient treatment effects, radiation necrosis, and tumor progression on post-treatment imaging. Misinterpretation of an enlarging lesion may lead to inappropriate treatment and contribute to disagreements about treatment efficacy. In an effort to clarify this problem, we reviewed our experience with interpreting post-radiosurgical imaging in patients with malignant primary and secondary brain tumors. We reviewed results of radiosurgery of 30 malignant gliomas and 35 metastatic brain tumors with minimum follow up of 1 year or until death. Of 30 gliomas, 73% were larger a mean of 13 weeks after radiosurgery. Of 35 metatstatic tumors, 22% were larger a mean of 10 weeks after radiosurgery. Eleven had 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) of enlarging lesions. Eight showed increased activity with respect to brain; three decreased activity. Of the eight, six predicted incorrectly based upon the patients' subsequent courses (all alive, mean follow up of 27 months), and two correctly, with the patients dying from the imaged lesions 8 and 13 months later. Of the three with FDG uptake less than brain, one patient was alive with 32 weeks of follow up, and two patients died from the imaged lesion 13 and 21 months later. Radiographic enlargement after radiosurgery is common, especially for gliomas. Physicians caring for these patients should be aware of this phenomenon and be cautious in interpreting post-treatment images. MRI appearance may be useful for metastases. FDG-PET seems unreliable. Further evaluation of Tl-201 and HMPAO SPECT or MRS is warranted.
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PMID:Imaging changes after stereotactic radiosurgery of primary and secondary malignant brain tumors. 1199 19

Subcutaneous in vivo injections of cells of the mastocytoma line P815 in syngenic DBA/2 mice induce locally fast growing solid tumors. These have been used extensively as a cancer model to analyze and manipulate the relationship between tumor cells and host's immune defenses. We report that progression of P815 tumors in vivo was accompanied by a burst (Days 5-7) of local inflammatory cells recruitment and angiogenesis observed histologically, corroborated in vivo by MRI with gadolinium, overtranscription of macrophage activation marker genes, secretion of TNF-alpha by regional lymph node cells and concomitant systemic inflammation. No substantial overtranscriptions of either VEGF or IL-10 or TGF-beta genes were observed. Induction of COX-2 gene was a late event. To establish a possible relationship between the tumor-induced local, regional and systemic increase of pro-inflammatory mediators and progression of tumors in vivo, we carried out experiments deliberately modulating the inflammatory status of the recipient animals. Pretreatment of recipient animals by i.p. injection of thioglycolate accelerated P815 tumor growth. At the opposite, treatment of mice with either a COX-1 + COX-2 inhibitor (aspirin, 1 mg/day/mouse) or a specific COX-2 inhibitor (celecoxib, 0.13 mg/day/mouse) for 2 weeks after injection of tumor cells, significantly reduced the size and growth rate of tumors compared to control mice. Experiments carried out in vitro indicated that peritoneal macrophages from untreated animals were strongly activated by live P815 cells and by P815 membrane preparations. The tumor-induced inflammatory reaction could establish a local micro environment favoring tumor progression. The P815 tumor model might be helpful to recognize important factors controlling host/tumor relationship.
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PMID:Inflammation and cancer, the mastocytoma P815 tumor model revisited: triggering of macrophage activation in vivo with pro-tumorigenic consequences. 1212 7

We propose a point by point response to the questions raised at this round table concerning the spontaneous and postoperative course of grade I and II vestibular schwannomas, focusing on hearing function. The questions concerning non-operated schwannomas are: For operated schwannomas, the questions are: Spontaneously, 75-80% of these schwannomas progress significantly with a degradation of hearing function in more than half of the cases. We monitor clinical disorders and order routine audiometry and MRI. For us, Gardner and Roberson class A or 1 is truly useful hearing function. Preservation of truly useful hearing function after microsurgery is no better than 10%; satisfactory facial motor function is preserved in 70-80% of the cases with grade I, II, or III schwannomas and in more than 50% for grade IV schwannomas. Incomplete excision to preserve hearing function is compromised by recurrence. We preferably treat the smaller grade I schwannomas by radiosurgery to halt tumor progression and attempt to preserve hearing function.
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PMID:[Grade I and II vestibular schwannomas: hearing, clinical course. Pre- and postoperative aspects]. 1248 18

Current treatments for brain cancer have, for the most part, equivocal survival benefit. However, clinical trials of new anticancer agents do not adequately assess potential clinical benefits for patient function other than survival and time to tumor progression. We evaluated 56 patients with recurrent brain tumors who were recruited on phase 1 and phase 2 clinical trials and given assessments of cognitive function, quality of life (QOL), and ability to perform activities of daily living (ADL) prior to receiving treatment and at intervals coinciding with MRI scans, generally monthly. Meaningful change on the cognitive and functional assessments was determined by the reliable change index. Cognitive or functional deterioration was then used as a time-dependent covariate in a Cox proportional hazards regression model with tumor progression, as defined by standard criteria, as the end point. Cognitive deterioration occurred 6 weeks prior to radiographic failure (median 7.4 weeks vs. 13.4 weeks). In contrast, median time for QOL to deteriorate was not achieved. Median time for instrumental ADL to decline was 43 weeks, long after tumor progression. For patients with brain cancer, brain function began to worsen before MRI evidence of tumor progression. QOL and ADL function were not strongly tied to cognitive decline or to time to tumor progression, suggesting that these measures may not be sufficiently sensitive to change in clinical trials of new anticancer agents, although they are important measures in terms of patient care. This study also demonstrates the feasibility of performing neurocognitive testing in this patient population. New drugs that slow the cognitive decline of brain tumor patients may be of clinical benefit regardless of the impact on overall survival.
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PMID:Multifaceted end points in brain tumor clinical trials: cognitive deterioration precedes MRI progression. 1267 80

MLS ovarian epithelial carcinoma multicellular spheroids xenografted subcutaneously in CD-1 nude mice displayed growth delay, or dormancy, of up to 52 days. In the study reported here, implanted MLS spheroids were used for testing the role of angiogenesis and vascular maturation in triggering the initiation of tumor progression. The kinetics and impact of neovascular maturation and functionality, in dormancy, and growth of MLS spheroid xenografts were studied noninvasively by BOLD contrast MRI. MR data were supported by histologic staining for biotinylated albumin as a blood pool marker and alpha-smooth muscle actin (alpha-SMA) as marker for perivascular mural cells. Although the tumor periphery showed higher levels of total and mature vasculature than normal skin, the fraction of mature out of the total vessels as detected by MRI vascular maturation index (VMI(MRI)) was significantly lower in the tumor both before and after tumor exit from dormancy. The neovasculature induced by the implanted spheroid was unstable and showed cycles of vessel growth and regression. Surprisingly, this instability was not restricted to the immature vessels, but rather included also regression of mature vessels. During dormancy, neovasculature was predominantly peripheral with no infiltration into the implanted spheroid. Infiltration of alpha-SMA positive stroma cells into the spheroid was associated with functional vascularization and tumor growth. Thus, stroma infiltration and vascular maturation are an important checkpoint linking the angiogenic switch with initiation of tumor progression.
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PMID:The role of angiogenesis, vascular maturation, regression and stroma infiltration in dormancy and growth of implanted MLS ovarian carcinoma spheroids. 1469 16

The purpose of this study was to assess the ability of [(18)F]FDG-PET, CT/MRI and serum tumor marker (TM) to predict the viability of residual masses after high-dose chemotherapy (HD-Ctx) in patients with metastatic germ cell tumors (GCT). In a prospective study, 60 residual tumors in 28 GCT patients were classified as viable/nonviable by FDG-PET, CT/MRI and TM levels. The results were validated either by histological examination of a resected mass and/or biopsy or by clinical/radiological follow-up for at least 6 months. There were no significant differences among the sensitivities observed with PET, CT/MRI and TM, but PET was significantly more specific than CT/MRI in predicting residual mass viability. TM showed the highest specificity. The highest accuracy in classification of residual tumors was achieved by a combination of PET, CT/MRI and TM (area under the ROC curve =0.91). All mature teratomas showed false-negative PET results with SUVs in the same range as necrosis. For classification of residual masses after HD-Ctx of metastatic GCT, [(18)F]FDG-PET is a valuable diagnostic method to complement the established procedures CT and TM. Positive PET results are highly correlated with the presence of viable tumor, but residual masses with negative PET findings still require resection. In cases of tumor progression diagnosed by CT and elevated TM, additional PET examinations are without benefit. PET seems useful in patients with stable disease or partial remission in CT/MRI and normalized TM as well as in marker-negative disease.
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PMID:The role of [(18)F] FDG-PET, CT/MRI and tumor marker kinetics in the evaluation of post chemotherapy residual masses in metastatic germ cell tumors--prospects for management. 1473 10

The purpose of this study was to evaluate the activity, measured in terms of progression-free survival (PFS) and response rates, of 1,3-bis(chloro-ethyl)-1-nitrosourea (BCNU) plus temozolomide in adult patients with recurrent glioblastoma multiforme. The phase 2 dose and schedule for this trial was BCNU 150 mg/m(2) i.v. followed in 2 h by temozolomide 550 mg/m(2) as a single oral dose. Treatment was repeated every 6 weeks for up to 8 cycles unless tumor progression was documented. The primary end point was PFS at 6 months (PFS-6). Response was a secondary end point, measured by MR imaging, neurological status, and steroid requirements prior to each 6-week cycle. The median age of eligible patients was 53, and 89.5% had no prior chemotherapy. All patients were evaluable for toxicity and time to progression. The PFS-6 was 21%. Overall survival was 68% at 6 months and 26% at 1 year. The MRI response for 36 patients was 2 partial responses, 2 minor responses, 19 cases of stable disease, and 13 immediate progressions. Median survival was 34 weeks, and median PFS was 11 weeks. Toxicity was primarily myelosuppression; no toxic deaths occurred. Historical phase 2 study data in this patient population show a PFS-6 of 15%. Recent data for use of temozolomide alone have shown a PFS-6 of 21%. We conclude that BCNU plus temozolomide when used in these doses and schedule has only modest activity, with significant toxicity, and appears to be no more effective than single-agent temozolomide.
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PMID:Phase 2 study of BCNU and temozolomide for recurrent glioblastoma multiforme: North American Brain Tumor Consortium study. 1476 38

Nephrogenic rests (NRs) are thought to originate from persistent nephrogenic blastema and are considered precursor lesions of Wilms' tumor (WT). These rests usually occur as perilobar and intralobar lesions in the kidney and, rarely, in ectopic sites. We report a midline lumbosacral ectopic NR in a healthy full-term newborn male with no family history of WT or WT-associated syndromes. The NR presented as a soft polypoid mass covered by normal skin. An MRI study revealed no lumbosacral spine abnormalities and no communication with the vertebral canal. The resected mass measured 3 cm and contained fat and had a central 1.2-cm solid nodule. The nodule was composed of blastema, epithelial elements (mature tubules and nephrons), and abundant stroma. No other somatic tissue elements were identified after complete microscopic examination. There are 4 cases of NRs reported in the lumbosacral area associated with spinal dysraphism, and only 2 cases, in addition to our report, unassociated with spinal abnormalities. The pathogenesis of heterotopic immature nephrogenic tissue remains a source of conjecture and speculation. If these lesions are heterotopic rests, their potential for neoplastic progression is probably quite limited, but if a monodermal teratoma, then more scrupulous clinical follow-up is warranted.
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PMID:Lumbosacral ectopic nephrogenic rest unassociated with spinal dysraphism. 1537 57

Breast cancer remains a public-health issue on a global scale. We report new information about the disease from the past 5 years. Early age at first birth, increasing parity, and tamoxifen use are related to long-term lifetime reduction in breast-cancer risk. Ductal carcinomas in situ has been suggested to be renamed ductal intraepithelial neoplasia to emphasise its non-life-threatening nature. An alternative approach, the progenitor/stem cell theory, predicts that only some tumour cells cause cancer progression and that these should be targeted by treatment. Mammography and ultrasonography are still the most effective for women with non-dense and dense breast tissues, respectively. Additionally, MRI, lymphatic mapping, the nipple-sparing mastectomy, partial breast irradiation, neoadjuvant systemic therapy, and adjuvant treatments are promising for subgroups of breast-cancer patients. Although tamoxifen can be offered for endocrine-responsive disease, aromatase inhibitors are increasingly used. Assessment of potential molecular targets is now important in primary diagnosis. Tyrosine-kinase inhibitors and other drugs with anti-angiogenesis properties are currently undergoing preclinical investigations.
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PMID:Breast cancer. 1627 38

Oligoastrocytomas (OAs) are WHO grade II or III tumors composed of a mixture of 2 neoplastic cell types morphologically resembling the cells in oligodendrogliomas and diffuse astrocytomas. Investigations on the genetic profile of OAs may yield important information for their classification and help for their clinical management. We have studied, in 94 OAs (46 WHO grade II and 48 WHO grade III), the patterns of loss of heterozygosity (LOH) of 4 genomic regions: 1p, 19q, 17p and 10q. Results were as follows: LOH 1p was present in 46% of the tumors; LOH 19q in 45%; LOH 17p in 22%; LOH 10q in 16%. LOH 1p and 19q were associated in 32%, other LOH associations were rare (<3%). Patients had a median follow-up of 30 months. Patients without LOH on 1p had shorter progression free survival than patients with LOH on 1p: 30 vs. 132 months, p < 0.0001. MRI indicated that tumors without LOH on 1p were often temporal (p < 0.02), and showed signal inhomogeneity on T1 and T2 images (p < 0.02) and contrast enhancement (p < 0.04). Thus, LOH on 1p identifies two subgroups of OAs. OAs without LOH on 1p behave like WHO grade II or III diffuse astrocytomas: they have shorter survival, MRI characteristics implying malignancy and genetic alterations associated with tumor progression. OAs with LOH on 1p, on the other hand, behave like WHO grade II or III oligodendrogliomas with 1p loss: they are associated with longer survival and do not have MRI or genetic alterations associated with malignancy. These findings suggest that the definition of OAs or mixed gliomas could be reshaped in agreement with the genetic information.
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PMID:Reclassification of oligoastrocytomas by loss of heterozygosity studies. 1643 42


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