Biomedical subjects

J Landry

Publications and source records attributed to J Landry.

At least 37 records · Page 2Linked to original sources

PubMed2000

p38 MAP kinase pathway regulates angiotensin II-induced contraction of rat vascular smooth muscle.

Angiotensin II (ANG II) is a multifunctional hormone that exerts potent vasoconstrictor and hypertrophic effects on vascular smooth muscle. Here, we demonstrate that the p38 mitogen-activated protein (MAP) kinase pathway is involved in ANG II-induced vascular contraction. Addition of ANG II to rat aortic smooth muscle cells (SMC) caused a rapid and transient increase of p38 activity through activation of the AT(1) receptor subtype. This response to ANG II was strongly attenuated by pretreating cells with antioxidants and diphenylene iodonium and was mimicked by exposure of cells to H(2)O(2). Stimulation of p38 by ANG II resulted in the enzymatic activation of MAP kinase-activated protein (MAPKAP) kinase-2 and the phosphorylation of heat shock protein 27 (HSP27) in aortic SMC. Pretreatment of cells with the specific p38 MAP kinase inhibitor SB-203580 completely blocked the ANG II-dependent activation of MAPKAP kinase-2 and phosphorylation of HSP27. ANG II also caused a robust activation of MAPKAP kinase-2 in the intact rat aorta. Incubation with SB-203580 significantly decreased the potency of ANG II to induce contraction of rat aortic rings and depressed the maximal hormone response. These results suggest that the p38 MAP kinase pathway selectively modulates the vasoconstrictor action of ANG II in vascular smooth muscle.

Angiotensin II↗

PubMed2000

Outcome of patients receiving radiation for cancer of the esophagus: results of the 1992-1994 Patterns of Care Study.

PURPOSE: A Patterns of Care Study examined the records of patients with esophageal cancer (EC) treated with radiation in 1992 through 1994 to determine the national practice processes of care and outcomes and to compare the results with those of clinical trials. PATIENTS AND METHODS: A national survey of 63 institutions was conducted using two-stage cluster sampling, and specific information was collected on 400 patients with squamous cell (62%) or adenocarcinoma (37%) of the thoracic esophagus who received radiation therapy (RT) as part of primary or adjuvant treatment. Patients were staged according to a modified 1983 American Joint Committee on Cancer staging system. Fifteen percent of patients had clinical stage (CS) I disease, 40% had CS II disease, and 30% had CS III disease. Twenty-six percent of patients underwent esophagectomy. Seventy-five percent of patients received chemotherapy; 84% of these received concurrent chemotherapy and radiation (CRT). RESULTS: Significant variables for overall survival in multivariate analysis include the use of esophagectomy (risk ratio [RR] = 0.62), the use of chemotherapy (RR = 0.63), Karnofsky performance status (KPS) greater than 80 (RR = 0.61), CS I or II disease (RR = 0.66), and facility type (RR = 0.72). Age, sex, and histology were not significant. Preoperative CRT resulted in a nonsignificantly higher 2-year survival rate compared with definitive CRT alone (63% v 39%; P =.11), whereas 2-year survival by planned treatment rather than treatment given was 47.7% for preoperative CRT and 35.4% for definitive CRT (P =.23). Definitive CRT compared with definitive RT alone resulted in significantly higher 2-year survival (39% v 20.6%; P =.027) and lower 2-year local regional failure (30% v 57.9%; P =. 0031). CONCLUSION: This study confirms the value of CRT in EC treatment. It indicates that the results obtained in practice settings nationwide are similar to those obtained in clinical trials and that KPS and the 1983 clinical staging system are useful prognostic indicators. The suggested value of esophagectomy and superiority of preoperative CRT over CRT alone in this study should be tested in a randomized trial.

Adenocarcinoma↗

PubMed2000

Perinatal expression of heat-shock protein 27 in brain regions and nonneural tissues of the piglet.

Important stressful events occur at birth or within the few hours that follow this event. To unravel a possible involvement of stress proteins, it is important to determine their levels of expression. Expression of HSP27 protein was determined by Western blotting in several nonneural tissues and in brain regions of the developing pig (fetal to adult). Maximum levels of expression were observed in heart, liver, and lung. In kidney, the expression was reduced during the first hours of life. Brain parts included whole brain, cerebellum, cortex, hippocampus, hypothalamus, and striatum. HSP27 immunogenicity was observed in all the brain regions studied. In whole brain, cerebellum, cortex, hippocampus, and hypothalamus extracts, the levels of HSP27 were decreased during the first hours of age (4 h to 2 d). In striatum, levels of expression were very low--if detectable--during the early postnatal days of life. Changes in environmental parameters, like temperature and/or hypoxia can be possibly related to differential expressions of HSPs, which can result in severe adverse developmental outcomes. The results are discussed in terms of using the newborn piglet as a model to study different forms of stress on the heat-shock protein postnatal expression.

Animals↗

PubMed1999

A short lived protein involved in the heat shock sensing mechanism responsible for stress-activated protein kinase 2 (SAPK2/p38) activation.

The stress-activated protein kinase 2 (SAPK2/p38) is activated by various environmental stresses and also by a vast array of agonists including growth factors and cytokines. This implies the existence of multiple proximal signaling pathways converging to the SAPK2/p38 activation cascade. Here, we show that there is a sensing mechanism highly specific to heat shock for activation of SAPK2/p38. After mild heat shock, cells became refractory to reinduction of the SAPK2/p38 pathway by a second heat shock. This was not the result of a toxic effect because the cells remained fully responsive to reinduction by other stresses, cytokines, or growth factors. Neither the activity of SAPK2/p38 itself nor the accumulation of the heat shock proteins was essential in the desensitization process. The cells were not desensitized to heat shock by other treatments that activated SAPK2/p38. Moreover, inhibiting SAPK2/p38 activity during heat shock did not block desensitization. Also, overexpression of HSP70, HSP27, or HSP90 by gene transfection did not cause desensitization, and inhibiting their synthesis after heat shock did not prevent desensitization. Desensitization rather appeared to be linked closely to the turnover of a putative upstream activator of SAPK2/p38. Cycloheximide induced a progressive and eventually complete desensitization. The effect was specific to heat shock and minimally affected activation by other stress inducers. Inhibiting protein degradation with MG132 caused the constitutive activation of SAPK2/p38, which was blocked by a pretreatment with either cycloheximide or heat shock. The results thus indicate that there is a sensing pathway highly specific to heat shock upstream of SAPK2/p38 activation. The pathway appears to involve a short lived protein that is the target of rapid successive up- and down-regulation by heat shock.

Amino Acid Sequence↗

PubMed1999

The evaluation and treatment of patients receiving radiation therapy for carcinoma of the esophagus: results of the 1992-1994 Patterns of Care Study.

BACKGROUND: For the first time, a Patterns of Care Study (PCS) was conducted in 1992-1994 to determine the national practice standards in evaluating and treating patients with esophageal carcinoma and to determine the degree to which clinical trials have been incorporated into national practice. METHODS: A national survey of 61 institutions using 2-stage cluster sampling was conducted, and specific information was collected on 400 patients with squamous cell carcinoma or adenocarcinoma of the thoracic esophagus who received radiation therapy (RT) as part of definitive or adjuvant management of their disease. Patients were staged according to a modified 1983 American Joint Committee on Cancer staging system. Chi-square tests for significant differences between academic and nonacademic institutions for a particular variable were performed. RESULTS: The median age of patients was 66.7 years (range, 26-89 years); 76.5% were male and 23.5% were female. Karnofsky performance status was > or = 80 for 88.3% of patients. Squamous cell carcinoma was diagnosed in 61.5% and adenocarcinoma in 36.8%. Fifteen percent were Clinical Stage (CS) I, 39.5% CS II, and 29.5% CS III. Evaluative procedures included endoscopy (>93%), computed tomography (CT) of the chest (86%), CT of the abdomen (75%), esophagography (68.5%), and endoscopic ultrasound (3.5%). Endoscopic ultrasound and CT of the chest were performed significantly more frequently at academic than nonacademic facilities (6.1% vs. 1.0% and 91.9% vs. 81.3%, respectively). Three-quarters of all patients received chemotherapy and RT and 62.5% received concurrent chemotherapy and RT as part of their treatment. Treatments included chemotherapy plus RT (54.0%), RT alone (20.3%), preoperative chemotherapy + RT (13.3%), postoperative chemotherapy + RT (7.7%), postoperative RT (3.5%), and preoperative RT (1.2%). The chemotherapeutic agents most frequently used were 5-fluorouracil (84%), cisplatin (64%), and mitomycin (9%); academic instututions used cisplatin significantly more often and mitomycin significantly less often than nonacademic institutions. Brachytherapy was used in 8.5% of cases. The median total dose of external beam radiation was 50.4 gray and the median dose per fraction was 1.8 gray. CONCLUSIONS: This study establishes the national benchmarks for the evaluation and treatment of patients with esophageal carcinoma at radiation facilities in the U.S. It also indicates that the majority of patients given RT as a component of treatment for esophageal carcinoma receive chemoradiation rather than RT alone, as supported by clinical trials. Although some differences in the evaluation of esophageal carcinoma were noted between academic and nonacademic facilities, there was no difference in the frequency of use of chemoradiation versus RT by facility type.

Adenocarcinoma↗

PubMed1999

Cloning and characterization of hGMEB1, a novel glucocorticoid modulatory element binding protein.

A 21-bp element called glucocorticoid modulatory element (GME) modulates the glucocorticoid receptor-mediated responses via the binding of an as yet poorly characterized transacting complex of proteins containing the 88-kDa GMEB1 and the 67-kDa GMEB2. Using heat shock protein 27 (HSP27) as bait in the yeast two-hybrid assay, we cloned a 1.83-kb cDNA encoding a novel 573-amino acid protein called human GMEB1 (hGMEB1). hGMEB1 possesses a KDWK domain, contains sequences almost identical (36/38) to three tryptic peptides of rat GMEB1 and shares 38% identity with rat GMEB2. hGMEB1 is ubiquitously expressed as a 85-kDa protein in all cell lines and tissues examined. In vitro translated hGMEB1 bound specifically to GME oligonucleotides yielding a complex of similar size to the complex obtained using rat liver nuclear extracts. Both complexes were supershifted with an antibody specific to hGMEB1. Co-immunoprecipitation experiments confirmed the in vivo interaction of HSP27 with hGMEB1.

3T3 Cells↗

PubMed1999

Embryonic death of Mek1-deficient mice reveals a role for this kinase in angiogenesis in the labyrinthine region of the placenta.

Mek is a dual-specificity kinase that activates the extracellular-signal-regulated (Erk) mitogen-activated protein (MAP) kinases upon agonist binding to receptors. The Erk MAP kinase cascade is involved in cell-fate determination in many organisms. In mammals, this pathway is proposed to regulate cell growth and differentiation. Genetic studies have shown that although a single mek gene is present in Caenorhabditis elegans, Drosophila and Xenopus, two mek homologs, Mek1 and Mek2, are present in the mammalian cascade. In the present study, we describe a mutant mouse line in which the mek1 gene has been disrupted by insertional mutagenesis. The null mutation was recessive lethal, as the homozygous mutant embryos died at 10.5 days of gestation. Histopathological analyses revealed a reduction in vascularization of the placenta that was due to a marked decrease of vascular endothelial cells in the labyrinthine region. The failure to establish a functional placenta probably explains the death of the mek1-/- embryos. Cell-migration assays indicated that mek1-/- fibroblasts could not be induced to migrate by fibronectin, although the levels of Mek2 protein and Erk activation were normal. Re-expression of Mek1 in the mutant mouse embryonic fibroblasts (MEFs) restored their ability to migrate. Our findings provide genetic evidence that establishes the unique role played by Mek1 in signal transduction. They also suggest that mek1 function is required for normal response to angiogenic signals that might promote vascularization of the labyrinthine region of the placenta.

Animals↗

PubMed1999

HSP27 multimerization mediated by phosphorylation-sensitive intermolecular interactions at the amino terminus.

Distinct biochemical activities have been reported for small and large molecular complexes of heat shock protein 27 (HSP27), respectively. Using glycerol gradient ultracentrifugation and chemical cross-linking, we show here that Chinese hamster HSP27 is expressed in cells as homotypic multimers ranging from dimers up to 700-kDa oligomers. Treatments with arsenite, which induces phosphorylation on Ser15 and Ser90, provoked a major change in the size distribution of the complexes that shifted from oligomers to dimers. Ser90 phosphorylation was sufficient and necessary for causing this change in structure. Dimer formation was severely inhibited by replacing Ser90 with Ala90 but not by replacing Ser15 with Ala15. Using the yeast two-hybrid system, two domains were identified that were responsible for HSP27 intermolecular interactions. One domain was insensitive to phosphorylation and corresponded to the C-terminal alpha-crystallin domain. The other domain was sensitive to serine 90 phosphorylation and was located in the N-terminal region of the protein. Fusion of this N-terminal domain to firefly luciferase conferred luciferase with the capacity to form multimers that dissociated into monomers upon phosphorylation. A deletion within this domain of residues Arg5-Tyr23, which contains a WDPF motif found in most proteins of the small heat shock protein family, yielded a protein that forms only phosphorylation-insensitive dimers. We propose that HSP27 forms stable dimers through the alpha-crystallin domain. These dimers further multimerize through intermolecular interactions mediated by the phosphorylation-sensitive N-terminal domain.

3T3 Cells↗

PubMed1999

Critical survey of interrelationships of nitrogen and amino acids in seeds.

The present paper is intended for removing inconsistencies from available information concerning the interrelationhips of nitrogen (N) and amino acids in seeds (or grains). It consists of a critical survey of data reported in a series of papers by Mossé and collaborators (see Mossé and Huet, Sci. Aliments 1990, 10, 151 for review). These authors contended for perfectly linear relationships (A(i) = a(i)N + b(i)) to hold between N and amino acid i (g/100 g seed dry matter) for seeds of a given species on the basis of correlation coefficient (r) found to be close to 1. Three linear regressions are called upon to analyze variations in the amino acid compositions of 33 samples of pea seeds. The regression C(i) (g amino acid i/16gN) = 16a(i) + 16b(i)N(-)(1), not used customarily, is the more amenable to accommodate all the facts in pointing out values significantly lower than 1 for r(i)(2), and parameters a(i) and b(i) similar to those found with the regression A(i) = NC(i)/16 = a(i)N + b(i) whose r(i)(2) values, very close to 1, are overestimated on account of the presence of N in both sides of equation and sampling limited in number. Examination of variations in lysine content of maize grains as a function of N shows that the phenotypic variations for a given genotype are a poor fit to the linear relationship A(lys) = aN + b available in the literature, as determined from 153 commercial samples. It is concluded that linear N-amino acid relationships hold only approximately for predicting amino acid composition of seed of a given species from its N content.

Amino Acids↗

PubMed1999

Long-term follow-up of patients with rectal cancer managed by local excision with and without adjuvant irradiation.

OBJECTIVE: The long-term outcomes of patients undergoing local excision with or without pelvic irradiation were examined to define the role of adjuvant irradiation after local excision of T1 and T2 rectal cancers. METHODS: Ninety-nine patients with T1 or T2 rectal cancers underwent local excision with or without adjuvant irradiation at Massachusetts General Hospital and Emory University Hospital between January 1966 and January 1997. Of these, 52 patients were treated by local excision alone and 47 patients by local excision plus adjuvant irradiation. Twenty-six of these 47 patients were treated by irradiation in combination with 5-fluorouracil chemotherapy. The outcomes of these groups were compared. RESULTS: The 5-year actuarial local control and recurrence-free survival rates were 72% and 66%, respectively, for the local excision alone group and 90% and 74%, respectively, for the adjuvant irradiation group. This improvement in outcome was evident despite the presence of a higher-risk patient population in the adjuvant irradiation group. Adverse pathologic features such as poorly differentiated histology and lymphatic or blood vessel invasion decreased local control and recurrence-free survival rates in the local excision only group. Adjuvant irradiation significantly improved 5-year outcomes in patients with high-risk pathologic features. Four cases of late local recurrence were seen at 64, 72, 86, and 91 months in the adjuvant irradiation group. CONCLUSIONS: The authors recommend adjuvant chemoradiation for all patients undergoing local excision for T2 tumors, and for T1 tumors with high-risk pathologic features. The four cases of late local failures beyond 5 years in the adjuvant irradiation group underscores the need for careful long-term follow-up in these patients.

Actuarial Analysis↗

PubMed1999

Assessment and intervention with clients with apraxia: contributions from the literature.

Individuals with praxis problems encounter difficulties engaging in occupation, and the occupational therapists who work with these clients are challenged to provide intervention that enables occupational performance. This extensive review of the current literature provides clinicians with information regarding the relevant descriptions and suggested mechanisms of apraxia. Errors noted in performance, different classification systems and the implications of the current knowledge will be discussed. The paper concludes by providing information for clinicians regarding occupational therapy evaluation and intervention strategies for praxis problems.

Apraxias↗

PubMed1999

Regulation of actin dynamics by stress-activated protein kinase 2 (SAPK2)-dependent phosphorylation of heat-shock protein of 27 kDa (Hsp27).

Activation of the mitogen-activated protein kinase (MAP kinase) SAPK2 (stress-activated protein kinase 2) leads to the phosphorylation of several transcription factors and cytoplasmic proteins, and thereby presumably orchestrates important specific cellular responses to numerous cytokines, stressing agents and agonists of tyrosine kinase or serpentine receptors. The heat-shock protein of 27 kDa (Hsp27), a downstream target of the SAPK2-activated MAP-kinase-activated protein kinase-2/3, has a documented function as an actin polymerization modulator. Accordingly, recent evidence implicates the SAPK2 pathway in the modulation of microfilament dynamics in response to stress and agonist stimulation. In vascular endothelial cells, where the basal level of expression of Hsp27 is high, SAPK2 mediates oxidative stress- and vascular endothelial growth factor (VEGF)-induced actin reorganization and VEGF-induced cell migration, suggesting a key role for this MAP kinase pathway in inflammation and angiogenic processes.

Actins↗

PubMed1998

SAPK2/p38-dependent F-actin reorganization regulates early membrane blebbing during stress-induced apoptosis.

In endothelial cells, H2O2 induces the rapid formation of focal adhesion complexes at the ventral face of the cells and a major reorganization of the actin cytoskeleton into dense transcytoplasmic stress fibers. This change in actin dynamics results from the activation of the mitogen-activated protein (MAP) kinase stress-activated protein kinase-2/p38 (SAPK2/p38), which, via MAP kinase-activated protein (MAPKAP) kinase-2/3, leads to the phosphorylation of the actin polymerization modulator heat shock protein of 27 kD (HSP27). Here we show that the concomitant activation of the extracellular signal-regulated kinase (ERK) MAP kinase pathway by H2O2 accomplishes an essential survival function during this process. When the activation of ERK was blocked with PD098059, the focal adhesion complexes formed under the plasma membrane, and the actin polymerization activity led to a rapid and intense membrane blebbing. The blebs were delimited by a thin F-actin ring and contained enhanced levels of HSP27. Later, the cells displayed hallmarks of apoptosis, such as DEVD protease activities and internucleosomal DNA fragmentation. Bleb formation but not apoptosis was blocked by extremely low concentrations of the actin polymerization inhibitor cytochalasin D or by the SAPK2 inhibitor SB203580, indicating that the two processes are not in the same linear cascade. The role of HSP27 in mediating membrane blebbing was assessed in fibroblastic cells. In control fibroblasts expressing a low level of endogenous HSP27 or in fibroblasts expressing a high level of a nonphosphorylatable HSP27, H2O2 did not induce F-actin accumulation, nor did it generate membrane blebbing activity in the presence or absence of PD098059. In contrast, in fibroblasts that expressed wild-type HSP27 to a level similar to that found in endothelial cells, H2O2 induced accumulation of F-actin and caused bleb formation when the ERK pathway was inhibited. Cis-platinum, which activated SAPK2 but induced little ERK activity, also induced membrane blebbing that was dependent on the expression of HSP27. In these cells, membrane blebbing was not followed by caspase activation or DNA fragmentation. We conclude that the HSP27-dependent actin polymerization-generating activity of SAPK2 associated with a misassembly of the focal adhesions is responsible for induction of membrane blebbing by stressing agents.

Actins↗

PubMed1998

Treatment systems guidelines for primary rectal cancer from the 1996 Patterns of Care Study.

PURPOSE: The Patterns of Care Rectal Cancer Committee was formed to develop consensus recommendations for patients with adenocarcinoma of the rectum limited to the pelvis. METHODS AND MATERIALS: The Committee was composed of a multidisciplinary group of oncologists, and clinical scenarios were chosen to address most of the major treatment controversies in the combined modality treatment of rectal cancer. A literature search was then conducted and the major articles were identified. A modified Delphi technique was used to arrive at consensus. Serial surveys were conducted by distributing questionnaires to the Committee members to consolidate expert opinion. Voting was conducted using a scoring system and opinions were unified to the highest degree possible. RESULTS: Consensus voting was performed for 4 clinical scenarios. Acceptability ratings for treatment were grouped into 3 broad categories: not acceptable, acceptable, and most acceptable. Based on the treatment options, a decision tree was developed that reflects the consensus of the committee. CONCLUSION: These options may help guide treatment decisions in rectal cancer.

Adenocarcinoma↗

PubMed1998

Role of the mitogen-activated protein kinases in the expression of the kinin B1 receptors induced by tissue injury.

Several cytokines and LPS regulate the population of the B1 receptors (B1Rs) for kinins; these are responsive to des-Arg9-bradykinin (BK) and Lys-des-Arg9-BK. B1R activation contributes to inflammatory vascular changes and pain. Aortic rings isolated from normal rabbits and incubated in vitro in Krebs physiological medium were used as a model of tissue injury. From a null level of response, these rings exhibit a time- and protein synthesis-dependent increase in the maximal contractile response to des-Arg9-BK. Exposure to exogenous IL-1beta or epidermal growth factor (EGF) considerably increases the process of sensitization to the kinins. Freshly isolated control aortic rings showed high mitogen-activated protein (MAP) kinase activities (persistent activation of p38, but less prolonged for extracellular signal-regulated kinase and c-Jun-N-terminal kinase/stress-activated protein kinase pathways) relatively to the basal activities found in various types of cultured cells. IL-1beta or EGF further increased the activities of the extracellular signal-regulated kinase and c-Jun-N-terminal kinase/stress-activated protein kinase MAP kinases. The inhibitor of the p38 MAP kinase, SB 203580 (10 microM), massively (approximately 75%) and selectively inhibited the spontaneous sensitization to des-Arg9-BK over 6 h. SB 203580 also significantly reduced the development of the response to des-Arg9-BK as stimulated by IL-1 or EGF. Both spontaneous and IL-1beta-stimulated up-regulation of responsiveness to des-Arg9-BK were significantly inhibited by the MAP kinase extracellular signal-regulated kinase kinase 1 inhibitor PD 98059 (approximately 40%). The protein kinase inhibitors failed to inhibit protein synthesis and to acutely inhibit the contractile effect of des-Arg9-BK, suggesting that they do not influence B1 receptor transduction mechanisms. In cultured aortic smooth muscle cells stimulated with EGF, MAP kinase activation preceded B1R mRNA induction. Protein kinase inhibitors reveal the role of cell injury-controlled MAP kinase pathways, and singularly of the p38 pathway, in the induction of B1R.

Animals↗

PubMed1998

Practical considerations of outpatient infusion therapy in the HIV arena.

In conclusion, OPAT is a cost-effective, quality-controlled alternative setting for treating patients with HIV. The program provides a desirable situation for the patient, physician, and nurse. Continuity of care provided by the health care team in the physician's office is a unique situation that can meet the treatment modalities necessary to care for the HIV patient with dignity and pride. In short, OPAT offers an attractive alternative to long-term hospitalization for a variety of HIV-related infections. Such therapy is rapidly becoming a standard of treatment that provides both cost savings and efficacious medical care to patients with HIV-related complications.

AIDS-Related Opportunistic Infections↗

PubMed1998

Expression of heat shock proteins in mouse skin during wound healing.

Wound healing conditions generate a stressful environment for the cells involved in the regeneration process and are therefore postulated to influence the expression of heat shock proteins (Hsps). We have examined the expression of four Hsps (Hsp27, Hsp60, Hsp70 and Hsp90) and a keratin (keratin 6) by immunohistochemistry during cutaneous wound repair from Day 1 to Day 21 after wounding in the mouse. Hsps were constitutively expressed in normal mouse epidermis and their patterns of expression were modified during the healing process. The changes were not directly linked to the time course of the healing process but rather were dependent on the location of cells in the regenerating epidermis. In the thickened epidermis, Hsp60 was induced in basal and low suprabasal cells, Hsp70 showed a reduced expression, and Hsp90 and Hsp27 preserved a suprabasal pattern with an induction in basal and low suprabasal cells. All Hsps had a uniform pattern of expression in the migrating epithelial tongue. These observations suggest that the expression of Hsps in the neoepidermis is related to the proliferation, the migration, and the differentiation states of keratinocytes within the wound.

Animals↗

PubMed1998

Radiation therapy for rectosigmoid and rectal cancer: results of the 1992-1994 Patterns of Care process survey.

PURPOSE: To determine the US national practice standards for patients with adenocarcinoma of the rectum treated in radiation oncology facilities. MATERIALS AND METHODS: A national survey of 57 institutions identified 507 eligible patients who received radiation therapy as a component of their treatment for rectal cancer. A stratified two-stage cluster sampling with simple random sampling at each stage for each stratum was used and on-site surveys were performed. RESULTS: Of the 507 patients, 378 (75%) received postoperative therapy, 110 (22%) received preoperative therapy, 17 (2%) received both preoperative and postoperative therapy, and less than 0.5% received intraoperative radiation alone. To more accurately assess the utilization of modern radiation techniques as well as recommendations of the National Cancer Institute (NCI)-sponsored, randomized, postoperative, adjuvant combined modality therapy rectal cancer trials into current practice, the analysis was limited to the 243 (48%) patients with tumor, node, and metastasis staging system classification T3 and/or N1-2M0 disease who underwent conventional surgery with negative margins. Although only 7% were treated on a clinical trial, 90% received chemotherapy for a median of 21 weeks. Most were treated with modern radiation treatment techniques. In contrast, techniques to identify and help exclude the small bowel from the radiation field were not routinely used. CONCLUSION: Despite the fact that only 7% of patients with T3 and/or N1-2M0 disease were treated on a clinical trial, such trials appear to have resulted in a positive influence on the standard of practice within the oncology community. Although there are still some deficiencies, the majority of these patients received combined modality therapy and were treated with modern radiation therapy techniques.

Adenocarcinoma↗