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T Nojima

Publications and source records attributed to T Nojima.

At least 19 recordsLinked to original sources

Mobile phone base station-emitted radiation does not induce phosphorylation of Hsp27.

An in vitro study focusing on the effects of low-level radiofrequency (RF) fields from mobile radio base stations employing the International Mobile Telecommunication 2000 (IMT-2000) cellular system was conducted to test the hypothesis that modulated RF fields act to induce phosphorylation and overexpression of heat shock protein hsp27. First, we evaluated the responses of human cells to microwave exposure at a specific absorption rate (SAR) of 80 mW/kg, which corresponds to the limit of the average whole-body SAR for general public exposure defined as a basic restriction in the International Commission on Non-Ionizing Radiation Protection (ICNIRP) guidelines. Second, we investigated whether continuous wave (CW) and Wideband Code Division Multiple Access (W-CDMA) modulated signal RF fields at 2.1425 GHz induced activation or gene expression of hsp27 and other heat shock proteins (hsps). Human glioblastoma A172 cells were exposed to W-CDMA radiation at SARs of 80 and 800 mW/kg for 2-48 h, and CW radiation at 80 mW/kg for 24 h. Human IMR-90 fibroblasts from fetal lungs were exposed to W-CDMA at 80 and 800 mW/kg for 2 or 28 h, and CW at 80 mW/kg for 28 h. Under the RF field exposure conditions described above, no significant differences in the expression levels of phosphorylated hsp27 at serine 82 (hsp27[pS82]) were observed between the test groups exposed to W-CDMA or CW signal and the sham-exposed negative controls, as evaluated immediately after the exposure periods by bead-based multiplex assays. Moreover, no noticeable differences in the gene expression of hsps were observed between the test groups and the negative controls by DNA Chip analysis. Our results confirm that exposure to low-level RF field up to 800 mW/kg does not induce phosphorylation of hsp27 or expression of hsp gene family.

Brain Neoplasms↗

DNA strand breaks are not induced in human cells exposed to 2.1425 GHz band CW and W-CDMA modulated radiofrequency fields allocated to mobile radio base stations.

We conducted a large-scale in vitro study focused on the effects of low level radiofrequency (RF) fields from mobile radio base stations employing the International Mobile Telecommunication 2000 (IMT-2000) cellular system in order to test the hypothesis that modulated RF fields may act as a DNA damaging agent. First, we evaluated the responses of human cells to microwave exposure at a specific absorption rate (SAR) of 80 mW/kg, which corresponds to the limit of the average whole body SAR for general public exposure defined as a basic restriction in the International Commission on Non-Ionizing Radiation Protection (ICNIRP) guidelines. Second, we investigated whether continuous wave (CW) and Wideband Code Division Multiple Access (W-CDMA) modulated signal RF fields at 2.1425 GHz induced different levels of DNA damage. Human glioblastoma A172 cells and normal human IMR-90 fibroblasts from fetal lungs were exposed to mobile communication frequency radiation to investigate whether such exposure produced DNA strand breaks in cell culture. A172 cells were exposed to W-CDMA radiation at SARs of 80, 250, and 800 mW/kg and CW radiation at 80 mW/kg for 2 and 24 h, while IMR-90 cells were exposed to both W-CDMA and CW radiations at a SAR of 80 mW/kg for the same time periods. Under the same RF field exposure conditions, no significant differences in the DNA strand breaks were observed between the test groups exposed to W-CDMA or CW radiation and the sham exposed negative controls, as evaluated immediately after the exposure periods by alkaline comet assays. Our results confirm that low level exposures do not act as a genotoxicant up to a SAR of 800 mW/kg.

Cell Line↗

Phosphorylation and gene expression of p53 are not affected in human cells exposed to 2.1425 GHz band CW or W-CDMA modulated radiation allocated to mobile radio base stations.

A large-scale in vitro study focusing on low-level radiofrequency (RF) fields from mobile radio base stations employing the International Mobile Telecommunication 2000 (IMT-2000) cellular system was conducted to test the hypothesis that modulated RF fields induce apoptosis or other cellular stress response that activate p53 or the p53-signaling pathway. First, we evaluated the response of human cells to microwave exposure at a specific absorption rate (SAR) of 80 mW/kg, which corresponds to the limit of the average whole-body SAR for general public exposure defined as a basic restriction by the International Commission on Non-Ionizing Radiation Protection (ICNIRP) guidelines. Second, we investigated whether continuous wave (CW) and wideband code division multiple access (W-CDMA) modulated signal RF fields at 2.1425 GHz induced apoptosis or any signs of stress. Human glioblastoma A172 cells were exposed to W-CDMA radiation at SARs of 80, 250, and 800 mW/kg, and CW radiation at 80 mW/kg for 24 or 48 h. Human IMR-90 fibroblasts from fetal lungs were exposed to both W-CDMA and CW radiation at a SAR of 80 mW/kg for 28 h. Under the RF field exposure conditions described above, no significant differences in the percentage of apoptotic cells were observed between the test groups exposed to RF signals and the sham-exposed negative controls, as evaluated by the Annexin V affinity assay. No significant differences in expression levels of phosphorylated p53 at serine 15 or total p53 were observed between the test groups and the negative controls by the bead-based multiplex assay. Moreover, microarray hybridization and real-time RT-PCR analysis showed no noticeable differences in gene expression of the subsequent downstream targets of p53 signaling involved in apoptosis between the test groups and the negative controls. Our results confirm that exposure to low-level RF signals up to 800 mW/kg does not induce p53-dependent apoptosis, DNA damage, or other stress response in human cells.

Amino Acid Sequence↗

The melanocyte inducing factor MITF is stably expressed in cell lines from human clear cell sarcoma.

Clear cell sarcoma (CCS) is associated with the EWS/ATF1 oncogene that is created by chromosomal fusion of the Ewings Sarcoma oncogene (EWS) and the cellular transcription factor ATF1. The melanocytic character of CCS suggests that the microphthalmia-associated transcription factor (Mitf), a major inducer of melanocytic differentiation, may be miss-expressed in CCS. Accordingly, we show that the mRNA and protein of the melanocyte-specific isoform of Mitf (Mitf-M) are present in several cultured CCS cell lines (Su-ccs-1, DTC1, Kao, MST-1, MST-2 and MST-3). The above cell lines thus provide a valuable experimental resource for examining the role of Mitf-M in both CCS and melanocyte differentiation. Melanocyte-specific expression of Mitf-M is achieved via an ATF-dependent melanocyte-specific cAMP-response element in the Mitf-M promoter, and expression of Mitf-M in CCS cells suggests that EWS/ATF1 (a potent and promiscuous activator of cAMP-inducible promoters) may activate the Mitf-M promoter. Surprisingly, however, the Mitf-M promoter is not activated by EWS/ATF1 in transient assays employing CCS cells, melanocytes or nonmelanocytic cells. Thus, our results indicate that Mitf-M promoter activation may require an appropriate chromosomal context in CCS cells or alternatively that the Mitf-M promoter is not directly activated by EWS/ATF1.

Blotting, Western↗

Centrosome hyperamplification and chromosomal instability in bladder cancer.

OBJECTIVE: Chromosomal instability (CIN) is a common feature of malignant tumors. Centrosome hyperamplification (CH) occurs frequently in human cancers, and may be a contributing factor in CIN. In this study, we investigated the relationship between CH and CIN in bladder cancer. METHODS: Clinical samples obtained by transurethral resection from 22 patients with bladder cancer were examined (histological grade G1, 5 cases; G2, 6 cases; G3, 11 cases). CH was evaluated by immunohistochemistry using anti-pericentrin antibody. CIN was evaluated by fluorescence in situ hybridization (FISH). FISH probes for pericentromeric regions of chromosomes 3, 7, and 17 were hybridized to touch preparations of nuclei from frozen tissues. We also analyzed the centrosome replication cycle of bladder cancer by laser scanning cytometry (LSC). RESULTS: Of the 22 cases examined, 18 (81.8%) had centrosome hyperamplification: CH 0, 4 cases (18.1%); CH I, 5 cases (22.7%); CH II, 5 cases (22.7%); CH III, 8 cases (36.4%). The grade of CH was directly proportional to the histological grade (p=0.03, chi(2) test). LSC analysis showed that the centrosome replication cycle was well regulated in pathologically low-grade bladder cancer, which did not have chromosomal instability. In contrast, we found marked variability of centrosomes in pathologically high-grade bladder cancer, which had chromosomal instability. CH and CIN were both detected in pathologically high-grade tumors. The grade of CH was directly proportional to the CIN grade (p=0.0079, chi(2) test). CONCLUSION: The results of the present study suggest that CH may be involved in CIN in bladder cancer.

Aged↗

Treatments of hamartoma with neuroendoscopic surgery and stereotactic radiosurgery: a case report.

Hypothalamic hamartoma is a non-neoplastic tumor manifesting as gelastic seizure, precocious puberty, and abnormal behavior. Treatment of it is very complicated due to its location. We report a case of hypothalamic hamartoma treated by neuroendoscopic surgery and stereotactic radiosurgery. A 5-year-old girl presented with violent behavior, precocious puberty, gelastic seizure and atonic seizure. She was diagnosed with hypothalamic hamartoma by CT and magnetic resonance imaging at 11 months of age. Tumor size did not change, but tumor intensity had changed on the MR image at 5 years of age. Magnetic resonance spectroscopy revealed decreased N-acetylaspartate and increased choline and creatine in the tumor. After neuroendoscopic biopsy, she underwent linear accelerator stereotactic radiosurgery. But her symptoms remained unchanged for 6 months. She then underwent partial resection and laser coagulation of the tumor by a neuroendoscopic approach. After the procedure, the frequency of her seizures was remarkably decreased, and her violent behavior improved. The transventricular neuroendoscopic approach to the hypothalamus is less invasive than the radical surgery. Neuroendoscopic surgery can be one of the treatments of choice for hypothalamic hamartoma.

Brain Diseases↗

Cyclic changes of granulocyte colony-stimulating factor (G-CSF) mRNA in the human follicle during the normal menstrual cycle and immunolocalization of G-CSF protein.

BACKGROUND: Ovulation has several similarities with inflammation and is closely connected to the activity of leukocytes and inflammatory cytokines. Since granulocytes are one of the major leukocytes, we focused our attention on the presence and local production of granulocyte colony-stimulating factor (G-CSF) in the human ovary. METHODS: The presence of G-CSF protein in the follicular fluid and perifollicular tissues was examined by Western blot analysis (n = 5) and immunohistochemical staining (n = 10). The relative expression levels of G-CSF mRNA in relation to GAPDH in granulosa, theca and luteal cells during the menstrual cycle were measured by quantitative RT-PCR using TaqMan technology (n = 15). RESULTS: G-CSF protein was detected in all follicular fluid and located mainly in granulosa cells of the follicle and luteal cells. The expression level of G-CSF mRNA in the late follicular phase was 137.6 +/- 18.5, which was approximately 10-fold greater than other phases during the menstrual cycle (P < 0.05). CONCLUSIONS: These results demonstrate that G-CSF is produced in the human follicle shortly before the ovulatory phase and may play an important role in the mechanism of ovulation.

Adult↗

Multicentric occurrence of esophageal cancer after gastrectomy: a preliminary report.

The effect of gastrectomy on the subsequent development of esophageal cancer was investigated, focusing on its multicentric occurrence. We retrospectively evaluated 28 patients who underwent subtotal esophagectomy for intrathoracic esophageal cancer between 1985 and 1999. They were divided into two groups according to whether or not they had previously undergone a gastrectomy: group 1, comprising 7 patients who had undergone gastrectomy and group 2, comprising 21 patients who had not. Clinical profiles of the patients were obtained from the medical records and the whole resected esophagus was histopathologically examined. The interval between gastrectomy and esophagectomy in group 1 was significantly shorter in the patients who had undergone gastrectomy for gastric cancer than in those who had undergone gastrectomy for a peptic ulcer, and also in the patients for whom anastomosis had been performed by Billroth I compared with Billroth II. The patients in group 1 were significantly younger than those in group 2. The multiple occurrence of esophageal cancer was found in 4 of 5 patients (80%) in group 1, and in 2 of 18 patients (11%) in group 2, with significantly higher frequency being seen in group 1. More than two coexisting cancer lesions apart from the primary tumor were detected in all four patients. Histological examination of all the coexisting cancer lesions showed well-differentiated squamous cell carcinoma confined within the superficial mucosal layer. No significant differences were noted in the location of the coexisting lesions between the oral and anal side of the primary tumors. Squamous dysplasia was randomly observed, especially around the cancer lesions. These findings suggest that gastrectomy precipitated subsequent chronic gastroesophageal reflux which in turn induced the development of squamous dysplasia and carcinoma at multiple locations in the esophagus.

Aged↗

A spontaneously ruptured gastric stromal tumor presenting as generalized peritonitis: report of a case.

Among the diverse clinical presentations of gastrointestinal stromal tumor (GIST), spontaneous rupture with peritonitis is extremely rare. We report herein the unusual case of a 75-year-old man found to have a spontaneously ruptured gastric stromal tumor after presenting with generalized peritonitis. The patient was brought to the emergency department of our hospital by ambulance, with generalized severe abdominal pain. On examination, his abdomen was extensively distended with generalized severe rebound tenderness. Abdominal computed tomography scan showed a giant mass arising from the anterior gastric wall with an irregular internal low-density area and a small amount of ascites. An emergency laparotomy revealed a ruptured gastric tumor with dissemination of its necrotic tissue throughout the peritoneal cavity. The tumor was excised together with normal gastric tissue around its base. The tumor, which was 15 x 11 x 4.4cm in size, had a coarse laceration over its well-capsulated smooth serosal surface with massive necrosis and clotted blood inside. Immunohistochemical examination revealed positive reactivity to C-kit protein, which was consistent with the newly introduced diagnostic criteria of GIST. The patient had an uneventful postoperative course and remains well.

Aged↗

A rare case of carcinosarcoma of the maxillary sinus with osteosarcomatous differentiation.

A unique case of carcinosarcoma in the maxillary sinus is reported. A 47-year-old man visited our hospital with complaints of right nasal obstruction and bloody rhinorrhea. Examination revealed a hemorrhagic mass with necrosis in the maxillary sinus that infiltrated the right nasal cavity. Histologically, the tumor was composed of both carcinomatous and sarcomatous elements. Nests of squamous cell carcinoma and adenocarcinoma were scattered in the sarcomatous element with osteosarcomatous differentiation. No distinct demarcation between the two elements was observed and some spindle-shaped cells in the sarcomatous component were immunoreactive to epithelial markers by immunohistochemical staining. Although the histogenesis of carcinosarcoma remains unclear, the histologic pattern of the present case indicates the possibility that a multipotential cell, capable of both epithelial and mesenchymal differentiation, was the origin of the rare tumor.

Carcinosarcoma↗

Granulocytic sarcoma of megakaryoblastic differentiation in the lymph nodes terminating as acute megakaryoblastic leukemia in a case of chronic idiopathic myelofibrosis persisting for 16 years.

A 43-yr-old Japanese woman presented with mild anemia, leukocytosis and splenomegaly in May 1984. Splenomegaly and anemia gradually progressed. Sixteen years later, in October 2000, she developed inguinal lymphadenopathy. Biopsy of the lymph node revealed infiltration of blasts, megakaryocytes, fibroblasts and myeloid cells. Large blasts with basophilic cytoplasm with cytoplasmic projections appeared in the peripheral blood. These blasts were negative in peroxidase stain, positive in acid phosphatase and weakly positive in periodic acid-Schiff stain. Immunohistochemical staining with monoclonal antibodies revealed that these blasts were positive with anti-CD41 (glycoprotein IIb/IIIa) and negative with other monoclonal antibodies. So diagnosis of granulocytic sarcoma in megakaryoblastic transformation from chronic idiopathic myelofibrosis was made. A cytogenetic study revealed that bone marrow cells were 46,XX del(13)(q?) initially and additional abnormalities including der(5,5,11)(q11;q13)ins(5;?)(q11;?) were found when she developed megakaryoblastic transformation. Granulocytic sarcoma of megakaryoblastic transformation from chronic idiopathic myelofibrosis is a rare event. Immunophenotyping with monoclonal antibody for CD41(glycoprotein IIb/IIIa) confirmed the diagnosis.

Cell Differentiation↗

Accuracy of histologic grading of synovial inflammation in temporomandibular joints with internal derangement using Gynther's system.

PURPOSE: The purpose of this study was to evaluate the accuracy of the system by Gynther et al (J Oral Maxillofac Surg 56:1281, 1998) for histologic grading of synovial inflammation in the temporomandibular joint (TMJ) in arthroscopically obtained synovial biopsy specimens. PATIENT AND METHODS: Thirty-three human TMJ synovial biopsy specimens from patients with internal derangement of the TMJ were evaluated using the system of Gynther et al. The results were compared statistically with the intensity of synovitis seen arthroscopically using Spearman ranked correlation coefficient. RESULTS: In 2 of the 3 parameters tested, a statistically significant correlation was found between the histologic findings by the system of Gynther et al and arthroscopic findings using the scale of Murakami et al (J Oral Maxillofac Surg 49:1159, 1991) CONCLUSION: These results suggest that histologic grading of synovial inflammation by the system of Gynther et al has considerable accuracy. However, more investigations are necessary to confirm the results.

Adolescent↗

Immunohistochemical localization of bone morphogenetic protein-2 in the oral and maxillofacial area of the human embryo.

The purpose of this study was to investigate the bone morphogenetic protein-2 (BMP-2) expression in oral and maxillofacial tissue of the human embryo. A human embryo was obtained from a patient with hysterorrhexis. The oral and maxillofacial area of the embryo was analyzed immunohistochemically using specific antibodies to BMP-2. BMP-2 was found mainly localized in developing teeth buds, jaw bone, striated and smooth muscle, spinal cord and nasal tracheal and oesophagal epithelium. However, it was not found in hair follicles. These findings are similar to those of BMP-2 and -4 gene expression in mouse and rat embryos. BMP-2 may be involved in the morphogenesis of oral and maxillofacial tissue in human embryos as well as those of other animals. These results will be of considerable benefit in the restoration and regeneration of the oral and maxillofacial tissue clinically.

Bone Morphogenetic Protein 2↗

Detection of DNA hybridization by use of a lanthanide fluorescent intercalator that specifically binds to double stranded DNA.

Toward development of a DNA microarray system in which neither labeling nor amplification of the nucleic acids from living cell is required, we have developed a new method for the detection and quantification of target DNA hybridized with probe DNA fixed on a solid surface. This method utilizes a fluorescent intercalator: naphthalene diimide derivative carrying two fluorescent tetradentate beta-diketone-Eu3+ chelates. This compound selectively binds to double stranded DNA (dsDNA) fixed on a plastic assay plate. The amount of the compound bound to single stranded DNA (ssDNA) is negligible. The fluorescent intensity of Eu3+ was in proportion to the amount of the fixed DNA, showing that the compound quantitatively binds to dsDNA. Therefore, this method can be used not only to detect dsDNA, but also to measure the amount of DNA on a solid surface.

DNA↗

Cytokine and immunogenetic profiles in Japanese patients with adult Still's disease. Association with chronic articular disease.

OBJECTIVE: To determine cytokines and MHC class II alleles in Japanese patients with adult Still's disease (ASD) and clarify the association between those profiles and chronic articular disease. METHODS: Of 35 patients with ASD (13 men, 22 women, mean age at onset 34.0 yr), 17 (49%) had chronic arthritis (>6 months, chronic articular ASD) and 18 (51%) lacked chronic arthritis (systemic ASD). Cytokines and cytokine receptors in sera were measured by ELISA. Correlations of each cytokine with disease activity or C-reactive protein (CRP) were determined. MHC class II alleles were examined by polymerase chain reaction methods. RESULTS: In chronic articular ASD, female gender was more frequent and liver dysfunction and myalgia were rarer than in systemic ASD. In active disease, the white blood cell count was lower, but total IgG was greater in patients with chronic articular ASD than in those with systemic ASD. Tumour necrosis factor (TNF) alpha, soluble TNF receptor 2 and interleukin (IL)-18 were increased in both types of ASD, even in remission. Soluble IL-2 receptors, IL-4 and IL-18 levels were correlated with disease activity or CRP value only in chronic articular ASD. Interferon gamma and IL-8 remained increased only in chronic articular ASD, even when disease activity, including IL-6 and CRP, was low. DRB1*1501 (DR2) and DRB1*1201 (DR5) alleles were more frequent in chronic articular than in systemic ASD, whereas DQB1*0602 (DQ1) was frequently observed in both types of ASD. CONCLUSION: The present study suggests that ASD with chronic articular disease has distinct clinical, cytokine and immunogenetic profiles.

Adult↗

Modified ultrafiltration removes serum interleukin-8 in adult cardiac surgery.

Cardiopulmonary bypass (CPB) causes an increase in serum cytokine levels and systemic inflamatory responses, which may trigger the onset of various types of postoperative organ failure. In the present study, modified ultrafiltration (MUF) was applied in cases of adult cardiac surgery and an attempt was made to determine whether MUF reduces serum interleukin-8 (IL-8) levels. Nine patients who underwent cardiovascular surgery with CPB and MUF between June 1996 and June 1997 were compared with nine control patients who underwent cardiovascular surgery without MUF in the same period. Modified ultrafiltration was performed, based on a method proposed elsewhere. Serum IL-8 was measured by enzyme immunoassay at the start of CPB, immediately after CPB, immediately after MUF and 3 h after MUF. The mean filtrated volume was 1550.0 +/- 173.2 ml. In the MUF group, haematocrit increased significantly from 21.2 +/- 2.0 to 24.9 +/- 3.3% (p = 0.0008), while systolic blood pressure increased from 97.5 +/- 16.7 to 116.5 +/- 23.9 mmHg (p = 0.0024) after MUF. In contrast, there were no changes in either haematocrit or blood pressure in the control group. In the MUF group, serum IL-8 was reduced from 69.5 +/- 33.5 to 58.9 +/- 32.4 pg/ml after MUF (p = 0.0029), whereas it was not reduced in the control group. The results of the present study suggest that MUF has beneficial effects on postoperative haemodynamics, and can reduce serum IL-8 levels in adult cardiac surgery.

Adult↗

Congenital-infantile fibrosarcoma. A clinicopathologic study of 10 cases and molecular detection of the ETV6-NTRK3 fusion transcripts using paraffin-embedded tissues.

Congenital-infantile fibrosarcoma (CIFS) is a relatively indolent sarcoma that should be distinguished from more aggressive spindle cell sarcomas of childhood. CIFSs have been found to have a novel recurrent reciprocal translocation t(12;15)(p13;q25) resulting in the gene fusion ETV6-NTRK3 (ETS variant gene 6; neurotrophic tyrosine kinase receptor type 3). We studied immunohistochemical expression of NTRK3, and conducted a reverse transcription-polymerase chain reaction (RT-PCR) assay to detect the ETV6-NTRK3 fusion transcripts using archival formalin-fixed paraffin-embedded tissues from 10 CIFSs. Thirty-eight other spindle cell tumors were included as controls. The ETV6-NTRK3 fusion transcripts were identified in 7 (70%) of 10 CIFSs. Nucleotide sequence analysis showed that the fusion occurred between ETV6 exon 5 and NTRK3 exon 13. The 38 control tumors were negative for the fusion transcript. Immunohistochemically, CIFSs consistently expressed NTRK3. But the expression of NTRK3 also was observed in 22 of 38 control tumors. These results show the diagnostic usefulness of RT-PCR methods to detect ETV6-NTRK3 fusion transcripts in archival formalin-fixed paraffin-embedded tissue and the important role of NTRK3 in the development of CIFS, despite its being a protein of little importance in differential diagnosis.

Child↗

[Extraction of RNA from paraffin embedded tissues and analysis of p53 gene expression in colonic cancer].

We examined, immunohistochemically and molecular biologically, p53 gene expression in 10 patients with colonic cancer. RNA was extracted from paraffin embedded normal and colonic cancer tissues by using RNA isolator kit and proteinase K. The most effective time and concentration of proteinase K for RNA extraction was 24 hours and 100 micrograms/ml, respectively. P53 gene expression was analyzed by ABI PRISM 7700 Sequence Detection System(ABI 7700 System, Perkinelmer). Gene expression level in each sample was estimated on the basis of the standard curve of ABI 7700 System. Human G3PDH gene was used as the internal control. Immunohistochemically, the tumor cells in all examined cases showed a strong positivity for anti-p53 gene antibody. In ABI 7700 System, expression of p53 gene in the malignant tissues revealed a high level in only 2 cases that had a clinical stage IV, however, in remaining 8 cases a clinical stage was I to III and expression level of p53 was relatively lower. These results suggest that colonic cancer cells show mutant-p53 gene expression, and a ratio of mutant- to wild-p53 gene may have something to do with a relationship between gene expression and clinical stage.

Adenocarcinoma↗