BACKGROUND Pancreatic cancer with ovarian metastases is rare and easily misdiagnosed.Most patients are first diagnosed with ovarian cancer.We report a rare case of ovarian metastases secondary to pancreatic adenocarci...BACKGROUND Pancreatic cancer with ovarian metastases is rare and easily misdiagnosed.Most patients are first diagnosed with ovarian cancer.We report a rare case of ovarian metastases secondary to pancreatic adenocarcinoma.We also review the literature to analyze the clinical characteristics of,diagnostic methods for,and perioperative management strategies for this rare malignancy.CASE SUMMARY A 48-year-old woman with an abdominal mass presented to our hospital.Computed tomography revealed lesions in the pancreas and lower abdomen.Radiological examination and histological investigation of biopsy specimens revealed either an ovarian metastasis from a pancreatic neoplasm or two primary tumors,with metastasis strongly suspected.The patient simultaneously underwent distal pancreatectomy plus splenectomy by a general surgeon and salpingo-oophorectomy with hysterectomy by a gynecologist.Histological examination of the surgical specimen revealed a pancreatic adenocarcinoma(intermediate differentiation,mucinous)and a metastatic mucinous adenocarcinoma in the ovary.CONCLUSION For this rare tumor,surgical resection is the most effective treatment,and the final diagnosis depends on tumor pathology.展开更多
Background： Thyrotropin-secreting pituitary adenomas （TSHomas） are a rare cause of hyperthyroidism. Somatostatin （SST） analogs work by interacting with somatostatin receptors （SSTRs）. This study aimed to evalua...Background： Thyrotropin-secreting pituitary adenomas （TSHomas） are a rare cause of hyperthyroidism. Somatostatin （SST） analogs work by interacting with somatostatin receptors （SSTRs）. This study aimed to evaluate short-term preoperative octreotide （OCT） use in TSHoma patients and to investigate SSTR2 and SSTR5 expression and observe structural changes in tumor tissue. Methods： We reviewed records and samples from eight TSHoma patients treated between July 2012 and July 2015. We tested immunohistochemically for SSTR2/5 expression and examined TSHoma cells for morphological changes. Signed rank sum test was used to compare the efficacy of short-term preoperative OCT treatment. Results： OCT treatment （median time： 7.9 days, range： 3-16 days; median total dose： 1.8 mg, range： 0.94.2 mg） led to significant decrease in all patients＇ thyroid hormone levels （FT3 [nmol/L]： 8.33 [7.02, 12.29] to 4.67 [3.52, 5.37] [P = 0.008]; FT4 [pmol/L]： 25.36 [21.34, 28.99] to 16.66 [14.88, 21.49] [P = 0.016]; and TSH [gU/ml]： 5.80 [4.37, 6.78] to 0.57 [0.19, 1.24] [P = 0.008]）. All the eight tumor specimens expressed high SSTR2 protein levels; 5/8 expressed high SSTRS, but 3/8 that expressed low SSTR5 presented a significantly higher TS H suppression rate （P = 0.036）. Electron microscopy showed subcellular level impairments, including clumped nuclear chromatin and reduced cytoplasmic volume. Golgi complexes were observed in the OCT-treated TSHoma specimens. Conclusions： OCT can control hormone levels and damage the ultrastructure of tumor cells and organelles. Short-term response to OCT may be related to SSTR5 expression. Preoperative SST analog treatment for TSHoma could be considered as a combination therapy.展开更多
Background:Hyperbaric oxygen treatment(HBOT)has been demonstrated to influence the keloid recurrence rate after surgery and to relieve keloid symptoms and other pathological processes in keloids.To explore the mechani...Background:Hyperbaric oxygen treatment(HBOT)has been demonstrated to influence the keloid recurrence rate after surgery and to relieve keloid symptoms and other pathological processes in keloids.To explore the mechanism of the effect of HBOT on keloids,tumor immune gene expression and immune cell infiltration were studied in this work.Methods:From February 2021 to April 2021,HBOT was carried out on keloid patients four times before surgery.Keloid tissue samples were collected and divided into an HBOT group(keloid with HBOT before surgery[HK]group,n=6)and a non-HBOT group(K group,n=6).Tumor gene expression was analyzed with an Oncomine Immune Response Research Assay kit.Data were mined with R package.The differentially expressed genes between the groups were compared.Hub genes between the groups were determined and verified with Quantitative Real-time PCR.Immune cell infiltration was analyzed based on CIBERSORT deconvolution algorithm analysis of gene expression and verified with immunohistochemistry(IHC).Results:Inflammatory cell infiltration was reduced in the HK group.There were 178 upregulated genes and 217 downregulated genes.Ten hub genes were identified,including Integrin Subunit Alpha M(ITGAM),interleukin(IL)-4,IL-6,IL-2,Protein Tyrosine Phosphatase Receptor Type C(PTPRC),CD86,transforming growth factor(TGF),CD80,CTLA4,and IL-10.CD80,ITGAM,IL-4,and PTPRC with significantly downregulated expression were identified.IL-10 and IL-2 were upregulated in the HK group but without a significant difference.Infiltration differences of CD8 lymphocyte T cells,CD4 lymphocyte T-activated memory cells,and dendritic resting cells were identified with gene CIBERSORT deconvolution algorithm analysis.Infiltration levels of CD4 lymphocyte T cell in the HK group were significantly higher than those of the K group in IHC verification.Conclusion:HBOT affected tumor gene expression and immune cell infiltration in keloids.CD4 lymphocyte T cell,especially activated memory CD4+T,might be the key regulatory immune cell,and its related gene expression needs further study.展开更多
Tumor-induced osteomalacia(TIO)is a rare paraneoplastic syndrome caused by excessive fibroblast growth factor 23(FGF23)production by a tumor,which often arises from a mesenchymal origin.[1-3]Most clinical symptoms of ...Tumor-induced osteomalacia(TIO)is a rare paraneoplastic syndrome caused by excessive fibroblast growth factor 23(FGF23)production by a tumor,which often arises from a mesenchymal origin.[1-3]Most clinical symptoms of TIO are the consequences of prolonged FGF23-mediated hypophosphatemia as muscle weakness,bone pain,impaired mobility,and fractures.[4]Clinical diagnosis and management of TIO are challenging because knowledge about this condition is still restricted to a few specialized centers,leading to delay in diagnosis and appropriate treatment.The scope of the present consensus is to provide up-to-date guidance on the assessment and treatment of TIO.展开更多
Relative to the length and surface area of the gastrointestinal tract, malignant tumors of the small intestine are remarkably rare, with a global incidence of〈1 per 100,000 population. Among the forty different histo...Relative to the length and surface area of the gastrointestinal tract, malignant tumors of the small intestine are remarkably rare, with a global incidence of〈1 per 100,000 population. Among the forty different histological subtypes of small intestinal cancers, primary squamous cell carcinoma （SCC） is exceptionally rare with only occasional case reports in literature. The present study reported a case of primary SCC of the small intestine and reviewed all cases reported in English literature to provide a systematic overview of this rare disease.展开更多
Although DNA 5-hydroxymethylcytosine(5 hmC)is recognized as an important epigenetic mark in cancer,its precise role in lymph node metastasis remains elusive.In this study,we investigated how 5 hmC associates with lymp...Although DNA 5-hydroxymethylcytosine(5 hmC)is recognized as an important epigenetic mark in cancer,its precise role in lymph node metastasis remains elusive.In this study,we investigated how 5 hmC associates with lymph node metastasis in breast cancer.Accompanying with high expression of TET1 and TET2 proteins,large numbers of genes in the metastasis-positive primary tumors exhibit higher 5 hmC levels than those in the metastasis-negative primary tumors.In contrast,the TET protein expression and DNA 5 hmC decrease significantly within the metastatic lesions in the lymph nodes compared to those in their matched primary tumors.Through genomewide analysis of 8 sets of primary tumors,we identified 100 high-confidence metastasis-associated5 hmC signatures,and it is found that increased levels of DNA 5 hmC and gene expression of MAP7 D1 associate with high risk of lymph node metastasis.Furthermore,we demonstrate that MAP7 D1,regulated by TET1,promotes tumor growth and metastasis.In conclusion,the dynamic5 hmC profiles during lymph node metastasis suggest a link between DNA 5 hmC and lymph node metastasis.Meanwhile,the role of MAP7 D1 in breast cancer progression suggests that the metastasis-associated 5 hmC signatures are potential biomarkers to predict the risk for lymph node metastasis,which may serve as diagnostic and therapeutic targets for metastatic breast cancer.展开更多
基金Supported by CAMS Innovation Fund for Medical Sciences,No.2016-I2M-3-005Beijing Municipal Science&Technology Commission,No.Z171100001017017018.
文摘BACKGROUND Pancreatic cancer with ovarian metastases is rare and easily misdiagnosed.Most patients are first diagnosed with ovarian cancer.We report a rare case of ovarian metastases secondary to pancreatic adenocarcinoma.We also review the literature to analyze the clinical characteristics of,diagnostic methods for,and perioperative management strategies for this rare malignancy.CASE SUMMARY A 48-year-old woman with an abdominal mass presented to our hospital.Computed tomography revealed lesions in the pancreas and lower abdomen.Radiological examination and histological investigation of biopsy specimens revealed either an ovarian metastasis from a pancreatic neoplasm or two primary tumors,with metastasis strongly suspected.The patient simultaneously underwent distal pancreatectomy plus splenectomy by a general surgeon and salpingo-oophorectomy with hysterectomy by a gynecologist.Histological examination of the surgical specimen revealed a pancreatic adenocarcinoma(intermediate differentiation,mucinous)and a metastatic mucinous adenocarcinoma in the ovary.CONCLUSION For this rare tumor,surgical resection is the most effective treatment,and the final diagnosis depends on tumor pathology.
文摘Background： Thyrotropin-secreting pituitary adenomas （TSHomas） are a rare cause of hyperthyroidism. Somatostatin （SST） analogs work by interacting with somatostatin receptors （SSTRs）. This study aimed to evaluate short-term preoperative octreotide （OCT） use in TSHoma patients and to investigate SSTR2 and SSTR5 expression and observe structural changes in tumor tissue. Methods： We reviewed records and samples from eight TSHoma patients treated between July 2012 and July 2015. We tested immunohistochemically for SSTR2/5 expression and examined TSHoma cells for morphological changes. Signed rank sum test was used to compare the efficacy of short-term preoperative OCT treatment. Results： OCT treatment （median time： 7.9 days, range： 3-16 days; median total dose： 1.8 mg, range： 0.94.2 mg） led to significant decrease in all patients＇ thyroid hormone levels （FT3 [nmol/L]： 8.33 [7.02, 12.29] to 4.67 [3.52, 5.37] [P = 0.008]; FT4 [pmol/L]： 25.36 [21.34, 28.99] to 16.66 [14.88, 21.49] [P = 0.016]; and TSH [gU/ml]： 5.80 [4.37, 6.78] to 0.57 [0.19, 1.24] [P = 0.008]）. All the eight tumor specimens expressed high SSTR2 protein levels; 5/8 expressed high SSTRS, but 3/8 that expressed low SSTR5 presented a significantly higher TS H suppression rate （P = 0.036）. Electron microscopy showed subcellular level impairments, including clumped nuclear chromatin and reduced cytoplasmic volume. Golgi complexes were observed in the OCT-treated TSHoma specimens. Conclusions： OCT can control hormone levels and damage the ultrastructure of tumor cells and organelles. Short-term response to OCT may be related to SSTR5 expression. Preoperative SST analog treatment for TSHoma could be considered as a combination therapy.
基金supported by a grant from the National Natural Science Foundation of China(No.81871538).
文摘Background:Hyperbaric oxygen treatment(HBOT)has been demonstrated to influence the keloid recurrence rate after surgery and to relieve keloid symptoms and other pathological processes in keloids.To explore the mechanism of the effect of HBOT on keloids,tumor immune gene expression and immune cell infiltration were studied in this work.Methods:From February 2021 to April 2021,HBOT was carried out on keloid patients four times before surgery.Keloid tissue samples were collected and divided into an HBOT group(keloid with HBOT before surgery[HK]group,n=6)and a non-HBOT group(K group,n=6).Tumor gene expression was analyzed with an Oncomine Immune Response Research Assay kit.Data were mined with R package.The differentially expressed genes between the groups were compared.Hub genes between the groups were determined and verified with Quantitative Real-time PCR.Immune cell infiltration was analyzed based on CIBERSORT deconvolution algorithm analysis of gene expression and verified with immunohistochemistry(IHC).Results:Inflammatory cell infiltration was reduced in the HK group.There were 178 upregulated genes and 217 downregulated genes.Ten hub genes were identified,including Integrin Subunit Alpha M(ITGAM),interleukin(IL)-4,IL-6,IL-2,Protein Tyrosine Phosphatase Receptor Type C(PTPRC),CD86,transforming growth factor(TGF),CD80,CTLA4,and IL-10.CD80,ITGAM,IL-4,and PTPRC with significantly downregulated expression were identified.IL-10 and IL-2 were upregulated in the HK group but without a significant difference.Infiltration differences of CD8 lymphocyte T cells,CD4 lymphocyte T-activated memory cells,and dendritic resting cells were identified with gene CIBERSORT deconvolution algorithm analysis.Infiltration levels of CD4 lymphocyte T cell in the HK group were significantly higher than those of the K group in IHC verification.Conclusion:HBOT affected tumor gene expression and immune cell infiltration in keloids.CD4 lymphocyte T cell,especially activated memory CD4+T,might be the key regulatory immune cell,and its related gene expression needs further study.
基金by grants from the CAMS Innovation Fund for Medical Science(No.2016-I2M-3-003)the National Natural Science Foundation of China(No.81970757 and No.81670714).
文摘Tumor-induced osteomalacia(TIO)is a rare paraneoplastic syndrome caused by excessive fibroblast growth factor 23(FGF23)production by a tumor,which often arises from a mesenchymal origin.[1-3]Most clinical symptoms of TIO are the consequences of prolonged FGF23-mediated hypophosphatemia as muscle weakness,bone pain,impaired mobility,and fractures.[4]Clinical diagnosis and management of TIO are challenging because knowledge about this condition is still restricted to a few specialized centers,leading to delay in diagnosis and appropriate treatment.The scope of the present consensus is to provide up-to-date guidance on the assessment and treatment of TIO.
文摘Relative to the length and surface area of the gastrointestinal tract, malignant tumors of the small intestine are remarkably rare, with a global incidence of〈1 per 100,000 population. Among the forty different histological subtypes of small intestinal cancers, primary squamous cell carcinoma （SCC） is exceptionally rare with only occasional case reports in literature. The present study reported a case of primary SCC of the small intestine and reviewed all cases reported in English literature to provide a systematic overview of this rare disease.
基金supported by the Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences(Grant Nos.2016ZX310182-2 and 2016ZX310176-6 to NY)the Medical Epigenetics Research Center,Chinese Academy of Medical Sciences(Grant Nos.2017PT31035 and 2018PT31035 to NY)the National Natural Science Foundation of China(Grant No.81773163 to JF)
文摘Although DNA 5-hydroxymethylcytosine(5 hmC)is recognized as an important epigenetic mark in cancer,its precise role in lymph node metastasis remains elusive.In this study,we investigated how 5 hmC associates with lymph node metastasis in breast cancer.Accompanying with high expression of TET1 and TET2 proteins,large numbers of genes in the metastasis-positive primary tumors exhibit higher 5 hmC levels than those in the metastasis-negative primary tumors.In contrast,the TET protein expression and DNA 5 hmC decrease significantly within the metastatic lesions in the lymph nodes compared to those in their matched primary tumors.Through genomewide analysis of 8 sets of primary tumors,we identified 100 high-confidence metastasis-associated5 hmC signatures,and it is found that increased levels of DNA 5 hmC and gene expression of MAP7 D1 associate with high risk of lymph node metastasis.Furthermore,we demonstrate that MAP7 D1,regulated by TET1,promotes tumor growth and metastasis.In conclusion,the dynamic5 hmC profiles during lymph node metastasis suggest a link between DNA 5 hmC and lymph node metastasis.Meanwhile,the role of MAP7 D1 in breast cancer progression suggests that the metastasis-associated 5 hmC signatures are potential biomarkers to predict the risk for lymph node metastasis,which may serve as diagnostic and therapeutic targets for metastatic breast cancer.
