Journal articles: 'Pulmonary adenocarcinoma, immunohistochemistry, molecular biology'

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Picot, Etienne, Robin Jouan, Emma Bach, Gregory Murcier, and Florent Borgnat. "Oral metastasis of pulmonary adenocarcinoma: diagnosis and treatment." Journal of Oral Medicine and Oral Surgery 25, no. 1 (2019): 9. http://dx.doi.org/10.1051/mbcb/2018026.

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Introduction: Oral metastases are rare and represent 1% oro-facial neoplasms. The lung is the most common primary site for oral metastatic tumors. The diagnosis is based on histological analysis. Oral metastases have been associated with poor prognosis and is no longer a proven treatment. It was found in a 58-year old man diagnosed with lung cancer with a voluminous mandibular tumefaction following dental avulsion. The panoramic X-ray showed an area of osteolysis compared to the extraction site. The histological and immunohistochemistry of the lesion showed a positivity of the marker CK7 and a negativity of TTF1, in favor of a lung origin. The biomolecular analysis revealed a mutation on the BRAF gene confirming the metastasis primitive origin. Treatment by surgical resection was performed palliatively. Comments: The diagnosis of an oral metastasis remains difficult and is based on the histological analysis and finding immune markers. Molecular biology is sometimes required for theranostics. Treatment options include surgical resection, radiotherapy, and/or chemotherapy. They are sometimes limited to preserve the quality of life. The prognosis of patients with oral metastases is very poor. Conclusion: Oral metastases are rare, and the diagnosis remains difficult.

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Guo, Fei, Xueyan Li, Guodong Yao, Guangchun Zeng, and Lijuan Yu. "Correlation between 18F-FDG maximum standardized uptake value with CD147 expression in lung adenocarcinomas: a retrospective study." PeerJ 7 (September 9, 2019): e7635. http://dx.doi.org/10.7717/peerj.7635.

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Background The pro-tumoral action of the cluster of differentiation 147 (CD147), which is associated with the chemotherapy resistance of lung adenocarcinoma, is partly due to accelerated tumor cell glycolysis. 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) metabolic parameters included maximal standardized uptake value (SUVmax), mean standardized uptake value (SUVmean), metabolic tumor volume (MTV), and total lesion glycolysis (TLG), which are non-invasive markers of the glucose metabolism of tumor cells in vivo. This study aimed to clarify the correlation between PET metabolic parameters and CD147 expression, and to evaluate the prognostic value of CD147 expression in resectable lung adenocarcinoma patients. Methods A total of 89 lung adenocarcinoma chemotherapy-naive patients who underwent 18F-fluorodeoxyglucose positron emission tomography and computerized tomography scan before pulmonary surgery were retrospectively analyzed. The PET metabolic parameters were calculated by 18F-FDG PET imaging, and CD147 expression was analyzed by immunohistochemistry. SUVmax, SUVmean, MTV, and TLG compared for their performance in predicting the expression of CD147 were illustrated with statistical analysis. All patients were then followed-up for survival analysis. Results The SUVmax was significantly correlated with the CD147 expression and was the primary predictor for the CD147 expression of lung adenocarcinoma. A cut-off value of the SUVmax, 9.77 allowed 85.1% sensitivity and 64.3% specificity for predicting the CD147 positive lung adenocarcinoma. CD147 expression was correlated with tumor differentiation and metastasis. Univariate survival analysis showed that CD147 expression was significantly associated with a shorter overall survival (OS) time. Multivariate analysis revealed that CD147 was an independent prognostic factor of lung adenocarcinoma patients. Conclusion The SUVmax of a primary tumor measured with 18F-FDG PET may be a simple and non-invasive marker for predicting CD147 expression in lung adenocarcinoma. CD147 is an independent prognostic factor related to OS of postoperative lung adenocarcinoma patients.

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Chernyaev, A. L., M. V. Samsonova, A. V. Averyanov, M. A. Makarova, and K. Yu Mikhaylichenko. "Anatomic pathology and computed tomography of diffuse cystic lung diseases." CLINICAL AND EXPERIMENTAL MORPHOLOGY 10, S4 (2021): 23–33. http://dx.doi.org/10.31088/cem2021.10.s4.23-33.

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Introduction. Cystic lung diseases are rare (orphan) diseases. Lung cysts are an important X-ray and morphological sign that contributes to the correct diagnosis. The aim of the researchwas to describe histologic features and computed tomography findings in patients with pulmonary Langerhans cell histiocytosis (PLCH), lymphangioleiomyomatosis (LAM), primary malignant lung tumors, and endometriosis of the lung. Materials and methods. We evaluated video-assisted surgical lung biopsies from 139 patients, with 86 patients having LAM, 47 having PLCH, and in threes having primary peripheral lung adenocarcinoma and endometriosis of the lung. The average age of patients with LAM was 41±10 years, LCG – 32±11 years, lung adenocarcinoma – 62±3.5 years, and endometriosis of the lung – 32±4.1 years. All patients had undergone high-resolution computed tomography of the lungs (HRCT) before the biopsy was obtained. We performed histological and immunohistochemical examinations of lung tissue specimens. Antibodies to CD1a, SMA, HMB-45, CD207 (langerin), CD10, receptors to progesterone, and estrogen were used in the study. Results. We described HRCT, histological, and immunohistochemical features of cystic lung diseases, including characteristics of the walls of cystic cavities in patients with PLCH, LAM, primary malignant lung tumors, and endometriosis of the lung. Conclusion. The variety of causes of lung cysts required a differential diagnosis, considering the patients’ ages, HRCT data indicating the localization of the pathological process, histology, and immunohistochemistry if necessary. Keywords: сystic lung diseases, computed tomography, pathological anatomy, Langerhans cell histiocytosis, lymphangioleiomyomatosis, malignant tumors, endometriosis

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Jriri, S., M. Ben Majdouba, S. Ben Jemaa, A. Feki, R. Akrout, M. Ezzeddine, M. H. Kallel, H. Fourati, and S. Baklouti. "AB1032 CONTRIBUTION OF BONE BIOPSY DURING REVELATORY BONE METASTASES." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1808.3–1808. http://dx.doi.org/10.1136/annrheumdis-2020-eular.6285.

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Background:Bone metastases (BM) are tumor cells that originate in a primary malignant tumor and are localized remotely in bone tissue. They more or less faithfully reproduce the morphological and biological characteristics of the primary tumor. Histological analysisis essential to confirm the diagnosis of BM and to identify the primary tumor if possible and sometimes to help in the selection of treatment.Objectives:The aim of this work is to study the contribution of bone biopsy during revealing BM in diagnostic strategy and therapeutic decision.Methods:We retrospectively studied the files of 105 patients hospitalized in a Rheumatology department of for BM revealing from January 2000 until December 2015. For each patient we collected epidemioclinical and anatomopathological data to arrive at the diagnosis of primary neoplasm and histological type.Results:The patients were divided into 86 men (81.9%) and 19 women (18.1%) with a sex ratio (M / F) of 4.52. The average age of our patients was 64.91 ± 13.29 years. Pain was the most frequent reason for consultation found in 97.1%. This pain was either of bone site (61.9%) or of radicular topography (41.9%). Bone swelling or a pathological fracture revealed BM in 4.8% and 8.6% of the cases, respectively. The onset of neurological damage was noted in 13.3% of the cases.Histologically, the bone biopsy performed in 64 patients made it possible to specify the histological type (carcinoma, adenocarcinoma) in 64% of the cases and to lead to primary cancer in 57.8%. A non-radio-guided percutaneous bone biopsy was performed in 44 patients (68.75%) including 41 osteo-medullary biopsy in iliac crest (BOM) and 3 in the sternum, a bone biopsy directed under scanner in 16 cases (25%) and a surgical bone biopsy in 4 cases.The BOM was positive in 21 cases (51.2%) showing a poorly or moderately differentiated adenocarcinoma or carcinoma. It allowed referral to a primitive in 20 cases: a prostatic origin in 11 cases, a pulmonary origin in 5 cases, a digestive origin in 2 cases, a mammary origin in one case and a neuroblastoma in one case.Conclusion:Thanks to improved sampling and immunohistochemistry techniques, the precise histological type and location of the primary tumor could be identified, there by improving the quality of care for patients with increased life expectancy.Disclosure of Interests:None declared

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Carey, Francis A. "Pulmonary adenocarcinoma: classification and molecular biology." Journal of Pathology 184, no. 3 (March 1998): 229–30. http://dx.doi.org/10.1002/(sici)1096-9896(199803)184:3<229::aid-path18>3.0.co;2-0.

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Marci, Valerio, Marco Volante, Susanna Cappia, Luisella Righi, Corrado Novello, Giorgio V. Scagliotti, Elisabeth Brambilla, and Mauro Papotti. "Basaloid adenocarcinoma. A new variant of pulmonary adenocarcinoma." Virchows Archiv 451, no. 3 (July 6, 2007): 729–36. http://dx.doi.org/10.1007/s00428-007-0458-8.

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Melocchi, Laura, Michele Mondoni, Umberto Malapelle, and Giulio Rossi. "Langerhans Cell Histiocytosis-Associated Pulmonary Adenocarcinoma: A Word of Caution during Molecular Determinations." Journal of Molecular Pathology 3, no. 4 (November 3, 2022): 286–92. http://dx.doi.org/10.3390/jmp3040024.

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Background: Smoking habit is a common cause of pulmonary Langerhans cell histiocytosis (PLCH) and lung cancer and both diseases may coexist in the lung and share genetic alterations, such as V600E BRAF mutations. We collected a small series of three cases of PLCH-associated lung adenocarcinoma in order to evaluate the molecular setup in both components and underline the critical role of careful tissue selection for predictive molecular driver testing. Methods: Three cases of PLCH-associated adenocarcinoma were collected from consultation files. Clinical data from referring physicians and clinical data were obtained. The surgical biopsies were tested by immunohistochemistry and molecular analysis after separate dissection of adenocarcinoma cells and Langerhans histiocytes. Results: There were three active smoking men with a median age at diagnosis of 60.6 years. PLCH was disclosed at imaging during work-up for suspected lung cancer. Molecular analysis revealed KRAS (G12C and G13C) mutations in two cases and V600E BRAF mutation in one case of PLCH. Immunostaining with the V600E BRAF mutation specific primary antibody VE1 correctly recognized BRAF-mutated LCH. One case was wild-type in both diseases. Two similar cases were found in the literature, one of which showed a discrepant KRAS (G12D) mutation in adenocarcinoma and a V600E BRAF mutation in LCH; Conclusions: This case series of PLCH-associated adenocarcinoma underline the possibility to disclose identical genetic alterations in co-existing benign and malignant pathologies, then potentially creating erroneous interpretation of molecular analysis leading to inadequate therapeutic options in case of incorrect diagnostic recognition and inappropriate selection of both components through microdissection.

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Kreus, Mervi, Siri Lehtonen, Sini Skarp, and Riitta Kaarteenaho. "Extracellular matrix proteins produced by stromal cells in idiopathic pulmonary fibrosis and lung adenocarcinoma." PLOS ONE 16, no. 4 (April 27, 2021): e0250109. http://dx.doi.org/10.1371/journal.pone.0250109.

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Idiopathic pulmonary fibrosis (IPF) and lung cancer share common risk factors, epigenetic and genetic alterations, the activation of similar signaling pathways and poor survival. The aim of this study was to examine the gene expression profiles of stromal cells from patients with IPF and lung adenocarcinoma (ADC) as well as from normal lung. The gene expression levels of cultured stromal cells derived from non-smoking patients with ADC from the tumor (n = 4) and the corresponding normal lung (n = 4) as well as from patients with IPF (n = 4) were investigated with Affymetrix microarrays. The expression of collagen type IV alpha 1 chain, periostin as well as matrix metalloproteinase-1 and -3 in stromal cells and lung tissues were examined with quantitative real-time reverse transcriptase polymerase chain reaction and immunohistochemistry, respectively. Twenty genes were similarly up- or down-regulated in IPF and ADC compared to control, while most of the altered genes in IPF and ADC were differently expressed, including several extracellular matrix genes. Collagen type IV alpha 1 chain as well as matrix metalloproteinases-1 and -3 were differentially expressed in IPF compared to ADC. Periostin was up-regulated in both IPF and ADC in comparison to control. All studied factors were localized by immunohistochemistry in stromal cells within fibroblast foci in IPF and stroma of ADC. Despite the similarities found in gene expressions of IPF and ADC, several differences were also detected, suggesting that the molecular changes occurring in these two lung illnesses are somewhat different.

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Todisco, Annalisa, Valeria Internò, Luigia Stefania Stucci, Carmela Ostuni, Domenica Lovero, Stella D’Oronzo, Fabio Mele, Loren Duda, Raffaele Palmirotta, and Franco Silvestris. "Cutaneous metastasis as a primary presentation of a pulmonary enteric adenocarcinoma." International Journal of Biological Markers 34, no. 4 (September 26, 2019): 421–26. http://dx.doi.org/10.1177/1724600819877190.

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Background: Primary pulmonary enteric adenocarcinoma (PEAC) is a rare non-small cell lung cancer subtype sharing morphologic and immunohistochemical features with colorectal adenocarcinoma. Given the frequency of lung metastases in colorectal cancer, the differential diagnosis of PEAC according to routine morphological and immunohistochemical findings may be difficult. Genome sequence by next-generation sequencing has recently introduced new perspectives to better define the diagnosis and tumor sensitivity to treatments, while the rarity of this subtype of cancer still limits the current knowledge of its molecular features and provides no information to address patients to tailored therapies. Methods: We diagnosed a rare case of subcutaneous metastasis as a first symptom of a PEAC. Formalin-fixed paraffin-embedded samples of the primary tumor and subcutaneous metastases were examined by immunohistochemistry, and subsequently by targeted next-generation sequencing analysis. Results: Morphological and immunohistochemical findings suggested a rare case of metastatic pulmonary adenocarcinoma with enteric aspects. Next-generation sequencing analysis performed on both the primary tumor sample and the cutaneous lesion identified two pathogenic variants on CDKN2A and KRAS in both of them. However, the metastasis showed two additional pathogenic mutations located in SMAD4 and FLT3 genes. Conclusions: We describe for the first time an extensive molecular analysis on a rare case of PEAC with an unusual cutaneous metastasis. Our observation suggests that a specific pattern of mutations is harbored in this neoplasm, and that additional molecular studies may provide further information to identify prognostic and hopefully predictive genes of response to treatment.

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Rodriguez, Erika F., Ricardo Pastorello, Lais Osmani, Mark Hopkins, Maria Kryatova, Satomi Kawamoto, and Zahra Maleki. "Ultrasound-Guided Transthoracic Fine-Needle Aspiration: A Reliable Tool in Diagnosis and Molecular Profiling of Lung Masses." Acta Cytologica 64, no. 3 (July 30, 2019): 208–15. http://dx.doi.org/10.1159/000501421.

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Introduction: Pulmonary adenocarcinoma is a major cause of mortality worldwide. The majority of patients present with advanced stage disease, and minimally invasive procedures are desirable for diagnosis and treatment plans. Herein, we report our experience with percutaneous/transthoracic needle aspiration (TT-NA) in the cytologic diagnosis of pulmonary adenocarcinoma. Material and Methods: After institutional review board approval, the cytopathology electronic data system was searched for all consecutive TT-NA of the lung masses from January 2011 to November 2015. Patients’ medical records were reviewed and cytologic materials were evaluated. Results: A total of 151 specimens were identified, with a mean age of 62.8 years; 62.9% of the patients had a prior history of malignancy. Carcinoma/adenocarcinoma was the most common (80%) diagnosis. The targeted lesions were predominantly located in the lung (56.3%, 81/151) and pleural based (27.8%, 42/151). The mean size of the lesions was 3.6 cm. Cytology specimens were adequate in 70.9% of the cases, while 72.8% (110/151) of the cases also had concurrent core biopsy. A malignant diagnosis was rendered in the majority of the cases (64.9%). In 71% of the cases, immunohistochemistry/histochemistry studies were successfully performed. Molecular/genetic studies were requested in 80% of the cases and had adequate material. Complications of the procedure were seen in 9.9% of the patients including pneumothorax (7.9%) and hemoptysis (1.9%). Conclusion: TT-NA is a relatively safe and reliable technique in the assessment of pulmonary lesions.

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Saal, K., Th Papadopoulos, J. Dämmrich, and H. K. Müller-Hermelink. "Cytogenetic studies in two subtypes of pulmonary adenocarcinoma." Cancer Genetics and Cytogenetics 63, no. 2 (October 1992): 180. http://dx.doi.org/10.1016/0165-4608(92)90537-i.

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Archer, Fabienne, Emilie Jacquier, Monique Lyon, Joëlle Chastang, Vincent Cottin, Jean-Francçois Mornex, and Caroline Leroux. "Alveolar Type II Cells Isolated from Pulmonary Adenocarcinoma." American Journal of Respiratory Cell and Molecular Biology 36, no. 5 (May 2007): 534–40. http://dx.doi.org/10.1165/rcmb.2006-0285oc.

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Luo, Jia-Wei, Yan-Hua Guo, Feng-Ying Wu, Xue-Fei Li, Xue-Cheng Sun, Jia-Lu Wang, and Cai-Cun Zhou. "Differences in Immunological Landscape between EGFR-Mutated and Wild-Type Lung Adenocarcinoma." Disease Markers 2021 (August 26, 2021): 1–8. http://dx.doi.org/10.1155/2021/3776854.

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Recent clinical trials of lung adenocarcinoma with immune checkpoint inhibitors revealed that lung adenocarcinoma patients with EGFR mutations have a poor response to immunotherapy. However, the mechanisms have not been addressed. We performed immunohistochemistry analyses of resected lung adenocarcinoma tissues with and without EGFR mutations to investigate and compare the characteristics of the tumor microenvironment (TME). We retrospectively enrolled a total of 323 lung adenocarcinoma patients (164 had EGFR mutations), and their corresponding tissue samples were analyzed by the EGFR mutation test and immunohistochemistry. We selected the markers of the immune checkpoint molecule (PD1, PD-L1, and LAG-3) and immune cell (CD3, CD4, CD8, and Foxp3) as markers of the tumor microenvironment. Our results revealed that patients had a distinct tumor microenvironment between EGFR-mutant and wild-type lung adenocarcinomas; the expression of CD3, CD4, PD-L1, and Foxp3 in EGFR-mutant tumors was significantly higher than that in wild-type tumors, while the expression of LAG3 and PD-1 showed a positive correlation with EGFR-wild-type tumors. In survival analysis, EGFR-wild-type patients had longer disease-free survival (DFS) than EGFR-mutant patients ( P = 0.0065 ). Our research demonstrates significant differences in tumor microenvironment composition between EGFR-mutant and wild-type patients. Our findings provide novel evidence that contributes to understanding the mechanism underlying the poor efficacy of immune checkpoint inhibitors.

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Liu, Ao-ran, Ying-nan Liu, Shi-xuan Shen, Li-rong Yan, Zhi Lv, Han-xi Ding, Ang Wang, Yuan Yuan, and Qian Xu. "Comprehensive Analysis and Validation of Solute Carrier Family 25 (SLC25) and Its Correlation with Immune Infiltration in Pan-Cancer." BioMed Research International 2022 (October 8, 2022): 1–23. http://dx.doi.org/10.1155/2022/4009354.

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As the largest gene family functioning in protein transport among human solute carriers, the SLC25 family (mitochondrial carrier family) can participate in development of cancer. However, a comprehensive exploration for the exactly roles of SLC family remains lacking. In the present study, a total of 15 functional SLC25 family genes were retrieved from all current publications. And multidimensional analyses were systematically performed based on the transcriptome and genome data of SLC25 family from a variety of online databases for their expression, immune cell infiltration, and cancer prognosis. Validation by qPCR and immunohistochemistry were further conducted for the expression of partial SLC25 family members in some tumor tissue. We found that the SLC25 family had strong correlation with immune cells, such as macrophages M2, CD8+ T cell, CD4+ T cell memory activated, and memory resting. Among them, SLC25A6 was most correlated with Macrophage M1 in uveal melanoma ( r = − 0.68 , P = 1.9 e − 0.5 ). Expression of mRNA level showed that SLC25A4 was downregulated in stomach adenocarcinoma and colon adenocarcinoma. SLC25A7 was highly expressed in stomach adenocarcinoma and colon adenocarcinoma. SLC25A23 was decreased in colon adenocarcinoma. qPCR and immunohistochemistry validation results were consistent with our bioinformatics prediction. SLC25A8 was associated with the prognosis of cancer. All these findings suggested that the SLC25 family might affects the immune microenvironment of the cancer and then had the potential to be predictive biomarkers for early diagnosis and prognosis as well as novel targets for individualized treatment of cancer.

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Gordon, Ilyssa O., Stephanie Sitterding, A. Craig Mackinnon, and Aliya N. Husain. "Update in Neoplastic Lung Diseases and Mesothelioma." Archives of Pathology & Laboratory Medicine 133, no. 7 (July 1, 2009): 1106–15. http://dx.doi.org/10.5858/133.7.1106.

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Abstract Context.—Lung cancer is a common disease frequently seen by the surgical pathologist. Although secondary to improvements in screening and radiologic techniques and aggressive resection of small pulmonary nodules, the diagnosis of preneoplastic lesions is increasing in frequency and importance. Consequently, a greater understanding of their role in the development of lung carcinoma is needed for optimal patient care. Two lesions often encountered as small pulmonary nodules are bronchioloalveolar carcinoma and adenocarcinoma, which can be challenging to distinguish. Recently, updates to the TNM classification of non–small cell lung carcinoma have been reported that directly impact prognosis and treatment algorithms. Identification of new molecular targets in pleural mesothelioma and in preneoplastic lesions may lead to improved therapeutic strategies. Objective.—To present recent advances in our understanding of neoplastic lung diseases and mesothelioma and to describe how these advances relate to the current practice of pulmonary pathology. Data Sources.—Published literature from PubMed (National Library of Medicine) and primary material from the authors' institution. Conclusions.—It is important for the surgical pathologist to understand current diagnostic classifications of non– small cell lung cancer and to be aware of the range of preneoplastic lesions, as well as the features useful for distinguishing bronchioloalveolar carcinoma from adenocarcinoma in small pulmonary nodules. Although pleural mesothelioma has distinct features, it can also overlap histologically with adenocarcinoma, and immunohistochemistry can greatly aid in accurate diagnosis. New therapies targeting molecular markers in both non–small cell lung cancer and mesothelioma rely on accurate histopathologic diagnosis of these entities.

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Chess, Patricia R., Liana Toia, and Jacob N. Finkelstein. "Mechanical strain-induced proliferation and signaling in pulmonary epithelial H441 cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 1 (July 1, 2000): L43—L51. http://dx.doi.org/10.1152/ajplung.2000.279.1.l43.

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Pulmonary epithelial cells are exposed to mechanical strain during physiological breathing and mechanical ventilation. Strain regulates pulmonary growth and development and is implicated in volutrauma-induced fibrosis. The mechanisms of strain-induced effects are not well understood. It was hypothesized that mechanical strain induces proliferation of pulmonary epithelial cells and that this is mediated by signals initiated within seconds of strain. To test this hypothesis, human pulmonary adenocarcinoma H441 cells were strained in vitro. Cyclic as well as tonic strain resulted in increased cellular proliferation. Western blot analysis of strained cells demonstrated three newly phosphorylated tyrosine residues within 30 s of strain. Phosphorylation of mitogen-activated protein kinases p42/44 increased, electrophoretic mobility shift assay demonstrated activation of transcription factor activating protein-1, and immunohistochemistry demonstrated increased phosphorylation of c- jun in response to strain. The tyrosine kinase inhibitor genistein blocked the strain-induced proliferation. We conclude that strain induces proliferation in pulmonary epithelial cells and that tyrosine kinase activity is necessary to signal the proliferative response to mechanical strain.

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Kuçuk, Hava, David Laville, Pierre Dal-Col, Violaine Yvorel, Abdulrazzak Sulaiman, Sophie Bayle-Bleuez, Philippe Cosmo, et al. "Value of immunohistochemistry in crushed areas of pulmonary neuroendocrine carcinoma." Experimental and Molecular Pathology 128 (October 2022): 104836. http://dx.doi.org/10.1016/j.yexmp.2022.104836.

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Li, Xiaohui, Hongfang Jin, Geng Bin, Li Wang, Chaoshu Tang, and Junbao Du. "Endogenous Hydrogen Sulfide Regulates Pulmonary Artery Collagen Remodeling in Rats with High Pulmonary Blood Flow." Experimental Biology and Medicine 234, no. 5 (May 2009): 504–12. http://dx.doi.org/10.3181/0807-rm-230.

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The mechanisms responsible for the structural remodeling of pulmonary vasculature induced by increased pulmonary blood flow are not fully understood. This study explores the effect of endogenous hydrogen sulfide (H2S), a novel gasotransmitter, on collagen remodeling of the pulmonary artery in rats with high pulmonary blood flow. Thirty-two Sprague-Dawley rats were randomly divided into sham, shunt, sham+PPG (D,L-propargylglycine, an inhibitor of cystathionine-γ-lyase), and shunt+PPG groups. After 4 weeks of shunting, the relative medial thickness (RMT) of pulmonary arteries and H2S concentration in lung tissues were investigated. Collagen I and collagen III were evaluated by hydroxyproline assay, sirius-red staining, and immunohistochemistry. Pulmonary artery matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and connective tissue growth factor (CTGF) were evaluated by immunohistochemistry. After 4 weeks of aortocaval shunting, resulting in an elevation of lung tissue H2S to 116.4%, rats exhibited collagen remodeling and increased CTGF expression in the pulmonary arteries. Compared with those of the shunt group, lung tissue H2S production was lowered by 23.4%, RMT of the pulmonary artery further increased by 39.5%, pulmonary artery collagen accumulation became obvious, and pulmonary artery CTGF expression elevated ( P < 0.01) in the shunted rats treated with PPG. However, pulmonary artery MMP-13 and TIMP-1 expressions decreased significantly in rats of shunt+PPG group ( P < 0.01). This study suggests that endogenous H2S exerts an important regulatory effect on pulmonary collagen remodeling induced by high pulmonary blood flow.

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Yamada, Mizuho, Kazuyoshi Kuwano, Takashige Maeyama, Naoki Hamada, Michihiro Yoshimi, Yoichi Nakanishi, and Michael Kasper. "Dual-immunohistochemistry provides little evidence for epithelial–mesenchymal transition in pulmonary fibrosis." Histochemistry and Cell Biology 129, no. 4 (January 31, 2008): 453–62. http://dx.doi.org/10.1007/s00418-008-0388-9.

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Zhang, Keshan, Hanjin Kong, Yongjie Liu, Youjun Shang, Bin Wu, and Xiangtao Liu. "Diagnosis and phylogenetic analysis of ovine pulmonary adenocarcinoma in China." Virus Genes 48, no. 1 (October 23, 2013): 64–73. http://dx.doi.org/10.1007/s11262-013-0988-x.

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Sun, M. H. "Neuroendocrine Differentiation in Sporadic CRC and Hereditary Nonpolyosis Colorectal Cancer." Disease Markers 20, no. 4-5 (2004): 283–88. http://dx.doi.org/10.1155/2004/379053.

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Extent neuroendocrine differentiation can be encountered in many human neoplasm derived from different organs and systems using immunohistochemistry and ultrastructural techniques. The tumor cells' behaviors resemble those of neurons and neuroendocrine cells. The presence of neuroendocrine differentiation reputedly appears to be associated with a poorer prognosis than the adenocarcinoma counterparts in sporadic human neoplasm. In this review the neuroendocrine carcinoma and the adenocarcinoma with neuroendocrine differentiation of colon and rectum both in sporadic colorectal carcinoma and the hereditary nonpolyposis colorectal cancer, the relationship of neuroendocrine differentiation and some possible molecular pathways in tumorogenesis of colorectal cancer will be discussed. Possible treatment strategy will also be addressed.

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Guo, Wei, Zhiming Dong, Ming He, Yanli Guo, Jianwen Guo, Zhifeng Chen, Zhibin Yang, and Gang Kuang. "Aberrant Methylation of Thrombospondin-1 and Its Association with Reduced Expression in Gastric Cardia Adenocarcinoma." Journal of Biomedicine and Biotechnology 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/721485.

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Aim. Investigate the promoter methylation of the Thrombospondin-1 (TSP1) gene in gastric cardia adenocarcinoma (GCA).Methods. MSP approach, immunohistochemistry method, and RT-PCR were used respectively to examine the promoter methylation of TSP1, its protein and mRNA expression in tumors and corresponding normal tissues. The expression and concentration of TGF-β1 were examined respectively by immunohistochemistry and ELISA method. The status of T cell immunity was examined by Flow cytometry analysis.Results. TSP1 was methylated in 34/96 (35.4%) tumor specimens, which was significantly higher than that in corresponding normal tissues (P<.001). Protein and mRNA expression of TSP1 in GCA tumor tissues were reduced significantly and were associated with TSP1 methylation. The protein expression of TGF-β1 was significantly higher in tumor tissues (P<.001) and was associated with TNM stage and histological differentiation. The concentration of active and total TGF-β1 did not show significant difference between the GCA patients with hypermethylation of TSP1 and without methylation of TSP1 (P>.05). The function of T cell immunity was significantly different between the GCA patients with hypermethylation of TSP1 and without methylation of TSP1.Conclusions. Epigenetic silencing of TSP1 gene by promoter hypermethylation may play an important role in GCA.

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Hwang, David H., David P. Szeto, Anthony S. Perry, Jacqueline L. Bruce, and Lynette M. Sholl. "Pulmonary Large Cell Carcinoma Lacking Squamous Differentiation Is Clinicopathologically Indistinguishable From Solid-Subtype Adenocarcinoma." Archives of Pathology & Laboratory Medicine 138, no. 5 (June 5, 2013): 626–35. http://dx.doi.org/10.5858/arpa.2013-0179-oa.

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Context Pulmonary large cell carcinoma (LCC) includes tumors not readily diagnosed as adenocarcinoma (ADC) or squamous cell carcinoma on morphologic grounds, without regard to immunophenotype, according to the World Health Organization (WHO). This ambiguous designation may cause confusion over selection of mutation testing and directed therapies. Several groups have proposed the use of immunohistochemistry (IHC) to recategorize LCC as ADC or squamous cell carcinoma; however, it remains unclear if strictly defined LCCs are a clinicopathologically distinct lung tumor subset. Objective —To compare the pathologic, molecular, and clinical features of 2 morphologically similar tumors: solid-subtype ADC and LCC. Design Tumors were included on the basis of solid growth pattern; tumors with squamous or neuroendocrine differentiation were excluded. Solid ADC (n = 42) and LCC (n = 57) were diagnosed by using WHO criteria (5 intracellular mucin droplets in ≥2 high-power fields for solid ADC) and tested for KRAS, EGFR, and ALK alterations. Results —Both solid ADC and LCC groups were dominated by tumors with “undifferentiated”-type morphology and both had a high frequency of thyroid transcription factor 1 expression. KRAS was mutated in 38% of solid ADCs versus 43% of LCCs (P = .62). One ALK-rearranged and 1 EGFR-mutated tumor were detected in the solid ADC and LCC groups, respectively. There were no significant differences in clinical features or outcomes; the prevalence of smoking in both groups was greater than 95%. Conclusions Other than a paucity of intracellular mucin, LCC lacking squamous or neuroendocrine differentiation is indistinguishable from solid-subtype ADC. We propose the reclassification of these tumors as mucin-poor solid adenocarcinomas.

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LI, FENGSHENG, LING GAO, ZHIDONG WANG, BO DONG, TAO YAN, QISHENG JIANG, and XIAOHUA CHEN. "Radiation enhances the invasion abilities of pulmonary adenocarcinoma cells via STAT3." Molecular Medicine Reports 7, no. 6 (April 25, 2013): 1883–88. http://dx.doi.org/10.3892/mmr.2013.1441.

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El-Zammar, Ola A., Shengle Zhang, and Anna-Luise A. Katzenstein. "Comparison of FISH, PCR, and Immunohistochemistry in Assessing EGFR Status in Lung Adenocarcinoma and Correlation With Clinicopathologic Features." Diagnostic Molecular Pathology 18, no. 3 (September 2009): 133–37. http://dx.doi.org/10.1097/pdm.0b013e3181857ea9.

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Wikman, Harriet, Eeva Kettunen, Jouni K. Seppänen, Antti Karjalainen, Jaakko Hollmén, Sisko Anttila, and Sakari Knuutila. "Identification of differentially expressed genes in pulmonary adenocarcinoma by using cDNA array." Oncogene 21, no. 37 (August 2002): 5804–13. http://dx.doi.org/10.1038/sj.onc.1205726.

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Mohamed, Dr Saeed Mahmoud Saeed, Afaf Mosaad Amin, Aisha Mohmmed Osman salih, Sabah Ali Mugahed Al-Qadasi, and Roa Mohmed Mahmoud Sultan. "Comparative Study of Immunohistochemical Expression of ER and PR as Prognostic Markers and Correlation with Clinicopathological Parameters in Human Endometrial Adenocarcinoma." Scholars Journal of Applied Medical Sciences 11, no. 1 (January 13, 2023): 74–86. http://dx.doi.org/10.36347/sjams.2023.v11i01.013.

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In human steroid sensitive tissue, progesterone receptors (PRs) and estrogen receptors (ERs) have been demonstrated at the mRNA and/or protein levels by using molecular biology and immunohistochemistry techniques. Estrogen and progesterone receptors are present both in endometrial hyperplasia and in neoplastic endometrium. The aim of the present work was to compare the expression of ER and PR as prognostic biomarkers in human endometrial adenocarcinoma versus benign tumors and normal endometrial tissues as well as their correlation with different pathological and histological parameters. Immunohistochemical technique was used to examine the expression of ER and PR in normal, benign as well as in endometrial adenocarcinoma. Present results showed higher expression of ER and PR in endometrial adenocarcinoma comparing to normal and benign endometrial tissues.

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Zhang, Liqian, Kathryn A. Wikenheiser, and Jeffrey A. Whitsett. "Limitations of Retrovirus-Mediated HSV-tk Gene Transfer to Pulmonary Adenocarcinoma CellsIn VitroandIn Vivo." Human Gene Therapy 8, no. 5 (March 20, 1997): 563–74. http://dx.doi.org/10.1089/hum.1997.8.5-563.

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Odida, Michael, Belen Lloveras, Nuria Guimera, and Elisabete Weiderpass. "The usefulness of immunohistochemistry in tissue microarrays of Human Papillomavirus negative adenocarcinoma of the uterine cervix." BMC Research Notes 3, no. 1 (2010): 54. http://dx.doi.org/10.1186/1756-0500-3-54.

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Cha, Yoon Jin, Jae Seok Lee, Hye Ryun Kim, Sun Min Lim, Byoung Chul Cho, Chang Young Lee, and Hyo Sup Shim. "Screening of ROS1 Rearrangements in Lung Adenocarcinoma by Immunohistochemistry and Comparison with ALK Rearrangements." PLoS ONE 9, no. 7 (July 24, 2014): e103333. http://dx.doi.org/10.1371/journal.pone.0103333.

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Cao, Lin-Lin, Changzheng Du, Hangqi Liu, Lin Pei, Li Qin, Mei Jia, and Hui Wang. "Lysine-specific demethylase 2A expression is associated with cell growth and cyclin D1 expression in colorectal adenocarcinoma." International Journal of Biological Markers 33, no. 4 (April 23, 2018): 407–14. http://dx.doi.org/10.1177/1724600818764069.

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Objective: Lysine-specific demethylase 2A (KDM2A), a specific H3K36me1/2 demethylase, has been reported to be closely associated with several types of cancer. In this study, we aimed to investigate the expression and function of KDM2A in colorectal adenocarcinoma. Methods: A total of 215 colorectal adenocarcinoma specimens were collected, and then subjected to immunohistochemistry assay to evaluate the expression levels of KDM2A, cyclin D1 and other proteins in colorectal adenocarcinoma tissues. Real-time polymerase chain reaction, Western blot, and other molecular biology methods were used to explore the role of KDM2A in colorectal adenocarcinoma cells. Results: In this study, we report that the expression level of KDM2A is high in colorectal adenocarcinoma tissues, and this high expression promotes the proliferation and colony formation of colorectal adenocarcinoma cells, as demonstrated by KDM2A knockdown experiments. In addition, the expression of KDM2A is closely associated with cyclin D1 expression in colorectal adenocarcinoma tissues and cell lines. Conclusions: Our study reveals a novel role for high-expressed KDM2A in colorectal adenocarcinoma cell growth, and that the expression of KDM2A is associated with that of cyclin D1 in colorectal adenocarcinoma.

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Wang, Xueyan, Huajing Wan, Shuo Yang, Rong Zhou, Yong Liao, Fan Wang, Ximin Chen, and Zhiling Wu. "Elevated Krüppel-like factor 5 expression in spatiotemporal mouse lungs is similar to human congenital cystic adenomatoid malformation of the lungs." Journal of International Medical Research 46, no. 7 (June 13, 2018): 2856–65. http://dx.doi.org/10.1177/0300060518774998.

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Objective The study aimed to investigate the role of high Krüppel-like factor 5 (KLF5) expression on the pathogenesis of congenital cystic adenomatoid malformation of the lungs (CCAML) in mice. Methods A mouse model of high KLF5 expression in the lungs was established. KLF5 expression and the pulmonary lumen diameter were examined by immunohistochemistry to determine a successful model. Basement membrane damage and activity of matrix metalloproteinase-9 (MMP-9) were examined. After an adenovirus carrying KLF5 gene transfection in lung adenocarcinoma (H441) was created, changes in expression and activity of MMP-9 were determined. Results In a mouse model with high KLF5 expression, the pulmonary lumen was markedly enlarged, indicating establishment of CCAML. The basement membrane was degraded, and MMP-9 activity was significantly higher in the model group compared with the control group. Moreover, mice in a cellular model after transfection also showed higher MMP-9 activity than did controls. Conclusion High KLF5 expression may play a pivotal role in the pathogenesis of CCAML, partly through regulating the activity of MMP-9.

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Zhao, Xiaoling, Yaran Li, Xu Yang, Xiaochong Zhang, Jing Xie, Shaoteng Li, Hongzhen Liu, et al. "T Lymphocyte Infiltration in Association with IDO1 Expression in Resected Lung Adenocarcinoma and Normal Adjacent Lung Tissues." BioMed Research International 2022 (February 10, 2022): 1–9. http://dx.doi.org/10.1155/2022/2381018.

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Background. Indoleamine 2,3-dioxygenase 1 (IDO1) catalyzes the first step of tryptophan catabolism in the kynurenine (Kyn) pathway. IDO1 downregulates natural killer cell receptors, and by mechanism, tumor cells escape immune surveillance. Methods. IDO1 protein and mRNA were assessed by immunohistochemistry, immunoblotting, and PCR in the 68 resected lung adenocarcinomas at stages I–III as well as adjacent normal lung tissues. Infiltration of CD3, CD8, and CD4 lymphocytes in the tumor and adjacent normal lung tissues was assessed by immunohistochemical staining. Results. IDO1 protein and mRNA were detected in various stages of lung adenocarcinoma with highest expression at stage III. In contrast, biomarkers of T cell subset, CD3, CD4, and CD8, were highly expressed in the normal lung tissues and stage I adenocarcinoma tissues but significantly reduced in the stage II and III tumor tissues. Conclusions. The current study demonstrated that the higher level of IDO1 expression in the lung adenocarcinoma was, the less infiltration of T lymphocytes was found in the tumors. Findings of this study indicated that IDO1 may contribute to the reduction of T lymphocyte infiltration into the lung adenocarcinoma.

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Castillo, Lesley, Adelaide I. J. Young, Amanda Mawson, Pia Schafranek, Angela M. Steinmann, Danielle Nessem, Ashleigh Parkin, et al. "MCL-1 antagonism enhances the anti-invasive effects of dasatinib in pancreatic adenocarcinoma." Oncogene 39, no. 8 (November 18, 2019): 1821–29. http://dx.doi.org/10.1038/s41388-019-1091-0.

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AbstractPancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest malignancies. It is phenotypically heterogeneous with a highly unstable genome and provides few common therapeutic targets. We found that MCL1, Cofilin1 (CFL1) and SRC mRNA were highly expressed by a wide range of these cancers, suggesting that a strategy of dual MCL-1 and SRC inhibition might be efficacious for many patients. Immunohistochemistry revealed that MCL-1 protein was present at high levels in 94.7% of patients in a cohort of PDACs from Australian Pancreatic Genome Initiative (APGI). High MCL1 and Cofilin1 mRNA expression was also strongly predictive of poor outcome in the TCGA dataset and in the APGI cohort. In culture, MCL-1 antagonism reduced the level of the cytoskeletal remodeling protein Cofilin1 and phosphorylated SRC on the active Y416 residue, suggestive of reduced invasive capacity. The MCL-1 antagonist S63845 synergized with the SRC kinase inhibitor dasatinib to reduce cell viability and invasiveness through 3D-organotypic matrices. In preclinical murine models, this combination reduced primary tumor growth and liver metastasis of pancreatic cancer xenografts. These data suggest that MCL-1 antagonism, while reducing cell viability, may have an additional benefit in increasing the antimetastatic efficacy of dasatinib for the treatment of PDAC.

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She, Yang, Aiyou Mao, Feng Li, and Xiaobin Wei. "P5CR1 protein expression and the effect of gene-silencing on lung adenocarcinoma." PeerJ 7 (May 14, 2019): e6934. http://dx.doi.org/10.7717/peerj.6934.

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The present study aimed to investigate the expression of pyrroline-5-carboxylate reductase 1 (P5CR1) protein in lung adenocarcinoma and paracancerous tissues and to explore the effect of silencing the encoding gene PYCR1 on the proliferation, migration, invasion, and cisplatin sensitivity in lung adenocarcinoma cells, thereby providing a novel therapeutic target for the treatment of the disease. Immunohistochemistry staining was used to detect the P5CR1 protein expression in lung adenocarcinoma and paracancerous tissues, and statistical analysis evaluated the correlation between P5CR1 protein expression and gender, age, tissue part, or pathological grade. The CCK8 assay was performed to detect the proliferation and cisplatin sensitivity, while the effect of PYCR1 on the migration and invasion of lung adenocarcinoma cells was detected by scratch test and transwell chamber assay. The findings demonstrated that the P5CR1 protein expression was significantly elevated in lung adenocarcinoma tissues and correlated with the pathological grade, whereas no significant correlation was established between the protein expression and gender, age, or tissue part. Furthermore, after PYCR1 gene silencing, the proliferation and invasion were significantly suppressed, while the sensitivity to cisplatin was significantly enhanced. Therefore, it can be speculated that the PYCR1 gene affects the biological behavior of lung adenocarcinoma and cisplatin resistance, serving as a potential therapeutic target for lung adenocarcinoma.

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Wang, Li-Li, Li Ding, Peng Zhao, Jing-Jing Guan, Xiao-Bin Ji, Xiao-Li Zhou, Shi-Hong Shao, Yu-Wei Zou, Wei-Wei Fu, and Dong-Liang Lin. "Clinicopathological, Radiological, and Molecular Features of Primary Lung Adenocarcinoma with Morule-Like Components." Disease Markers 2021 (June 12, 2021): 1–10. http://dx.doi.org/10.1155/2021/9186056.

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Background. Morule-like component (MLC) was a rare structure in primary lung adenocarcinoma. We aimed to reveal the clinicopathological, radiological, immunohistochemical, and molecular features of lung adenocarcinoma with MLCs. Methods. Twenty lung adenocarcinomas with MLCs were collected, and computed tomographic and histological documents were reviewed. Immunohistochemistry, targeted next-generation sequencing, and Sanger sequencing for β-catenin gene were performed. Results. There were 9 lepidic adenocarcinomas, 8 acinar adenocarcinomas, 2 papillary adenocarcinomas, and 1 minimally invasive adenocarcinoma. Most patients (16/17) were shown a pure solid nodule, and 1 patient was shown a partly solid nodule on chest computed tomography (CT). Nine cases were accompanied with micropapillary components, and 3 were with cribriform components in which 2 suffered a worse prognosis. No significant association was found between the MCLs and the overall survival of lung adenocarcinoma ( P = 0.109 ). The MLCs were often arranged in whorled or streaming patterns. The cells in MLCs showed syncytial and mild appearance. The MLCs were positive for E-cadherin, CK7, TTF-1, napsin-A, vimentin, and β-catenin (membrane), and negative for CK5/6, p40, p63, Synaptophysin, chromogranin A, and Cdx-2. EGFR mutation, ALK-EML4 fusion, HER2 amplification, and PIK3CA mutation were detected in 16 cases, 2 cases, 1 case, and 1 case, respectively. EGFR mutation was more frequent in adenocarcinomas with MLCs than those without MLCs ( P = 0.040 ). β-catenin gene mutation was not detected in any patients. Conclusions. MLC is often observed in the background of acinar, lepidic, and papillary adenocarcinomas. Lung adenocarcinomas with MLCs tend to appear as a solid mass on CT and harbor EGFR gene mutations. The micropapillary components and cribriform components may cause poor prognosis of lung adenocarcinomas with MLCs. Vimentin is always positive in MLCs, and it is a useful marker for the identification of MLCs.

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Yan, Hongjun, Ye Hua, Tingcui Zhang, and Wen Liu. "Differential Diagnosis of Preinvasive Lesions in Small Pulmonary Nodules by Dual Source Computed Tomography Imaging." Computational and Mathematical Methods in Medicine 2022 (July 4, 2022): 1–7. http://dx.doi.org/10.1155/2022/6255024.

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This study was aimed to explore the differential diagnosis value of preinvasive lesions/minimally invasive adenocarcinoma and invasive adenocarcinoma manifesting as small pulmonary nodules under dual source computed tomography (DSCT) imaging. The patients with nodular manifestations of adenocarcinoma in situ (AIS)/microinfiltrating adenocarcinoma (MIA) were selected as group X, including 14 cases. A total of 31 cases with nodular infiltrating adenocarcinoma were selected as group Y. The enhanced dual-energy image obtained by DSCT dual-energy scan was transferred to the software to obtain the energy image and iodine distribution map. SPSS 18.0 was used for statistical analysis. P < 0.05 was considered statistically significant. All measurements were labeled as mean x ͞ ± S standard deviation. In the CT findings of microinfiltrating adenocarcinoma and infiltrating adenocarcinoma, lobulation sign, burr sign, vacuole sign, and pleural depression sign can help the diagnosis of infiltrating adenocarcinoma. The results showed that lobulation sign, burr sign, vacuole sign, and pleural depression sign could be used as the distinguishing feature of preinvasive lesion/microinvasive adenocarcinoma and invasive adenocarcinoma. Receiver-operating characteristic (ROC) curve analysis showed that the critical value, sensitivity, and specificity of lesion diameter ≥1.4 cm and CT value ≥14.14HU for diagnosis of invasive lung adenocarcinoma were 1.32 and 14.14, 88.4% and 94.4%, and 67.3% and 75.8%, respectively. There were substantial differences in CT values between the two groups under low energy level (42-99 kev) ( P < 0.05 ). DSCT dual-energy imaging can quantitatively identify preinvasive pulmonary nodules with multiple parameters.

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FU, SHIJIE, XUFENG PAN, and WENTAO FANG. "Differential co-expression analysis of a microarray gene expression profiles of pulmonary adenocarcinoma." Molecular Medicine Reports 10, no. 2 (June 5, 2014): 713–18. http://dx.doi.org/10.3892/mmr.2014.2300.

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Egevad, Lars, Brett Delahunt, Hemamali Samaratunga, Toyonori Tsuzuki, Henrik Olsson, Peter Ström, Cecilia Lindskog, et al. "Interobserver reproducibility of perineural invasion of prostatic adenocarcinoma in needle biopsies." Virchows Archiv 478, no. 6 (February 3, 2021): 1109–16. http://dx.doi.org/10.1007/s00428-021-03039-z.

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AbstractNumerous studies have shown a correlation between perineural invasion (PNI) in prostate biopsies and outcome. The reporting of PNI varies widely in the literature. While the interobserver variability of prostate cancer grading has been studied extensively, less is known regarding the reproducibility of PNI. A total of 212 biopsy cores from a population-based screening trial were included in this study (106 with and 106 without PNI according to the original pathology reports). The glass slides were scanned and circulated among four pathologists with a special interest in urological pathology for assessment of PNI. Discordant cases were stained by immunohistochemistry for S-100 protein. PNI was diagnosed by all four observers in 34.0% of cases, while 41.5% were considered to be negative for PNI. In 24.5% of cases, there was a disagreement between the observers. The kappa for interobserver variability was 0.67–0.75 (mean 0.73). The observations from one participant were compared with data from the original reports, and a kappa for intraobserver variability of 0.87 was achieved. Based on immunohistochemical findings among discordant cases, 88.6% had PNI while 11.4% did not. The most common diagnostic pitfall was the presence of bundles of stroma or smooth muscle. It was noted in a few cases that collagenous micronodules could be mistaken for a nerve. The distance between cancer and nerve was another cause of disagreement. Although the results suggest that the reproducibility of PNI may be greater than that of prostate cancer grading, there is still a need for improvement and standardization.

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Song, Yang, Mei-Yue Tang, Wei Chen, Zhe Wang, and Si-Liang Wang. "High JAK2 Protein Expression Predicts a Poor Prognosis in Patients with Resectable Pancreatic Ductal Adenocarcinoma." Disease Markers 2020 (September 22, 2020): 1–8. http://dx.doi.org/10.1155/2020/7656031.

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Background. Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal malignancies worldwide. The JAK/STAT signaling pathway is involved in pancreatic cancer tumorigenesis. However, the prognostic value of JAK2 expression in resectable PDAC is unclear. Method. In this study, we performed a clinicopathological analysis of 62 resectable PDAC cases with a primary focus on survival. JAK2 expression was examined by immunohistochemistry. The relationship between JAK2 expression and clinicopathological features and prognosis was analyzed. Results. Survival curve analyses revealed that high levels of JAK2 expression predict a poor prognosis in resectable PDAC patients. Multivariate analysis confirmed that JAK2 expression can predict the prognosis of PDAC. Conclusions. Assessment of JAK2 protein expression may be a promising method to predict prognosis in patients with resectable PDAC.

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Ito, Akihiko, Morihito Okada, Kazuya Uchino, Tomohiko Wakayama, Yu-ichiro Koma, Shoichi Iseki, Noriaki Tsubota, Yutaka Okita, and Yukihiko Kitamura. "Expression of the TSLC1 Adhesion Molecule in Pulmonary Epithelium and Its Down-Regulation in Pulmonary Adenocarcinoma Other than Bronchioloalveolar Carcinoma." Laboratory Investigation 83, no. 8 (August 2003): 1175–83. http://dx.doi.org/10.1097/01.lab.0000081391.28136.80.

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Visscher, D. W., S. Yadrandji, P. Tabaczka, M. Kraut, and F. H. Sarkar. "Clinicopathologic Analysis of k-ras, p53, and ERBB-2 Gene Alterations in Pulmonary Adenocarcinoma." Diagnostic Molecular Pathology 6, no. 1 (February 1997): 64. http://dx.doi.org/10.1097/00019606-199702000-00010.

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Ohtsuki, Yuji, Masashi Uomoto, Yasuki Hachisuka, Miyuki Kato, Mitsuko Iguchi, Gang-Hong Lee, and Mutsuo Furihata. "A rare case of coexistence of pulmonary adenocarcinoma with Langerhans’ cell histiocytosis." Medical Molecular Morphology 41, no. 3 (September 2008): 175–78. http://dx.doi.org/10.1007/s00795-008-0402-2.

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Zhu, Zhen-Long, Zeng-Ren Zhao, Yu Zhang, Yan-Hong Yang, Zheng-Min Wang, Dong-Sheng Cui, Ming-Wei Wang, et al. "Expression and Significance of FXYD-3 Protein in Gastric Adenocarcinoma." Disease Markers 28, no. 2 (2010): 63–69. http://dx.doi.org/10.1155/2010/868037.

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Objective:FXYD-3, also known as Mat-8, is a member of the FXYD protein family. It was reported that this protein can associate with and modify the transport properties of Na, K-ATPase, and may play an important role in a variety of physiological and pathological states. This protein is up-regulated in certain types of cancers (such as breast, prostate and pancreatic cancer), but down-regulated in other types of cancers (such as colon and kidney cancer). No study has been performed in gastric cancer; therefore, the aim of this project was to investigate FXYD-3 expression and its clinicopathological significance in gastric adenocarcinoma.Patients and methods:FXYD-3 protein was examined by immunohistochemistry in normal gastric mucous (n= 29) and gastric adenocarcinoma (n= 51), obtained from surgical resection of gastric cancer patients.Results:FXYD-3 protein was present in the cytoplasm of normal gastric epithelial cells or gastric cancer cells. The rate of FXYD-3 strong expression was significantly higher in cancer (51% of 51) than in normal mucosa (10% of 29, X2=13.210, p < 0.0001). FXYD-3 expressed strongly in ulcerative/infiltrating types of cancers compared to polypoid/fungating ones (X2= 5.765,p= 0.016). However, FXYD-3 expression was not correlated with patient’s gender, age, tumor size, lymph node status and histological grade (p> 0.05).Conclosion:Up-regulated expression of FXYD-3 protein may be involved in tumourgenesis and invasion of gastric adenocarcinoma.

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Boldrin, Elisa, Maria Assunta Piano, Rita Alfieri, Marcodomenico Mazza, Loretta Vassallo, Antonio Scapinello, Pierluigi Pilati, and Matteo Curtarello. "MSI Analysis in Solid and Liquid Biopsies of Gastroesophageal Adenocarcinoma Patients: A Molecular Approach." International Journal of Molecular Sciences 22, no. 14 (July 6, 2021): 7244. http://dx.doi.org/10.3390/ijms22147244.

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Gastroesophageal adenocarcinoma (GEA) patients with the microsatellite instability (MSI) subtype emerged as optimal candidates for immunotherapy. To date, immunohistochemistry (IHC) is the gold standard for MSI assessment in formalin-fixed paraffin-embedded (FFPE) specimens. However, IHC, although useful for diagnostic typing, cannot be used to analyze cell-free DNA (cfDNA) in liquid biopsy, a tool that could overcome tumor heterogeneity and enable longitudinal monitoring. In order to find an alternative diagnostic method to IHC, we analyzed 86 retrospective GEAs FFPE samples with multiplex PCR. Moreover, to verify the feasibility of MSI detection in liquid biopsy, cfDNA samples of five patients that resulted in having MSI in a prospective cohort of 35 patients were evaluated by multiplex PCR, real-time PCR and droplet digital PCR (ddPCR). Analysis of FFPE showed 100% concordance between multiplex PCR and IHC (Cohen’s Kappa agreement = 1). On the contrary, only ddPCR was able to detect MSI in cfDNAs of T3/T4 GEA patients. In conclusion, data highlight the molecular analysis as an optimal alternative to IHC for the diagnostic typing and suggest that the ddPCR assay can be considered as the most reliable and promising molecular approach to detect MSI in the cfDNA of GEA patients.

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Holm, Jan, Steen Ingemann Hansen, Mimi Høier-Madsen, and Poul-Erik Helkjær. "A Folate Binding Protein in Ascitic Fluid, Serum and Ovarian Tissue of Patients with Ovarian Adenocarcinoma Immunoreacts with Antibodies Against Human Milk Folate Binding Protein." Bioscience Reports 18, no. 2 (April 1, 1998): 49–57. http://dx.doi.org/10.1023/a:1020174325204.

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The presence of a folate binding protein which immunoreacts with antibodies against human milk folate binding protein was demonstrated in ascitic fluids from seven patients with ovarian adenocarcinoma. Ascitic fluids collected from two patients with other malignancies contained non-immunoreactive FBP. Tumor tissue specimens from five patients with ovarian carcinoma contained immunoreactive FBP. By contrast to normal ovaries ovarian carcinoma tissue showed positive immunostaining on immunohistochemistry. Ascitic fluids from two patients with ovarian carcinoma exhibited single distinct bands on SDS-PAGE immunoblotting. The gel filtration profile of ovarian carcinoma tissue homogenate from two patients contained 25 and 100 kDa peaks of radioligand-bound and immunoreactive folate binding protein, while ascitic fluid from one of the patients exhibited a large 100 kDa immunoreactive peak with no radioligand binding activity. The immunoreactive non-functional 100 kDa FBP could represent unprocessed precursor FBP. Future studies are necessary to evaluate whether determination of immunoreactive FBP in ovarian adenocarcinomatosis is of any diagnostic value.

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Nagy, Krisztina, Zsolt Pálfia, and Gábor Réz. "Characterisation of the progression of azaserine-induced rat pancreatic adenocarcinoma by proliferative cell nuclear antigen, basement membrane laminin and trypsinogen immunohistochemistry." Histochemistry and Cell Biology 119, no. 5 (May 2003): 405–13. http://dx.doi.org/10.1007/s00418-003-0520-9.

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Qin, Dahui, Zhong Zheng, Shanxiang Shen, Prudence Smith, and Farah K. Khalil. "Necessity of Microdissecting Different Tumor Components in Pulmonary Tumor Pyrosequencing." BioMed Research International 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/8759267.

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Microdissection is a useful method in tissue sampling prior to molecular testing. Tumor heterogeneity imposes new challenges for tissue sampling. Different microdissecting methods have been employed in face of such challenge. We improved our microdissection method by separately microdissecting the morphologically different tumor components. This improvement helped the pyrosequencing data analysis of two specimens. One specimen consisted of both adenocarcinoma and neuroendocrine components. When both tumor components were sequenced together for KRAS (Kirsten rat sarcoma viral oncogene homolog) gene mutations, the resulting pyrogram indicated that it was not a wild type, suggesting that it contained KRAS mutation. However, the pyrogram did not match any KRAS mutations and a conclusion could not be reached. After microdissecting and testing the adenocarcinoma and neuroendocrine components separately, it was found that the adenocarcinoma was positive for KRAS G12C mutation and the neuroendocrine component was positive for KRAS G12D mutation. The second specimen consisted of two morphologically different tumor nodules. When microdissected and sequenced separately, one nodule was positive for BRAF (v-raf murine sarcoma viral oncogene homolog B1) V600E and the other nodule was wild type at the BRAF codon 600. These examples demonstrate that it is necessary to microdissect morphologically different tumor components for pyrosequencing.

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Youssef, G., W. A. H. Wallace, M. P. Dagleish, C. Cousens, and D. J. Griffiths. "Ovine Pulmonary Adenocarcinoma: A Large Animal Model for Human Lung Cancer." ILAR Journal 56, no. 1 (May 19, 2015): 99–115. http://dx.doi.org/10.1093/ilar/ilv014.

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Stern, Esther, Guy Pines, Li Or Lazar, Gilad W. Vainer, Nitzan Beltran, Omri Dodi, Lika Gamaev, et al. "CDC25C Protein Expression Correlates with Tumor Differentiation and Clinical Outcomes in Lung Adenocarcinoma." Biomedicines 11, no. 2 (January 26, 2023): 362. http://dx.doi.org/10.3390/biomedicines11020362.

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Given that, even after multimodal therapy, early-stage lung cancer (LC) often recurs, novel prognostic markers to help guide therapy are highly desired. The mRNA levels of cell division cycle 25C (CDC25C), a phosphatase that regulates G2/M cell cycle transition in malignant cells, correlate with poor clinical outcomes in lung adenocarcinoma (LUAD). However, whether CDC25C protein detected by immunohistochemistry can serve as a prognostic marker in LUAD is yet unknown. We stained an LC tissue array and a cohort of 61 LUAD tissue sections for CDC25C and searched for correlations between CDC25C staining score and the pathological characteristics of the tumors and the patients’ clinical outcomes. Clinical data were retrieved from our prospectively maintained departmental database. We found that high expression of CDC25C was predominant among poorly differentiated LUAD (p <0.001) and in LUAD > 1cm (p < 0.05). Further, high expression of CDC25C was associated with reduced disease-free survival (p = 0.03, median follow-up of 39 months) and with a trend for reduced overall survival (p = 0.08). Therefore, high expression of CDC25C protein in LUAD is associated with aggressive histological features and with poor outcomes. Larger studies are required to further validate CDC25C as a prognostic marker in LUAD.

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Journal articles on the topic 'Pulmonary adenocarcinoma, immunohistochemistry, molecular biology'

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