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Готові списки джерел за темами / Pulmonary adenocarcinoma / Статті в журналах

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Статті в журналах з теми "Pulmonary adenocarcinoma"

Автор: Grafiati

Опубліковано: 11 березня 2023

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1

Faccin, Mayane, Filipe Cestari, Mônica Matos, João Pedro Cavasin, Anna Zimmermann, Flávio Carvalho, Geane Pagliosa, and Aline Viott. "Pulmonary adenocarcinoma in mare." Brazilian Journal of Veterinary Pathology 11, no. 3 (November 29, 2018): 108–12. http://dx.doi.org/10.24070/bjvp.1983-0246.v11i3p108-112.

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2

Carey, F. A. "Pulmonary adenocarcinoma." Current Diagnostic Pathology 7, no. 3 (September 2001): 187–93. http://dx.doi.org/10.1054/cdip.2001.0070.

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3

Zhao, Wei, Tong-bing Chen, and Hui Wang. "Ikaros is heterogeneously expressed in lung adenocarcinoma and is involved in its progression." Journal of International Medical Research 48, no. 8 (August 2020): 030006052094586. http://dx.doi.org/10.1177/0300060520945860.

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Objective The aim of the present study was to assess the expression of the Ikaros transcription factor (IKZF1) in lung adenocarcinoma and investigate whether expression levels of Ikaros are correlated with lung adenocarcinoma progression. Methods We conducted a retrospective study of 325 cases of resected stage I pulmonary adenocarcinoma, in which histological subtyping was performed according to the 2015 World Health Organization classification. We performed immunohistochemical examinations to assess expression of Ikaros in pulmonary adenocarcinomas and evaluated the correlation between Ikaros expression and cancer progression. Results Immunohistochemical staining was heterogeneous, with the majority of well-differentiated and moderately differentiated lung adenocarcinomas being weakly positive and the majority of the poorly differentiated lung adenocarcinomas exhibiting strong positive staining. Higher expression of Ikaros was associated with tumor recurrence or metastasis. Conclusions Ikaros is heterogeneously expressed in different subtypes of lung adenocarcinoma; higher expression of Ikaros was found to be associated with cancer progression.

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4

Aulakh, Kanwaijit S., Cary D. Chisholm, Daniel A. Smith, and V. O. Speights. "TTF-1 and Napsin A Do Not Differentiate Metastatic Lung Adenocarcinomas From Primary Esophageal Adenocarcinomas: Proposal of a Novel Staining Panel." Archives of Pathology & Laboratory Medicine 137, no. 8 (August 1, 2013): 1094–98. http://dx.doi.org/10.5858/arpa.2012-0305-oa.

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Context.—When adenocarcinomas arise within the esophagus, particularly when located away from the gastroesophageal junction, it may be important in some patients to differentiate between a primary esophageal adenocarcinoma and metastasis from another site. Lung adenocarcinoma is one tumor that has been reported to frequently metastasize to the esophagus. Objectives.—To create a panel of immunohistochemical markers that can reliably distinguish between an esophageal and pulmonary primary; within the gastrointestinal pathology literature, including published articles and textbooks, common lung immunohistochemical markers, such as TTF-1, are assumed to be negative in esophageal adenocarcinoma, yet, to our knowledge, no study has yet investigated the veracity of that presumption. Design.—In this study, 24 cases each of pulmonary and esophageal adenocarcinomas were stained with TTF-1, napsin A, CDX2, 34βE12, N-cadherin, and IMP3 in an attempt to define an optimal panel for differentiation. Esophageal adenocarcinomas occurring at the gastroesophageal junction were excluded in this study because a gastric primary tumor cannot be excluded in those cases. Results.—Surprisingly, TTF-1 and napsin A were positive in similar proportions of tumors from both sites. Those markers that differentiated statistically between esophageal and pulmonary adenocarcinoma were IMP3, CDX2, and N-cadherin. Conclusions.—When differentiating the origin of a tumor as either esophageal or pulmonary, an immunohistochemical panel consisting of IMP3, CDX2, and N-cadherin is superior to either TTF-1 or napsin A.

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5

Usacheva, A. Yu, N. K. Silanteva, A. P. Petrosian, V. S. Usachev, A. V. Sidorin, and S. A. Ivanov. "Pulmonary Mucinous Adenocarcinoma." Journal of radiology and nuclear medicine 102, no. 1 (March 10, 2021): 42–46. http://dx.doi.org/10.20862/0042-4676-2021-102-1-42-46.

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Mucinous adenocarcinoma is a rare malignant tumor of the lung, which is accompanied by extremely scarce and nonspecific symptoms. This leads to an increase in the timing of its recognition, especially in young women. Given the poor prognosis of the pathlogy, the problem of its early diagnosis with histological and immuno-histochemical studies is extremely urgent. The presented clinical case demonstrates the possibilities of computed tomography with intravenous contrast enhancement in a young woman for the diagnosis of mucinous lung adenocarcinoma.

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6

Gong, Jiali, Ying Fan, and Hongyang Lu. "Pulmonary enteric adenocarcinoma." Translational Oncology 14, no. 8 (August 2021): 101123. http://dx.doi.org/10.1016/j.tranon.2021.101123.

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7

Ayub, Adil, Omar Nunez Lopez, Adam Booth, and Ikenna Okereke. "Pulmonary hepatoid adenocarcinoma." Journal of Thoracic and Cardiovascular Surgery 158, no. 4 (October 2019): e139-e140. http://dx.doi.org/10.1016/j.jtcvs.2019.06.023.

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8

Handa, Yoshinori, Yuichiro Kai, Takuhiro Ikeda, Hidenori Mukaida, Hiromi Egawa, and Mayumi Kaneko. "Pulmonary enteric adenocarcinoma." General Thoracic and Cardiovascular Surgery 64, no. 12 (July 3, 2015): 749–51. http://dx.doi.org/10.1007/s11748-015-0569-0.

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9

Moran, Cesar A. "Pulmonary Adenocarcinoma: The Expanding Spectrum of Histologic Variants." Archives of Pathology & Laboratory Medicine 130, no. 7 (July 1, 2006): 958–62. http://dx.doi.org/10.5858/2006-130-958-pateso.

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Abstract Pulmonary adenocarcinoma is one of the most common types of lung cancer. Traditionally, adenocarcinomas have been divided based on their degree of resemblance to their parent tissues into 3 histopathologic types: well, moderately, and poorly differentiated. In the majority of cases, this schema is sufficient to categorize these lung tumors. However, there is a considerable group of tumors in which the histology is not that of the classic gland-forming neoplasm. Thus, although the terminology of adenocarcinoma is applied in such cases, the histopathologic features are different from those of the more conventional variants. The current review addresses these unusual variants and the importance of recognizing and properly categorizing them to avoid unnecessary additional workup or possible misdiagnosis.

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10

Yang, Kun, Huifeng Jiang, and Qiuyao Li. "Primary pulmonary hepatoid adenocarcinoma." Medicine 98, no. 14 (April 2019): e15053. http://dx.doi.org/10.1097/md.0000000000015053.

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11

Weydert, Jamie A., and Michael B. Cohen. "Small Peripheral Pulmonary Adenocarcinoma." Advances in Anatomic Pathology 14, no. 2 (March 2007): 120–28. http://dx.doi.org/10.1097/pap.0b013e3180324519.

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12

Sato, Seijiro, Noriko Motoi, Miyako Hiramatsu, Eisaku Miyauchi, Hiroshi Ono, Yuichi Saito, Hiroko Nagano, et al. "Pulmonary Adenocarcinoma In Situ." American Journal of Surgical Pathology 39, no. 7 (July 2015): 912–21. http://dx.doi.org/10.1097/pas.0000000000000458.

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13

Maeda, R., N. Isowa, H. Onuma, and H. Miura. "Pulmonary intestinal-type adenocarcinoma." Interactive CardioVascular and Thoracic Surgery 7, no. 2 (December 3, 2007): 349–51. http://dx.doi.org/10.1510/icvts.2007.168716.

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14

Lawal, Lukman, Dimitrios Mikroulis, Savvas Eleftheriadis, Panagiotis Karros, Ioannis Bougioukas, and Georgios Bougioukas. "Adenocarcinoma in pulmonary sequestration." Asian Cardiovascular and Thoracic Annals 19, no. 6 (December 2011): 433–35. http://dx.doi.org/10.1177/0218492311419796.

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A 67-year-old male smoker presented with hemoptysis and recurrent pneumonia. Chest computed tomography showed an emphysematous cyst and air-fluid level cavities in the left lower lobe. A left lower lobectomy was performed. The intraoperative finding was intralobar sequestration. Histopathology revealed adenocarcinoma within the sequestrated lobe. Only 8 cases of lung cancer and sequestration have been reported since 1963.

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15

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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16

Karimi, S. S., T. Valyi-Nagy, and M. F. Gonzalez. "TTF-1 Immunoexpression in Primary Rectal Adenocarcinoma with Brain Metastasis." American Journal of Clinical Pathology 156, Supplement_1 (October 1, 2021): S63. http://dx.doi.org/10.1093/ajcp/aqab191.130.

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Abstract Introduction/Objective Rectal adenocarcinoma metastatic to the brain occurs in 0.6%-3% of cases and is associated with advanced-stage disease.TTF-1 expression in rectal adenocarcinoma is an uncommon finding and less than five cases of TTF-1 positive rectal adenocarcinomas have been reported in the literature. Herein, we report a primary rectal adenocarcinoma with biopsy-proven brain metastasis, radiographic evidence of hepatic and pulmonary involvement and unique expression of TTF-1, a marker with high sensitivity for primary pulmonary and thyroid lesions. Furthermore, we discuss the importance of distinguishing this entity from Pulmonary Enteric Adenocarcinoma (PEA). Methods/Case Report A 68-year-old male with hypertension presented with a two-day history of left facial drooping and dysarthria. Brain MRI revealed a 2.9 cm, contrast-enhancing, solitary, right insular mass. A pterional craniotomy and gross total resection of the lesion was performed. Microscopic examination revealed metastatic adenocarcinoma with immunohistochemical expression of CAM 5.2, CDX2, CK20, focal immunoreactivity with Napsin A and TTF-1, and lack of expression of CK7 and Synaptophysin. Radiographic investigation revealed a right posterior rectal lesion and multiple hepatic and bilateral pulmonary nodules. Sigmoidoscopy a fungating, partially circumferential, ulcerated, and friable rectal mass extending 6 cm proximally from the anal verge. Biopsy demonstrated invasive well- differentiated rectal adenocarcinoma with microsatellite stable phenotype, expression of CDX2, CD20, TTF-1 in the lesional cells, and lack of immunostaining with CK7. Given these findings, we favored a diagnosis of invasive well- differentiated rectal adenocarcinoma. Results (if a Case Study enter NA) N/A Conclusion TTF-1 positive rectal adenocarcinoma is an important differential diagnosis for PEA. As the two primary lesions share histomorphological features, clinical history, radiological findings and immunohistochemical staining with CK7 can aid in distinguishing between the two entities. Recent literature suggests a possible role for CDH17 and SATB2 immunostaining to increase the sensitivity and specificity of distinction between the two entities. Lack of expression of CK7 in both the rectal and brain lesion biopsies, radiological finding of numerous bilateral pulmonary infiltrates and one large, solitary rectal mass supports the diagnosis of advanced stage primary rectal adenocarcinoma with distal metastasis in our patient.

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17

Tang, Ping, Sheel K. Vatsia, Saul Teichberg, and Ellen Kahn. "Pulmonary Adenocarcinoma Simulating Malignant Mesothelioma." Archives of Pathology & Laboratory Medicine 125, no. 12 (December 1, 2001): 1598–600. http://dx.doi.org/10.5858/2001-125-1598-pasmm.

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Abstract Adenocarcinoma of the lung with pleural involvement frequently resembles pleural epithelioid mesothelioma clinically as well as macro- and microscopically. Special stains, immunohistochemical studies, and electron microscopic studies are needed to differentiate these 2 tumors. We report a case of pleural involvement by adenocarcinoma, mimicking in the hematoxylin-eosin stain an epithelioid mesothelioma, correctly identified only after immunohistochemical and electron microscopic examinations.

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18

Jung, Young-Eun, Jeong-Won Lee, Byoung-Gie Kim, and Duk-Soo Bae. "Ovarian metastasis from pulmonary adenocarcinoma." Obstetrics & Gynecology Science 56, no. 5 (2013): 341. http://dx.doi.org/10.5468/ogs.2013.56.5.341.

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19

Doctor, AM, S. Sharma, and M. Maheshwari. "Meningeal carcinomatosis from pulmonary adenocarcinoma." Indian Journal of Cancer 45, no. 2 (2008): 74. http://dx.doi.org/10.4103/0019-509x.41780.

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20

Scatena, Cristian, Camilla Eva Comin, Alberto Lapini, and Maria Rosaria Raspollini. "Renal Metastasis From Pulmonary Adenocarcinoma." Applied Immunohistochemistry & Molecular Morphology 21, no. 5 (October 2013): 460–63. http://dx.doi.org/10.1097/pai.0b013e31827101b1.

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21

Scott, Phil, and Chris Cousens. "Ultrasonography of ovine pulmonary adenocarcinoma." In Practice 40, no. 7 (August 31, 2018): 291–300. http://dx.doi.org/10.1136/inp.k3380.

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22

Kawai, Toshiaki, Chikao Torikata, and Minoru Suzuki. "Immunohistochemical Study of Pulmonary Adenocarcinoma." American Journal of Clinical Pathology 89, no. 4 (April 1, 1988): 455–62. http://dx.doi.org/10.1093/ajcp/89.4.455.

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23

McGregor, Douglas H., Christopher J. Papasian, and Pamela D. Pierce. "Aspergilloma Within Cavitating Pulmonary Adenocarcinoma." American Journal of Clinical Pathology 91, no. 1 (January 1, 1989): 100–103. http://dx.doi.org/10.1093/ajcp/91.1.100.

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24

Zander, Dani S. "Primary vs Metastatic Pulmonary Adenocarcinoma." Chest 137, no. 1 (January 2010): 3–4. http://dx.doi.org/10.1378/chest.09-1514.

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25

Mori, Kouki, Katsumi Yoshida, Toshiaki Kikuchi, Tomohiro Sakakibara, Osamu Hisata, Toshihiro Nukiwa, Takuya Moriya, Jun-ichi Tani, Saeko Hoshikawa, and Sadayoshi Ito. "Thyroid Metastasis of Pulmonary Adenocarcinoma." Thyroid 15, no. 2 (February 2005): 176–77. http://dx.doi.org/10.1089/thy.2005.15.176.

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26

Yang, Wei, Xiang Han, and Bei He. "PUB058 Pulmonary Intestinal-Type Adenocarcinoma." Journal of Thoracic Oncology 12, no. 1 (January 2017): S1481—S1482. http://dx.doi.org/10.1016/j.jtho.2016.11.2028.

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27

Lin, Yu-Li, and Yung-Hsiang Hsu. "Wegener's granulomatosis simulates pulmonary adenocarcinoma." Tzu Chi Medical Journal 27, no. 1 (March 2015): 38–40. http://dx.doi.org/10.1016/j.tcmj.2013.12.001.

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28

GONZÁLEZ-ARRIAGADA, WILFREDO ALEJANDRO, LARA MARIA ALENCAR RAMOS, JOSÉ RIBAMAR SABINO-BEZERRA, SÉRGIO ESTEVES, ALAN ROGER DOS SANTOS SILVA, OSLEI PAES DE ALMEIDA, and MÁRCIO AJUDARTE LOPES. "Mandibular Metastasis of Pulmonary Adenocarcinoma." Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology 117, no. 2 (February 2014): e127. http://dx.doi.org/10.1016/j.oooo.2013.10.052.

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29

Kerr, Keith M. "Current issues in pulmonary adenocarcinoma." Diagnostic Histopathology 14, no. 10 (October 2008): 509–18. http://dx.doi.org/10.1016/j.mpdhp.2008.07.010.

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30

Maeda, Ryo, Noritaka Isowa, Hideyuki Onuma, and Hiroshi Miura. "Primary pulmonary mucinous (colloid) adenocarcinoma." General Thoracic and Cardiovascular Surgery 56, no. 4 (April 2008): 195–98. http://dx.doi.org/10.1007/s11748-007-0217-4.

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31

Kim, Gou Young, Jhingook Kim, Tae Sung Kim, and Joungho Han. "Pulmonary Adenocarcinoma with Heterotopic Ossification." Journal of Korean Medical Science 24, no. 3 (2009): 504. http://dx.doi.org/10.3346/jkms.2009.24.3.504.

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32

Zhao, Wei, Hui Wang, Jun Xie, and Bo Tian. "A Clinicopathological Study of Small Lung Adenocarcinoma 1 cm or Less in Size: Emphasis on Histological Subtypes Associated With Lymph Node Metastasis and Recurrence." International Journal of Surgical Pathology 26, no. 1 (August 13, 2017): 4–11. http://dx.doi.org/10.1177/1066896917721649.

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Background. The aim of this study was to assess the prognostic significance of the newly proposed 2015 World Health Organization (WHO) lung adenocarcinoma classification for patients undergoing resection for small (≤1 cm) lung adenocarcinoma. We also investigated whether lobectomy offers prognostic advantage over limited resection for this category of tumors. Methods. A retrospective study of resected pulmonary adenocarcinomas (n = 83) in sizes 1 cm or less was carried out in which comprehensive histologic subtyping was assessed according to the 2015 WHO classification on all consecutive patients who underwent lobectomy or limited resection between 1998 and 2012. Correlation between clinicopathologic parameters and the difference in recurrence between lobectomy and limited resection group was evaluated. Results. Our data show that the proposed 2015 WHO classification identifies histological subsets of small lung adenocarcinomas with significant differences in prognosis. No recurrence was noted for patients with adenocarcinoma in situ and minimally invasive adenocarcinoma. Invasive adenocarcinomas displayed high heterogeneity and the presence of micropapillary component of 5% or greater in adenocarcinomas was significantly related to lymph node involvement and recurrence ( P < .001). Stage IA patients who underwent limited resection had a higher risk of recurrence than did those treated by lobectomy ( P < .05). Conclusions. Application of the 2015 WHO classification identifies patients with adenocarcinoma in situ and minimally invasive adenocarcinoma had excellent prognosis. Micropapillary pattern was associated with high risk of lymph node metastasis and recurrence.

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33

Householder, Jean Marie, Aaron Han, Mitchell I. Edelson, J. Michael Eager, and Norman G. Rosenblum. "Immunohistochemical Confirmation of Pulmonary Papillary Adenocarcinoma Metastatic to Ovaries." Archives of Pathology & Laboratory Medicine 126, no. 9 (September 1, 2002): 1101–3. http://dx.doi.org/10.5858/2002-126-1101-icoppa.

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Abstract Metastatic papillary adenocarcinomas of the ovary are rare compared to primary ovarian papillary serous carcinomas. We report a case of pulmonary papillary adenocarcinoma metastatic to the ovary and show how this tumor can be differentiated immunohistochemically from an ovarian primary. Paraffin blocks of the ovarian tumor were analyzed for carcinoembryonic antigen, CA 125, surfactant, E-cadherin, N-cadherin, and vimentin. These markers are useful in differentiating epithelial tumors of lung versus ovarian origin. The papillary tumor showed expression of carcinoembryonic antigen, surfactant, and E-cadherin, but was negative for CA 125, N-cadherin, and vimentin. These findings support a lung carcinoma metastatic to the ovary.

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34

Adrian, Benjamin, Pascaline Priou, Jacques Cadranel, Gonzague De Chabot, Marie-Christine Rousselet, Thierry Urban, and Frédéric Gagnadoux. "A Case of Pulmonary Adenocarcinoma Presenting with Diffuse Cystic Lesions." Case Reports in Oncology 14, no. 2 (June 17, 2021): 896–900. http://dx.doi.org/10.1159/000515863.

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The main causes of diffuse cystic lung diseases include lymphangioleiomyomatosis, pulmonary Langerhans cell histiocytosis, Birt-Hogg-Dubé syndrome, lymphoid interstitial pneumonia, light chain deposition disease, <i>Pneumocystis jirovecii</i> pneumonia, hypersensitivity pneumonitis, and desquamative interstitial pneumonia. Diffuse cystic lung diseases are rarely caused by a malignant process, which are secondary to metastases from sarcomas and gastrointestinal and gynecologic adenocarcinomas. Here, we present a rare case of invasive pulmonary adenocarcinoma associated with progressive diffusion of cystic lesions, revealed by chronic cough and progressive shortness of breath. It is important for clinicians to be aware of this unusual imaging manifestation of lung cancer, to avoid misdiagnoses.

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35

Behrend, Sabine J., Georgia A. Giotopoulou, Magda Spella, and Georgios T. Stathopoulos. "A role for club cells in smoking-associated lung adenocarcinoma." European Respiratory Review 30, no. 162 (October 20, 2021): 210122. http://dx.doi.org/10.1183/16000617.0122-2021.

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The cellular origin of lung adenocarcinoma remains a focus of intense research efforts. The marked cellular heterogeneity and plasticity of the lungs, as well as the vast variety of molecular subtypes of lung adenocarcinomas perplex the field and account for the extensive variability of experimental results. While most experts would agree on the cellular origins of other types of thoracic tumours, great controversy exists on the tumour-initiating cells of lung adenocarcinoma, since this histologic subtype of lung cancer arises in the distal pulmonary regions where airways and alveoli converge, occurs in smokers as well as nonsmokers, is likely caused by various environmental agents, and is marked by vast molecular and pathologic heterogeneity. Alveolar type II, club, and their variant cells have all been implicated in lung adenocarcinoma progeny and the lineage hierarchies in the distal lung remain disputed. Here we review the relevant literature in this rapidly expanding field, including results from mouse models and human studies. In addition, we present a case for club cells as cells of origin of lung adenocarcinomas that arise in smokers.

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36

Ichihara, Eiki, Masahiro Tabata, Nagio Takigawa, Yumiko Sato, Eisaku Kondo, Motoi Aoe, Katsuyuki Kiura, and Mitsune Tanimoto. "Synchronous Pulmonary MALT Lymphoma and Pulmonary Adenocarcinoma after Metachronous Gastric MALT Lymphoma and Gastric Adenocarcinoma." Journal of Thoracic Oncology 3, no. 11 (November 2008): 1362–63. http://dx.doi.org/10.1097/jto.0b013e31818b1b07.

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37

Itakura, Meiji, Masato Shingoji, and Toshihiko Iizasa. "Expressions of KLF2 and chemokine receptor CCR7 in pulmonary adenocarcinoma." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e21054-e21054. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e21054.

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e21054 Background: Chemokines and chemokine receptors not only have the powerful ability in cancer metastasis and tumorigenesis, but also act as anti-tumorgenic ability. Lung Krueppel-like factor (LKLF, KLF2) is a member of the family of the Krueppel-like factors (KLFs). KLF2 was initially described as a lung-specific transcription factor. KLF2 is reported to regulate some malignant cells. We examined and evaluated the effect of KLF2 on pulmonary adenocarcinoma and the relationship of their mRNA expression with CCR7, EGFR and p53 genetical mutations in pulmonary adenocarcinoma. Methods: 120 patients of stage I to IV with pulmonary adenocarcinoma were included in this retrospective analysis. The expression of CCR7 and KLF2 mRNA expression in surgically resected pulmonary adenocarcinoma specimens were examined and evaluated the relation to prognosis, the effect of EGFR and p53 genetical mutations. Results: High mRNA expression of KLF2 in lung cancer patients indicated significantly good prognosis than the groups of low expressions (p= 0.0066, HR= 2.008, 95% CI of ratio 1.215 to 3.319). The expression of KLF2 mRNA had relationships with CCR7 mRNA expression in pulmonary adenocarcinoma. Moreover the mRNA expression of KLF2 in pulmonary adenocarcinoma specimens was influenced by the mutation of p53 mutation in lung cancer specimens. There was no significant difference within KLF2 mRNA expression quantities of EGFR mutation positive and negative group. Conclusions: We propose KLF2 as clinical good prognostic factors and that KLF2 has strong relation with CCR7 and p53 genetical mutation mRNA expression in pulmonary adenocarcinoma.

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38

Rodríguez Alvarado, Israel, Maite Goicoechea Irigaray, and M. Teresa Gómez Hernández. "Adenocarcinoma pulmonar quístico." Archivos de Bronconeumología 55, no. 3 (March 2019): 157. http://dx.doi.org/10.1016/j.arbres.2018.09.004.

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39

Miyaoka, Masashi, Kazuhito Hatanaka, Masayuki Iwazaki, and Naoya Nakamura. "CK7/CK20 Double-Negative Pulmonary Enteric Adenocarcinoma With Histopathological Evaluation of Transformation Zone Between Enteric Adenocarcinoma and Conventional Pulmonary Adenocarcinoma." International Journal of Surgical Pathology 26, no. 5 (February 7, 2018): 464–68. http://dx.doi.org/10.1177/1066896918756737.

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We report a rare case of pulmonary enteric adenocarcinoma (PEA) exhibiting a immunohistochemical feature of CK7/CK20 double-negativity by evaluating the transformation zone between PEA and conventional pulmonary adenocarcinoma (CPA). A 75-year-old man was found to have a mass, 40 mm in diameter, in the right lower lobe on chest computed tomography, and underwent right lower lobectomy. Histologically, the tumor was composed of a PEA and CPA component. The dominant PEA component had medium to large complex glands with tall columnar cells with eosinophilic cytoplasm and brush-border. The CPA component comprised small to medium glands with cuboidal cells. Moreover, intermediate glands (INT), which had cuboidal to tall columnar cells, with morphological features between PEA and CPA, was also observed in the transformation area. Immunohistochemically, the PEA component was negative for CK7, CK20, and TTF-1, and positive for CDX2 and SATB2 (weak): the CPA component was negative for CK20, CDX2, and SATB2, and positive for CK7 and TTF-1: the INT were negative for SATB2, with intermingled positive signals for CK7, CK20, TTF-1, and CDX2. The final diagnosis was PEA based on the CPA component and not colorectal carcinoma. To distinguish CK7-negative PEA from metastatic colorectal carcinoma, careful examination for a CPA component is very useful along with clinical information. There are no reports that discuss about process of oncogenesis, de novo sequence or transformation from CPA of PEA. This is the first reported case of CK7/CK20 double-negative PEA, with analysis of the transformation zone between PEA and CPA components.

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Izumo, Takehiro, Shinji Sasada, Christine Chavez, Yuji Matsumoto, and Takaaki Tsuchida. "Radial endobronchial ultrasound images for ground-glass opacity pulmonary lesions." European Respiratory Journal 45, no. 6 (January 8, 2015): 1661–68. http://dx.doi.org/10.1183/09031936.00167914.

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Radial endobronchial ultrasound (R-EBUS) is a useful tool for precise localisation of peripheral pulmonary lesions, but there have been no detailed reports about the use of R-EBUS images for ground-glass opacity (GGO).The R-EBUS images of 116 patients with GGO, who were diagnosed as having adenocarcinoma by R-EBUS with a guide sheath (EBUS-GS), were compared with the respective chest computed tomography findings. In 103 patients, R-EBUS images were correlated with the histological surgical specimens.R-EBUS images of GGO were identified based on the internal structure of the lesion and classified into two groups. Blizzard showed an enlarged, diffuse hyperintense acoustic shadow. Mixed blizzard showed a combination of blizzard and some diffuse heterogeneity with several hyperechoic dots and vessels. All pure GGO lesions (nine out of nine) were blizzard on R-EBUS. For part-solid GGOs, the percentage of mixed blizzard was inversely related to the amount of the GGO component. Histological findings from surgery revealed that all blizzard lesions were on the spectrum of adenocarcinoma in situ to well differentiated adenocarcinoma while majority (33 out of 64) of mixed blizzard lesions were moderately to poorly differentiated adenocarcinoma.R-EBUS types are important to locate GGOs prior to transbronchial sampling with EBUS-GS.

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Kuwata, Taiji, Hidetaka Uramoto, Tomoko So, Takeshi Hanagiri, and Fumihiro Tanaka. "Pulmonary adenocarcinoma with pulmonary actinomycosis: Report of a case." Journal of the Japanese Association for Chest Surgery 26, no. 1 (2012): 060–63. http://dx.doi.org/10.2995/jacsurg.26.060.

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Solajic, Nenad, Jelena Krcedinac, Golub Samardzija, Miljan Milic, and Aleksandra Lovrenski. "Granular cell tumor of the bronchus coexisting with a bronchogenic adenocarcinoma: Case report." Archive of Oncology 19, no. 1-2 (2011): 31–33. http://dx.doi.org/10.2298/aoo1102031s.

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Pulmonary granular cell tumors (GCTs) are uncommon and usually benign and their coexistence with bronchogenic adenocarcinoma is rare. We report the case of 50-year-old woman with GCT located in the left lung hilum, which occurred simultaneously with a primary bronchogenic adenocarcinoma in the same area. Contrast CT scan of the head revealed secondary deposits in the right cerebellum, presumably of adenocarcinomas origin. Bronchoscopy revealed narrowing on the beginning of the left lingular bronchus and infiltration of the medial distal wall of the left main bronchus. Large tumor cells with eosinophilic granular cytoplasm were seen on light microscopic examination. Tumor cells fully occupied submucosa and had small, round nuclei with no signs of pleomorphism. Immunohistochemically, these cells were S-100 positive. In small area, groups of atypical oval-shaped cells of adenocarcinomas origin were noticed. This confirmed the diagnosis of GCT coexisting with adenocarcinoma. After consultation with oncologists, the patient was scheduled for further polychemotherapy and radiation treatment.

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Strickland-Marmol, Leah B., Andras Khoor, Sandra K. Livingston, and Amyn Rojiani. "Utility of Tissue-Specific Transcription Factors Thyroid Transcription Factor 1 and Cdx2 in Determining the Primary Site of Metastatic Adenocarcinomas to the Brain." Archives of Pathology & Laboratory Medicine 131, no. 11 (November 1, 2007): 1686–90. http://dx.doi.org/10.5858/2007-131-1686-uottft.

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AbstractContext.—Brain metastases of adenocarcinoma of unknown primary pose a diagnostic dilemma to the surgical pathologist. Although the most common source in these cases is the lung, determining a primary source is difficult on routinely stained slides. Immunohistochemical stain panels including differential cytokeratins, hormone receptors, and breast-specific proteins are commonly used in these cases. Recently, attention has turned to tissue-specific transcription factors, such as thyroid transcription factor 1 (TTF-1) and Cdx2, in the appraisal of metastatic adenocarcinomas.Objective.—To characterize the previously unpublished immunohistochemical expression of the relatively new tissue-specific transcription factor Cdx2 in metastatic adenocarcinomas to the brain.Design.—We reviewed the surgical pathology files of the H. Lee Moffitt Cancer Center and Research Institute, Tampa, Fla, and retrieved 38 consecutive cases of metastatic adenocarcinoma (22 pulmonary, 10 breast, 6 gastrointestinal [2 esophagus/gastroesophageal junction, 4 colorectal]) to the brain with confirmation of the primary site by chart review and histologic evaluation. Sections were immunohistochemically stained with antibodies to TTF-1, Cdx2, and cytokeratins 7 and 20 by standard methods.Results.—Specificities and positive predictive values for Cdx2 and TTF-1 equaled 100% for metastatic gastrointestinal and pulmonary adenocarcinomas, respectively. The negative predictive value of Cdx2 was also very high at 97%.Conclusions.—Cdx2 is a specific and valuable tool for the surgical pathologist when faced with the common problem of metastatic adenocarcinoma of unknown primary. In conjunction with TTF-1, cytokeratin 7, and cytokeratin 20, Cdx2 can accurately differentiate the most common sources of metastatic adenocarcinoma to the brain.

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Rajdev, Kartikeya, Ujjwal Madan, Sean McMillan, Kyle Wilson, Kurt Fisher, Ashley Hein, Amol Patil, Sabin Bista, Daniel Hershberger, and Brian Boer. "Pulmonary Tumor Embolism and Pulmonary Tumor Thrombotic Microangiopathy Causing Rapidly Progressive Respiratory Failure: A Case Series." Journal of Investigative Medicine High Impact Case Reports 10 (January 2022): 232470962210864. http://dx.doi.org/10.1177/23247096221086453.

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Pulmonary tumor embolism (PTE) and pulmonary tumor thrombotic microangiopathy (PTTM) are rare etiologies for rapidly progressive dyspnea in the setting of undiagnosed metastatic cancer. They occur most frequently in association with adenocarcinomas, with PTE being most frequently associated with hepatocellular carcinoma and PTTM being most commonly reported with gastric adenocarcinoma. Pulmonary tumor embolism and PTTM appear to be a disease spectrum where PTTM represents an advanced form of PTE. Pulmonary tumor embolism and PTTM are mostly identified postmortem during autopsy as the antemortem diagnosis remains a clinical challenge due to the rapidly progressive nature of these rare diseases. We report 2 cases of rapidly progressive respiratory failure leading to death, due to tumoral pulmonary hypertension resulting from PTE and PTTM, diagnosed postmortem. Both of the patients were middle-aged females, nonsmokers, and had a gastrointestinal source of their primary malignancy.

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Zheng, Di, Jiying Wang, and Bing Lu. "A practical decision-making strategy based on clinical triple features for EGFR-TKIs to treat advanced non-small cell lung cancer patients with unknown EGFR mutation status." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e19082-e19082. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e19082.

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e19082 Background: EGFR mutated lung cancers are strongly associated with clinical characteristics of never- smoking history and adenocarcinoma histology type, and tended to develop multiple pulmonary metastases.Whether multiple pulmonary metastatic lung adenocarcinomas with never-smoking history would respond to EGFR-TKIs as those harboring EGFR active mutation remains unclear. Methods: 223 consecutive metastatic non-small cell lung cancer (NSCLC) patients with unknown EGFR status who received EGFR-TKIs as salvage therapy after failure of previous platinum-based chemotherapy in Shanghai Pulmonary hospital between 2009 and 2011 were included to the study. Available CT scans, routinely performed at baseline and one month after the start of EGFR-TKIs therapy, were reviewed independently by two investigators. For the purposes of this study, diffuse pulmonary metastatic nodules were defined as multiple nodules distributed diffusely throughout the whole lung with at least 20 nodules within the unilateral lung field. Paraffin embedded tissues were available for 45 of 223 patients for EGFR gene mutation test. Results: Of 134 never-smokers with lung adenocarcinoma,70 patients responded to EGFR-TKIs with an objective response rate (ORR) of 52.2% (70/134), and the ORR for the 62 patients with diffuse pulmonary metastatic nodules was 79% (49/62). Among the 20 patients with confirmed EGFR mutation (based on the available 45 archived specimen), the ORR was 75% (15/20). The multivariate analyses showed that the presence of diffused multiple pulmonary metastatic nodules, activating EGFR mutation and female are independent predictive factors of the response to EGFR-TKIs. Conclusions: Patient selection based on specific clinical features to recieve EGFR-TKI treatment yield high response rate comparable to that selected by EGFR mutation status. It is practical to consider EGFR-TKI as salvage therapy in non-smoking patients with lung adenocarcinoma characterized by diffuse pulmonary nodules when EGFR mutation testing is a challenge.

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Ali Mohammed Hammamy, Riyadh, Khalid Farooqui, and Wisam Ghadban. "Sclerotic Bone Metastasis in Pulmonary Adenocarcinoma." Case Reports in Medicine 2018 (June 12, 2018): 1–5. http://dx.doi.org/10.1155/2018/1903757.

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Pulmonary adenocarcinoma is one of the major types of lung cancers in which metastasis is very common and it accounts approximately to one-third of all primary pulmonary cancers. Although a minority of patients with lung cancer are asymptomatic, which gets usually detected in routine chest radiography, most of the patients present with some symptoms. Lung cancer metastasis may occur virtually in every organ system. Patients with non-small-cell lung cancer commonly have extrathoracic metastases to the adrenal glands, liver, brain, bones, and lymph nodes at presentation. Approximately one-third of patients with lung cancer will present with symptoms related to extrathoracic spread. Metastasis to the bone is not uncommon in lung cancer; however, osteoblastic bone metastasis is very rare. Here we present a 30-year-old female diagnosed to have pulmonary adenocarcinoma with multiple sclerotic bony lesions in the vertebra.

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Zapata, Mauricio, Cynthia Cohen, and Momin T. Siddiqui. "Immunohistochemical expression of SMAD4, CK19, and CA19-9 in fine needle aspiration samples of pancreatic adenocarcinoma: Utility and potential role." CytoJournal 4 (June 22, 2007): 13. http://dx.doi.org/10.1186/1742-6413-4-13.

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Background Pancreatic adenocarcinoma comprises 85% of all cases of pancreatic malignancies. From a diagnostic standpoint, these tumors are readily diagnosed by fine needle aspiration, with an accuracy of greater than 90%; however it is often difficult to ascertain whether these are primary or metastatic in nature. This study was undertaken to see the usefulness of CK19, CA19-9 and a newly described marker, SMAD4 in confirming the pancreatic origin of these tumors. Briefly, SMAD4 (DPC4) is a tumor-suppressor gene located on chromosome 18q which has been shown to mediate the downstream effects of TGF-β superfamily signaling, resulting in growth inhibition. The loss of SMAD4, which as been reported to occur in 55% of pancreatic ductal adenocarcinomas may lead to up regulation of cell cycle proteins and hence increase cellular proliferation. In addition, SMAD4 has been suggested to possibly have prognostic potential, with the presence of SMAD4, indicating shorter survival after resection. Design Clinical data was reviewed to identify patients with proven, primary pancreatic adenocarcinoma. A total of 25 patients with diagnostic material from fine needle aspiration cell blocks, were retrieved from our files at Emory University Hospital. In addition cell blocks from clinically diagnosed non-pancreatic adenocarcinomas were also selected as controls for this study (10 cases of colonic adenocarcinoma, 10 cases of pulmonary adenocarcinoma, 10 cases of breast ductal carcinoma and 10 cases of ovarian mucinous adenocarcinoma). Formalin fixed, paraffin-embedded sections from these were stained with SMAD4, CK19, and CA19-9, using pressure cooker antigen retrieval, labeled polymer HRP (DAKO), and the DAKO autostainer. Results Immunohistochemical staining was reviewed based on intensity (negative, low-positive, and high-positive) and percentage of cells. In primary pancreatic ductal adenocarcinoma, CK 19 showed diffuse cytoplasmic positivity in 23 of 25 cases, CA 19-9 showed apical cytoplasmic staining in all 25 cases, and SMAD4 showed nuclear staining in 20 of 25 cases. In the control group comprising of non-pancreatic adenocarcinoma SMAD4 was negative (100%) in all 10 cases of colonic and pulmonary adenocarcinoma. However 1 of 10 cases (10%) of breast and ovarian adenocarcinoma did show low positivity nuclear staining. However the expression of CA19-9 and CK19 was more variable in these different non-pancreatic malignancies. Conclusion Pancreatic adenocarcinoma showed positive immunohistochemical staining for SMAD4 in 80%, CK19 in 100% and CA19-9 in 100% of the selected cases. These markers, when used as a panel, may confirm the diagnosis of pancreatic adenocarcinoma in fine needle aspiration samples, and help in differentiating from metastatic adenocarcinoma. This may help in determination of appropriate surgical and chemotherapeutic options.

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Ozbudak, Irem Hicran, Omer Ozbudak, Gokhan Arslan, Abdullah Erdogan, and Gulay Ozbilim. "Metachronous malignant mesothelioma and pulmonary adenocarcinoma." Turkish Journal of Pathology 29, no. 1 (2013): 83. http://dx.doi.org/10.5146/tjpath.2013.01156.

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Uchiyama, Shuhei, Jun Ehara, and Eiji Hiraoka. "Pulmonary Tuberculosis Coexisting with Lung Adenocarcinoma." American Journal of Medicine 134, no. 7 (July 2021): e437-e438. http://dx.doi.org/10.1016/j.amjmed.2020.12.029.

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Weidner, Noel. "Pulmonary Adenocarcinoma with Intestinal-Type Differentiation." Ultrastructural Pathology 16, no. 1-2 (January 1992): 7–10. http://dx.doi.org/10.3109/01913129209074543.

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