Changes In Adenocarcinoma Research Articles

Comparing the Expressions of Vitamin D Receptor, Cell Proliferation, and Apoptosis in Gastric Mucosa With Gastritis, Intestinal Metaplasia, or Adenocarcinoma Change

Background: This study aimed to compare the expression of vitamin D receptor (VDR), cell proliferation, and apoptosis in the gastric mucosa of patients with gastritis, intestinal metaplasia (IM), and adenocarcinoma using artificial intelligence.Material and Methods: This study retrospectively enrolled patients at the Keelung Chang Gung Memorial Hospital from November of 2016 to June, 2017, who were diagnosed with gastric adenocarcinoma. The inclusion criteria were patients' pathologic reports that revealed all compartments of Helicobacter pylori infection, gastritis, IM, and adenocarcinoma simultaneously in the same gastric sample. Tissue slides after immunohistochemical (IHC) staining were transformed into digital images using a scanner and counted using computer software (QuPath and ImageJ). IHC staining included PA1-711 antibody for VDR, Ki67 antigen for proliferation, and M30 antibody CK18 for apoptosis.Results: Twenty-nine patients were included in the IHC staining quantitative analysis. The mean age was 69.1 ± 11.3 y/o. Most (25/29, 86.2%) patients had poorly differentiated adenocarcinoma. The mean expression of Ki67 and CK18 increased progressively from gastritis and IM to adenocarcinoma, with statistical significance (P < 0.05). VDR expression did not correlate with Ki67 or CK18 expression. Survival time was only correlated with tumor stage (correlation coefficient = −0.423, P value < 0.05), but was not correlated with the expression of VDR, Ki67, and CK18.Conclusion: Ki67 expression and CK18 expression progressively increased in the areas of gastritis, IM, and adenocarcinoma. No correlation between VDR expression and Ki67 or CK18 expression was found in this study.

A Rare Case Of Retroperitoneal Enterogenous Cyst With Adenocarcinoma

Retroperitoneal Enterogenous cysts are uncommon and changes of Adenocarcinoma within it is a rare presentation with only 3 cases of such cysts being reported till date. We present the 4th case of such a presentation.

Mitochondrial Changes in Adenocarcinoma of the Pancreas

The aim of our study was to analyse the mitochondrial ultrastructure in primary ductal adenocarcinomas of the pancreas and to compare it with normal pancreatic cells. 52 samples of adenocarcinoma of the pancreas obtained by surgical resection or by endosonographic biopsy were examined. Compared to normal mitochondrial ultrastructure in non-tumorous cells, the mitochondria in cancer cells had a dense matrix and condensed configuration or with lucent-swelling matrix associated with disarrangement and distortion of cristae and partial or total cristolysis. Functionally, these structural alterations presume the presence of hypoxia-tolerant and hypoxia-sensitive cancer cells.

Adenocarcinoma of the Lung Progressing to Multiple Cystic Lesions in a 29-Year-Old Man

Cystic lesions or progressive cystic changes in adenocarcinoma of the lung have rarely been reported. We report a case of lung adenocarcinoma that progressed from ground-glass opacities (GGOs) and consolidations or nodules to extensive cystic lesions during 12 months in a young adult patient. A 29-year-old male was initially diagnosed with primary lung adenocarcinoma by transbronchial lung biopsy of the right lower lobe and lung to lung metastasis in both lungs according to imaging findings. The initial chest computed tomography (CT) scans showed multifocal GGOs, consolidations, and nodules in both lungs. Despite treatment with palliative chemotherapy, the patient's follow-up CT scans showed multiple, cystic changes in both lungs and that the lesions had progressed more extensively. He died of hypoxic respiratory failure one year after his diagnosis.

Clinical specificities of 246 Japanese with prostate anomalies: early bone metastases, aplastic anemia, lymphatic-related lung lesions, primary pleural and lung cancers, and fatty liver with insulin-resistant diabetes, which were related to prostate fusion gene anomalies

A total of 246 Japanese composed of 121 with benign prostatic hyperplasia (BPH) and 125 with prostatic cancer (PCa) were analyzed clinically to explain fusion gene anomalies between erythroblast transformation-specific family transcription factor-related gene (ERG) and transmembrane protease serine 2 (TMPRSS2) on chromosome 21q22. Among the 246 cases, 12 (10%) BPH and 18 (14%) PCa showed prostate-specific antigen (PSA) values of >20 ng/ml. It was shown that PSA was not only secreted from the prostates of BPH and PCa, but also actively from bone metastases, which occurred in the 18 PCa, although PCa bone metastases through lymphatic vessels were shown to be blocked by a cystic abscess formation or skin lipoma derived from lymphatic vessels. Among the 30 cases of >20 ng/ml PSA, lymphatic-related lung lesions were observed in 4 (33%) BPH and 12 (67%) PCa. Except for 1 case with pleural PCa metastasis, pleural, lung, and liver metastases were not observed in the 125 PCa. Instead, primary pleural squamous cell carcinoma was detected in two BPH and one PCa and primary lung adenocarcinoma/lung neuroendocrine cell carcinoma (LNCC) was detected in two BPH and five PCa in which adenocarcinoma changes to LNCC were shown. Besides early PCa bone metastases, hematopoietic normal stem cell suppression was observed in two BPH and two PCa, probably on the basis of periosteal stem cell activation. The correlation between insulin and blood sugar (BS) was examined in 66 BPH and 24 PCa. A negative correlation coefficient of −0.297 was calculated in the nine PCa with abnormal BS. Among 23 PCa and 52 BPH of the 90 cases measured insulin, 10 (43%) PCa and 7 (13%) BPH were diagnosed with diffuse fatty liver. Insulin-resistant diabetes mellitus was observed with a high spike of insulin. High levels of triglyceride and total cholesterol (TC) were well improved by prostatectomy. The TMPRSS2:ERG gene fusions/deletions had caused bone marrow and fat metabolism anomalies and other primary cancers not only in PCa, but also in BPH, which indicated a better prognosis of early prostatectomy.

Before and after GOG 99: Did our practice patterns for treatment of intermediate risk endometrial adenocarcinoma change?

Before and after GOG 99: Did our practice patterns for treatment of intermediate risk endometrial adenocarcinoma change?

Immunohistochemical analysis of selected molecular markers in esophagus precancerous, adenocarcinoma and squamous cell carcinoma in Iranian subjects

Background: The molecular and cellular mechanisms linking chronic inflammation and gastrointestinal malignancy are not known with certainty. Aim: To investigate changes in potential causative factors during progression of esophagus cancer in a population living in high-risk area in Iran. Subjects: Formalin-fixed, paraffin-embedded esophageal specimens ( n = 87) from patients with gastroesophageal reflux disease (GERD), Barrett's metaplasia, adenocarcinoma (ADC) and squamous cells carcinoma (SCC) were collected based on their pathological diagnosis. Methods: Immunohistochemical (IHC) technique was used to study tissue accumulation of P53, P21, cyclooxygenase-2 (COX-2), glutathione S-transferase-P (GST-Pi) and nitrotyrosine (NT) in patients and controls. Results: P53 expression was not detected in esophageal tissues from normal and GERD samples, whereas it was found positive in Barrett's, ADC, and SCC samples. P21 positive sample was relatively higher in ADC patients as compared to that in SCC (ADC: 52.6%; SCC: 25%). GST-Pi expression was equally accumulated in all the samples. NT was predominantly expressed in ADC (72.7%). COX-2 expression was significantly higher in Barrett's (60.0%) and ADC (66.6%) as compared to that in GERD, SCC and normal. These data were further confirmed by detecting the scores of immunostainings in all the positive samples. Conclusion: The pathological changes in ADC and SCC samples which were associated with increasing frequency of NT and COX-2 provides further evidence for involvement of these inflammatory factors in progression of esophagus cancer.

Small Bowel Cancer in the United States

Previous studies have shown an increasing incidence of small bowel tumors in the United States. Our objective was to assess this increase by examining changes in histology-specific incidence, treatment, and survival. Patients with small bowel malignancies were identified from the National Cancer Data Base (NCDB, 1985-2005) and the Surveillance Epidemiology and End Results (SEER, 1973-2004) database. Age-adjusted incidence rates were calculated using SEER. Treatment and survival trends over time were examined using the National Cancer Data Base. Regression models were developed to assess survival over time. Sixty-seven thousand eight hundred forty-three patients were identified with small bowel malignancies: 37.4% carcinoid, 36.9% adenocarcinomas, 8.4% stromal tumors, and 17.3% lymphomas. From 1973 to 2004, the incidence of carcinoid tumors increased more than 4-fold (2.1 to 9.3 per million), whereas changes in adenocarcinomas, stromal tumors, and lymphomas were less pronounced. From 1985 to 2005, utilization of surgery increased significantly for carcinoid tumors from 78.8% to 87.4% (P < 0.0001). Adjuvant chemotherapy utilization for adenocarcinoma increased from 8.1% in 1985 to 23.8% in 2005 (P < 0.0001). Treatment over time was generally unchanged for lymphoma and stromal tumors. Five-year survival after resection remained unchanged over time for all histologic subtypes even after adjusting for changes in patient demographics, tumor characteristics, and treatment approaches. The overall incidence of small intestine malignancies has increased considerably, primarily because of carcinoid tumors which are now the most common small bowel cancer. With current treatments, survival has remained relatively unchanged over the last 20 years. Novel therapeutic options need to be investigated.

Nasosinus Adenocarcinomas—A Molecular Point of View

Little is known about the genetic changes in adenocarcinoma (ACN). Because of its histopathological resemblance, most studies so far have focused on a limited number of genes and proteins often selected for their frequent involvement in colorectal adenocarcinoma. Indeed, mutations in K-ras and p53 occur also in ACN, although with lower frequencies. K-ras mutations varied in frequency bteween 0% and 15%. One study reported 50%, about the same as in colorectal adenocarcinoma. Also, H-ras mutations have been detected. Mutations in p53 ranged between 18% and 57%, and 50% of LOH was seen at 17p13, the chromosomal locus of p53. Further attempts to find genetic alterations as described in colorectal carcinoma concerned APC, b-catenin, and various mismatch repair genes and gave negative results. These results indicate that ACN and colorectal carcinoma have different genetic pathways of development and progression. Other investigations focused on genes involved in head and neck squamous carcinoma were reported as the promotor methylation of p14(ARF) and p16(INK4a) as well as LOH at the 9p21 locus. Gene amplification of CCND1, PIK3CA, and ERBB1 and ERBB2 was observed in low frequencies. Finally, c-erbB2 was also found overexpressed in 32% of 28 cases.

Nasosinus Adenocarcinomas—A Molecular Point of View

Little is known about the genetic changes in adenocarcinoma (ACN). Because of its histopathological resemblance, most studies so far have focused on a limited number of genes and proteins often selected for their frequent involvement in colorectal adenocarcinoma. Indeed, mutations in K-ras and p53 occur also in ACN, although with lower frequencies. K-ras mutations varied in frequency bteween 0% and 15%. One study reported 50%, about the same as in colorectal adenocarcinoma. Also, H-ras mutations have been detected. Mutations in p53 ranged between 18% and 57%, and 50% of LOH was seen at 17p13, the chromosomal locus of p53. Further attempts to find genetic alterations as described in colorectal carcinoma concerned APC, b-catenin, and various mismatch repair genes and gave negative results. These results indicate that ACN and colorectal carcinoma have different genetic pathways of development and progression. Other investigations focused on genes involved in head and neck squamous carcinoma were reported as the promotor methylation of p14(ARF) and p16(INK4a) as well as LOH at the 9p21 locus. Gene amplification of CCND1, PIK3CA, and ERBB1 and ERBB2 was observed in low frequencies. Finally, c-erbB2 was also found overexpressed in 32% of 28 cases.

Distinct patterns of genetic alterations in adenocarcinoma and squamous cell carcinoma of the lung

Squamous cell carcinoma (SqC) and adenocarcinoma (AdC) are the two most common subtypes of non-small cell lung cancer (NSCLC). Cumulative information suggests that the SqC and AdC subtypes progress through different carcinogenic pathways, but the genetic aberrations promoting such differences remain unclear. Here we have assessed the overall genomic imbalances and structural abnormalities in SqC and AdC . By parallel analyses with comparative genomic hybridisation (CGH) on tumorous lung tissues and spectral karyotyping (SKY) on short-term cultured primary tumours, genome-wide characterisation was carried out on 69 NSCLC (35 SqC, 34 AdC). Molecular cytogenetic characterisation indicated common and distinct genetic changes in SqC and AdC. Common events of +1q21-q24, +5p15-p14, and +8q22-q24.1, and −17p13-p12 were found in both groups, although hierarchical clustering simulation on CGH findings depicted +2p13-p11.2, +3q25-q29, +9q13-q34, +12p, +12q12-q15 and +17q21, and −8p in preferential association with SqC pathogenesis ( P<0.05). Corresponding SKY analysis suggested that these changes occur in simple and complex rearrangements, and further indicated the clonal presence of translocation partners leading to chromosomal over-representations. These recurring rearrangements involved chromosome pairs of t(1;13), t(1;15), t(7;8), t(8;15), t(8;9), t(2;17) and t(15;20). Of particular interest was the finding that the t(8;12) translocation partner was exclusive to AdC. The combined application of SKY and CGH has thus uncovered the genome-wide chromosomal aberrations in NSCLC. Specific chromosomal imbalances and translocation partners found in SqC and AdC have highlighted regions for further molecular investigation into gene(s) that may hold importance in the carcinogenesis of NSCLC.

Diet, cancer and aging in DNA mismatch repair deficient mice.

Diet is an important risk factor for many cancers. High fat/low calcium (HFLC) diets are associated with increased tumorigenesis, whereas caloric restriction (CR) reproducibly increases lifespan and decreases tumors. Mutations are involved in aging and cancer, and different diets may alter mutagenesis. However, a number of repair pathways normally counteract mutations by correcting errors before they can be fixed in the genome. To further understand interactions between diet, aging and cancer, mice deficient in a major repair pathway called DNA mismatch repair (MMR) were fed HFLC, CR or control diets. Mlh1 deficient mice are prone to lymphomas and intestinal adenomas and carcinomas. No significant changes in adenocarcinoma or lymphoma incidence were observed with HFLC or CR diets. Significantly more (2.2-fold) adenomas occurred with HFLC diets although adenoma numbers were unchanged with CR. Only a small increase in lifespan (116% of control) was achieved with CR. In addition, levels of microsatellite mutations in the small and large intestines were unchanged with the different diets. Our studies indicate that MMR deficiency may be epistatic to certain otherwise strong environmental influences on carcinogenesis or aging.

Isochromosomes i(8q) or i(9q) in three adenocarcinomas of the lung

We have cytogenetically analyzed three primary adenocarcinomas of the lung. All tumors had chromosome numbers in the triploid region. The multiple structural aberrations included rearrangements of 3p, in two cases affecting the segment 3p14–23, where deletions are characteristically found in small cell lung carcinomas. Isochromosomes for 8q were present in two tumors and i(9q) in one tumor. In the few previously reported cytogenetic analyses of pulmonary adenocarcinomas, all of which examined metastases or cell lines, i(8q) was found in one case and i(9q) in two cases. These isochromosomes, therefore, represent previously unrecognized nonrandom changes in adenocarcinomas of the lung, and might constitute primary aberrations in this tumor type.

Significance of neoplastic atypicalities in endocervical epithelium

Currently, adenocarcinoma in situ and early invasive adenocarcinoma of the cervix are poorly defined entities. The dangers inherent in such diagnoses are identified in this case report of “early adenoepidermoid” cervical cancer in which deepest glands were not involved; however, pelvic recurrence was recognized 5-years posthysterectomy and the patient died of widespread disease 1 1 2 years later. The danger of correlating the knowledge of cervical cancer with gland involvement to “apparently” similar changes in adenocarcinoma are emphasized. It is suggested that, at least at the present, “early adenocarcinoma” must be considered as invasive and treated as such.

Multiple phenotypic divergence of mammary adenocarcinoma cell clones. I. In vitro and in vivo properties.

The properties of cell clones derived from locally growing and spontaneous metastases of 13762NF mammary adenocarcinoma change during in vitro growth. This has been termed phenotypic drift and is reproducible in independent experiments using different cryoprotected cell stocks. To determine whether phenotypic drift in 13762NF cell clones is the result of an en bloc shift in the properties of all tumor cells, or independent phenotypic divergence of tumor cells to produce a mixed cell population, local tumor-derived clone MTF7 was subcloned at low and high culture passage numbers in vitro. Each subclone was analyzed in vitro for cell morphology, growth rate, saturation density, karyotype and ploidy, and in vivo for experimental metastatic behavior. Subclones derived from low passage clone MTF7 (T11; tissue culture passage number 11) were relatively homogeneous in their growth rates (doubling times of 16.8-17.4 h) and saturation densities (approximately 2 X 10(5) cells/cm2); yet, these same subclones were heterogeneous in their in vitro cell morphologies, experimental metastatic potentials (means range from 0 to greater than 100 tumor nodules per lung), size distributions of lung tumor nodules, marker chromosomes and modal chromosome numbers. High passage MTF7 (T35; tissue culture passage number 35) subclones had similar growth rates and saturation densities, except for subclone 2, which had a doubling time of approximately 26 h. Cell morphologies, experimental metastatic potentials (means range from 3 to greater than 600 tumor nodules per lung), size distribution of lung tumor nodules, marker chromosomes and modal chromosome numbers varied between MTF7 (T35) subclones. The results suggest that simultaneous, independent divergence of several phenotypes from a single cloned cell occurred to form a mixed cell population containing cells with independently segregated, unrelated phenotypes. Thus, the reproducibility of phenotypic drift in clonal cell populations was probably the result of tumor cell divergence and was not an en bloc shift in phenotypic properties of all cells.

Mucin Histochemistry of Human Gallbladder: Changes in Adenocarcinoma, Cystic Fibrosis, and Cholecystitis&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;

Mucin Histochemistry of Human Gallbladder: Changes in Adenocarcinoma, Cystic Fibrosis, and Cholecystitis&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;