Barrett’s esophagus, dysplasia, and adenocarcinoma
In Barrett’s esophagus the normal stratified squamous epithelium lining the esophagus becomes replaced by metaplastic columnar epithelium containing goblet cells; it develops as a complication of chronic gastroesophageal reflux disease and predisposes the patient to adenocarcinoma. The frequency with which it leads to adenocarcinoma is not established with certainty, but the reported prevalence averages approximately 10% when the diagnosis of Barrett’s esophagus is first made. The estimated incidence of adenocarcinoma varies from one in 152 to one in 441 cases per patient year, or a 30- to 125-fold excess risk. Esophageal adenocarcinoma arises only in patients with metaplastic columnar epithelium. Dysplasia precedes adenocarcinoma in Barrett’s esophagus and arises from the metaplastic epithelium; it has been proposed as a marker for detecting patients at high risk for developing carcinoma. Problems with the use of dysplasia as a marker for cancer risk include difficulty in differentiating it from reactive change, variability in diagnosis and grading between observers and when the same observer interprets the sections on different occasions, and lack of understanding of its natural history. Methods other than dysplasia for detecting patients at highest risk for developing carcinoma have been sought, but flow cytometric analysis of DNA content is the only one proven to be valuable to date. Flow cytometric abnormalities correlate well with histological progression in Barrett’s esophagus. The prevalence of elevated S phase and G2/tetraploid fractions and of aneuploid cell populations increases with histological progression from metaplasia to indefinite/low grade dysplasia to high grade dysplasia and cancer. Flow cytometric abnormalities in endoscopic biopsy specimens identify those patients with a higher risk of progression to high grade dysplasia or adenocarcinoma. 
Comprehensive molecular profiling of lung adenocarcinoma
Adenocarcinoma of the lung is the leading cause of cancer death worldwide. Here we report molecular profiling of 230 resected lung adenocarcinomas using messenger RNA, microRNA and DNA sequencing integrated with copy number, methylation and proteomic analyses. High rates of somatic mutation were seen (mean 8.9 mutations per megabase). Eighteen genes were statistically significantly mutated, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification. EGFR mutations were more frequent in female patients, whereas mutations in RBM10 were more common in males. Aberrations in NF1, MET, ERBB2 and RIT1 occurred in 13% of cases and were enriched in samples otherwise lacking an activated oncogene, suggesting a driver role for these events in certain tumours. DNA and mRNA sequence from the same tumour highlighted splicing alterations driven by somatic genomic changes, including exon 14 skipping in MET mRNA in 4% of cases. MAPK and PI(3)K pathway activity, when measured at the protein level, was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation. These data establish a foundation for classification and further investigations of lung adenocarcinoma molecular pathogenesis. 
Gefitinib or Carboplatin–Paclitaxel in Pulmonary Adenocarcinoma
Previous, uncontrolled studies have suggested that first-line treatment with gefitinib would be efficacious in selected patients with non–small-cell lung cancer.
In this phase 3, open-label study, we randomly assigned previously untreated patients in East Asia who had advanced pulmonary adenocarcinoma and who were nonsmokers or former light smokers to receive gefitinib (250 mg per day) (609 patients) or carboplatin (at a dose calculated to produce an area under the curve of 5 or 6 mg per milliliter per minute) plus paclitaxel (200 mg per square meter of body-surface area) (608 patients). The primary end point was progression-free survival.
The 12-month rates of progression-free survival were 24.9% with gefitinib and 6.7% with carboplatin–paclitaxel. The study met its primary objective of showing the noninferiority of gefitinib and also showed its superiority, as compared with carboplatin–paclitaxel, with respect to progression-free survival in the intention-to-treat population (hazard ratio for progression or death, 0.74; 95% confidence interval [CI], 0.65 to 0.85; P<0.001). In the subgroup of 261 patients who were positive for the epidermal growth factor receptor gene (EGFR) mutation, progression-free survival was significantly longer among those who received gefitinib than among those who received carboplatin–paclitaxel (hazard ratio for progression or death, 0.48; 95% CI, 0.36 to 0.64; P<0.001), whereas in the subgroup of 176 patients who were negative for the mutation, progression-free survival was significantly longer among those who received carboplatin–paclitaxel (hazard ratio for progression or death with gefitinib, 2.85; 95% CI, 2.05 to 3.98; P<0.001). The most common adverse events were rash or acne (in 66.2% of patients) and diarrhea (46.6%) in the gefitinib group and neurotoxic effects (69.9%), neutropenia (67.1%), and alopecia (58.4%) in the carboplatin–paclitaxel group.
Gefitinib is superior to carboplatin–paclitaxel as an initial treatment for pulmonary adenocarcinoma among nonsmokers or former light smokers in East Asia. The presence in the tumor of a mutation of the EGFR gene is a strong predictor of a better outcome with gefitinib. 
A Rare Case of Metastatic Adenocarcinoma of Stomach Metastasizing into Metachronous Gist of Small Intestine
Gastrointestinal stromal tumours (GIST) are rare mesenchymal neoplasms in the gastrointestinal tract. The metachronous existence of GIST and gastric adenocarcinoma, though are tumours of distinct histotype, and very rare, have been reported in medical case reports in recent years.
We report a case of a 74 year old man who initially presented with moderately differentiated adenocarcinoma of the stomach, underwent Billroth 2 gastrectomy followed by chemotherapy. Subsequently, after 15 months he developed a GIST of small bowel with metastasis from adenocarcinoma of stomach.
Taking into consideration the fact that metachronous occurrence of GIST of the gastrointestinal tract and adenocarcinoma of stomach is rare and further metastasis of one tumour into the other makes this case a rare one as per available literature. 
Could Monocytes Colonized by Circulating Epithelial Cells of the Prostate Gland be a Source of Metastasis of the Adenocarcinoma? A Hypothesis Based on a Previous Study
Background: Recently we reported the successful in vitro cultivation of prostatic epithelial and stromal cells from patients with benign prostatic hyperplasia and adenocarcinoma of the prostate by liquid biopsy. In that study we noticed monocytes that were colonized by prostatic epithelial cells; this was confirmed using a monoclonal antibody to prostate epithelial cells. We also detected a deleterious effect exerted on the monocyte cytoplasm by a process yet to be determined.
Aim: To develop a hypothesis that will explain the significance of monocytes colonized by prostatic epithelial cells in the pathogenesis of prostate adenocarcinoma.
Study Design: Retrospective analysis of images in the previous study.
Place and Duration: Kilimanjaro Christian Medical University College, Tumaini University, Moshi, Tanzania. One month.
Results: We found that all monocytes viewed, without exception, contained intra-cytoplasmic prostatic epithelial cells and most of them presented with apparent cytopathology. The cytopathology presented as strand formation and shrinkage of monocytes. Often the loss of integrity of monocyte cytoplasm could be arbitrarily graded as little to complete loss of cytoplasm.
Conclusion: We hypothesize that epithelial cells invade monocytes and colonize the cytoplasm. Monocytes colonized by epithelial cells then participate in the metastatic process of the prostate adenocarcinoma to different parts of the body. We report for the first time, a monocyte colonized by an epithelial cell of the prostate gland. This could also be an unrecognized phenomenon with other types of cancers. 
 Haggitt, R.C., 1994. Barrett’s esophagus, dysplasia, and adenocarcinoma. Human pathology, 25(10), pp.982-993.
 Cancer Genome Atlas Research Network, 2014. Comprehensive molecular profiling of lung adenocarcinoma. Nature, 511(7511), pp.543-550.
 Mok, T.S., Wu, Y.L., Thongprasert, S., Yang, C.H., Chu, D.T., Saijo, N., Sunpaweravong, P., Han, B., Margono, B., Ichinose, Y. and Nishiwaki, Y., 2009. Gefitinib or carboplatin–paclitaxel in pulmonary adenocarcinoma. New England Journal of Medicine, 361(10), pp.947-957.
 Rodrigues, J., Kumar, S., Vaz, O. P. and Salelkar, R. (2015) “A Rare Case of Metastatic Adenocarcinoma of Stomach Metastasizing into Metachronous Gist of Small Intestine”, Journal of Advances in Medicine and Medical Research, 13(1), pp. 1-4. doi: 10.9734/BJMMR/2016/22002.
 Nyindo, M., Hamid Lukambagire, A.- and Mimano, L. (2016) “Could Monocytes Colonized by Circulating Epithelial Cells of the Prostate Gland be a Source of Metastasis of the Adenocarcinoma? A Hypothesis Based on a Previous Study”, Journal of Cancer and Tumor International, 4(2), pp. 1-5. doi: 10.9734/JCTI/2016/28227.