Basic and Clinical Cancer Research
Volume:13 Issue: 4, Autumn 2021

The incidence of malignant esophageal-respiratory fistulas in esophageal cancer patients is not so frequent. Development of fistula in esophageal cancer may be due to advanced disease or may be a radiotherapy related complication. Rarely, pulmonary abscess may develop and it is the most dreadful complication resulting in dismal outcomes. Here, we reported 2-cases of esophageal-respiratory fistula; one with esophageal bronchial fistula and other with esophageal pleural fistula.

Case reports: 

A 46-year-aged man presented with complaints of difficulty in swallowing from 4-months. CECT chest showed an esophageal growth of 8.5 cm in lower esophagus. Patient received palliative radiotherapy followed by palliative chemotherapy and showed some improvement in dysphagia. After 9–months from start of treatment, patient’s dysphagia began to worsen and he was put on oral metronomic chemotherapy. After 1-year of metronomic chemotherapy, patient developed cough and chest pain and was diagnosed as a case of esophageal-pleural fistula with chest wall collection and pleural effusion. Patient was managed conservatively and later lost to follow up. Another, 65-year-old patient presented with dysphagia from 3-months. CECT chest showed an esophageal growth of 5.5 cm in middle esophagus. Patient received palliative radiotherapy after which the dysphagia improved. On 3rd month of follow up patient’s dysphagia worsened; barium swallow showed esophageal-bronchial fistula. Patient was managed symptomatically and later lost to follow up.

Fistula formation and subsequent abscess results in poor prognosis. With advancing disease and compromised general condition of the patient, palliation of symptoms is an important challenge. Treatment becomes difficult due to rare occurrence of fistulas and non-standardization of treatment protocol. Invasive treatment includes esophageal-pulmonary resection, endoscopic placement of self-expandable covered stents, drainage of empyema and obliteration of empyema cavity, esophageal diversion, and non-invasive treatment includes best supportive care. However, even with appropriate treatment, outcome is dismal.

In the last few years, researchers have regarded gene therapy as one of the most essential approaches to treating diseases such as cancer and a variety of genetic disorders. In this research, the capability of FeCo-Chitosan nanoparticles for gene delivery into the MCF-7 cells was investigated.

To this purpose, FeCo-Chitosan/DNA nanoparticles was prepared. Then, the physicochemical properties such as the morphology, size, zeta potential and their magnetic properties of nanoparticles were evaluated. In addition, the biological properties of the nanoparticles, such as biocompatibility, DNA protection, DNA release, and gene transfer capability to MCF-7 cells were investigated.

The results showed that the FeCo-Chitosan / DNA nanoparticles had a spherical structure with an average size of about 200 nm. The zeta potential of the FeCo-Chitosan/DNA complex increased with increasing the concentration of FeCo-Chitosan nanoparticles in FeCo-Chitosan/DNA complex. Electrophoretic analysis confirmed that the FeCo-Chitosan/DNA nanoparticles could protect DNA from nuclease degradation and ultrasound damages. The results of MTT test also showed that FeCo-Chitosan nanoparticles have high biocompatibility. The ability of the FeCo-Chitosan/DNA nanoparticles to deliver genes to MCF-7 cells were examined using fluorescent microscopy and flow cytometry.

The fluorescence microscopy and flow cytometry analysis showed that FeCo-Chitosan nanoparticles have the ability to transfer and release DNA safely to MCF-7 cells. These results also showed that efficiency of gene transfer was increased with increasing the concentration of the FeCo-Chitosan in FeCo-Chitosan/DNA complex.

DNA oxidation is one of the essential destructive effects of reactive oxygen species (ROS) on the cell membrane macromolecules leading to the deformation of cellular DNA. The most abundant oxidative DNA product on which most studies have focused is re-oxidized DNA, 8 oxo-deoxyguanosine (8-oxodG). This deformation of cellular DNA is associated with various cancer initiation and progression. DNA damage can be a cancer marker including 8-oxodG, thymidine glycol, 8-oxoadenine, etc. DNA oxidation is affected by environmental and non-environmental factors. Age, diet, and metabolism are at the heart of this process. This review study summarizes the types of cancer-related DNA oxidation that serve as a cancer biomarker. Also we will look at the factors influencing their formation.

Patients undergoing bone marrow transplantation (BMT) are at higher risk of immune system deficiency. The immunosuppression, followed by pre-transplant chemotherapy makes patients vulnerable to a variety of infections, and fever is one of the first symptoms, which could develop as a result of infectious or non-infectious diseases. In the present study, the features of the fever during the pre-engraftment stage in BMT receiving patients have been investigated.

Sixty-four patients receiving BMT were prospectively evaluated during the pre-engraftment phase to evaluate the evidence of the febrile reaction.  Data concerning the cause of fever, microbiological test, the treatments and fever onset pattern, and treatment outcomes were recorded and analyzed.

73.4% of the patients had an autologous transplant, and the others received allogeneic. After transplantation, 75% of patients encountered fever during the pre-engraftment period. Of the 48 patients, 47.9% of the patients suffered fever of unknown origin (FUO). Age, gender, underlying malignancy, type of transplantation, and acute phase reactants levels before transplantation were not associated with fever development. Among febrile patients, patients with autologous transplantation were significantly more likely to develop FUO (p-value = 0.036) There was also no significant difference in the onset of fever between patients with infectious fever and who suffered FUO.

During BMT, half of the patients developed a fever of unknown origin; nevertheless, it seems that patients undergoing allogeneic transplantation are at higher risk of FUO compared to patients who received an autologous transplant.

Tuberous sclerosis complex (TSC) is an autosomal dominant neurocutaneous syndrome that affects almost all of the organs of the body, including the brain, heart, lungs, liver, and kidneys. Brain tumors in TSC patients include cortical tubers, subependymal nodules (SENs), and Subependymal giant cell astrocytomas (SEGAs). Seizures that occur in 92% of patients with TSC are an important cause of sudden deaths in them. Other organ involvement includes renal angiomyolipomas, lymphangioleiomyomatosis, cardiac rhabdomyomas, and cutaneous manifestations (hypomelanotic macules, angiofibromas, ungual fibromas, shagreen patch, and 'confetti' skin lesions). There is a criterion for tuberous sclerosis complex that consists of 11 major and 6 minor clinical features that diagnosis occurs based on it. The best way for definitive diagnosis of TSC in a patient is using genetic tests and histopathology.  Immunohistochemistry is a helpful method in confirming the diagnosis of brain tumors in TSC. Immunostaining of SEGA shows positivity for GFAP and S-100 protein while neurofilament and synaptophysin are negative. Ki-67, which indicates nuclear proliferation, has a low proliferation index in immunostain. At the beginning of aggression the tumor or manifestation of hydrocephalus and symptoms of rising intracranial pressure and focal neurologic deficit, surgery is a necessity and can improve outcome. The aim of this study is a concise review of literature for clinicians and pathologists for better diagnosis and management of disease with variable manifestation.

Insulin is a big hormone (five,808 Da) generally produced with the aid of the pancreas. Insulin receptors (IR) are found in neurons and glial cells. Insulin resistance has been related to increased plasma insulin levels, glucose intolerance, elevated insulin-like growth factor-1 (IGF-I), glucose and free fatty acids, body mass index, and an elevated risk for colorectal cancers. Proinflammatory cytokines, boom components, and hormones secreted by adipocytes play a key role in colorectal cancer etiology. Acetyl-CoA acetyltransferase (ACAT1) mediates insulin-precipitated cell proliferation and metastatic outcomes in colorectal cancer cells. Therefore, miRNAs might serve as a biological connection between metabolic changes linked to obesity and the beginning and progression of colorectal cancer (CRC). Furthermore, these findings shed new light on weight problems as a CRC danger component in which miRNA dysregulation potentially plays a role. The role of IGFs in colorectal cancer is investigated by examining the association of two genetic polymorphisms in IGFBP-3 (a G → C single nucleotide polymorphism) and IGF-1 (a cytosine-adenosine dinucleotide repeat) with colorectal cancer risk in addition to the possibility of the other interventions, including physical activity, body mass index (BMI), and the use of postmenopausal hormones. These factors can exert their effects by modifying IGF-1 and the related binding proteins (IGFBP). Furthermore, the IGFBP-3 genotype can lead to a substantial effect modifier in the association between colorectal cancer and risk factors.  It has been found that functional polymorphisms in the pathway of insulin genes, including IGFBPI, INSR, INS, and insulin receptor substrate 1 and 2 (IRS1 and IRS2), can be related to CRC.

The application of radiation therapy (RT) in lung cancer has shown some exciting and sometimes disappointing advances in recent years. Protons compared with photons interact differently with human tissues, and can be used to improve patient care for suffering from lung cancer. A new strategy is the simultaneous injection of nanoparticles with proton radiation into the tumor which has been given over a decade to improve conventional RT. In this work, proton beam therapy (PBT) with gold nanoparticles (GNPs) is used as a part of a combination program to treat advanced localized lung cancers. This paper aims to develop the complex Geant4 model on the human lung and predict the distribution of absorbed dose in lung tumors during proton therapy without and with a high-Z injection of GNPs. Thus, the absorbed dose distribution in lung tumors for four modes such as (i) Bethe-Bloch’s relativistic quantum theory, (ii) GEANT4/ GATE7 simulation model, (iii) Hartree-Fock-Roothaan(HFR) wave functions, and the (vi) Bortfeld theoretical model without and with the injection of GNPs in predicted lung phantom are compared.

Fluorine 18-deoxyglucose is often used in Positron Emission Tomography device. Positron Emission Tomography imaging is one of the useful tool which is used to cancer detection and its management. Positron Emission Tomography growth is limited due to problems that depend on the production of Fluorine-18. Imaging results are strongly depending on the information of nuclear reaction cross section data. This study is presented to calculate different quantities such as stopping power, CSDA range, simulated and distributed absorbed dose of Fluorine-18 in water. In order to access these goals, we use Geant4/Gate7 simulation and theoretical Bethe-Bloch model. The results of this simulation and theoretical model presented are in good agreement with each other. The important point of this paper is the presentation of a theoretical approach in order to the production of Fluorine-18 using protons generated through the main D(d;p) Tand side 3 He(d;p)4 He nuclear fusion reaction in which uses Helium-3 as a catalyzed.