Metastasis is the leading cause of breast cancer-related mortality and involves cells from a primary tumor invading into adjacent tissue by using the circulatory system.During the process of metastasis, several dynamic and reciprocal interactions between cancer cells and inflammatory cells occur in the surrounding tumor microenvironment via the secretion of several cytokines, including tumor necrosis factor-α, and transforming growth factor-β.The present study aimed to investigate the functional role of recombinant apurinic apyrimidinic endonuclease 1(APE1)/Redox factor-1 (Ref-1) with reducing activity, [APE1/Ref-1-(SH)2] in the regulation of metastatic migration in cytokine-stimulated MDA-MB-231 breast cancer cells.The results reveal that [APE1/Ref-1-(SH)2], but not the oxidized form of recombinant APE1/Ref-1, attenuated migration, and invasion of cytokines-stimulated MDA-MB-231 cells.These effects were induced by the oxidative conformational changes due to the thiol-disulfide exchange reaction targeting disulfide bonds in extracellular domain of the cytokine receptors.Blocking of the binding of the cytokines to the corresponding receptors also reversed epithelial-to-mesenchymal transition (EMT) in cytokine-stimulated MDA-MB-231 cells.The reversal of EMT was accompanied by changes in the expression levels of representative EMT markers, E-cadherin, N-cadherin, vimentin, and snail.Remarkable phenotypic changes were also observed in MDA-MB-231 cells, as the cells adopted an epithelial like globular shape, with regular dimension, a reorganized cytoskeleton, and collapsing filopodia and lamellipodia.In conclusion, although devising a stable form of recombinant [APE1/Ref-1-(SH)2] requires further study, its ability to target cytokine receptors and to inhibit their intracellular signaling suggests the use of [APE1/Ref-1-(SH)2] as a promising agent for regulating metastatic cancer cells.
In the case of invasive breast carcinomas (BC) there are extremely rare late nonregional retroperitoneal lymph node recurrences, occurring after 10 years of disease diagnosis .We present a 32-year-old woman, who was diagnosed in 2010 with left HER2 positive invasive ductal BC-pT2N1M0.Complex treatment involving radical mastectomy with axillary dissection and complex adjuvant treatment (chemotherapy, radiotherapy, targeted therapy with trastuzumab, endocrine therapy with LHRH agonist plus tamoxifen) was conducted.After 4 years, disease progression with left supraclavicular lymph node enlargement has been manifested.After surgical resection of supraclavicular lymph node, the patohistological analysis establishes lymph metastasis from HER2 positive invasive ductal carcinoma.After 6 years of multimodal treatment, including eight chemotherapy cycles docetaxel, bilateral adnexectomy, 2 targeted agents trastuzumab/pertuzumab and endocrine therapy with aromatase inhibitor, PET/ CT visualizes a nonregional lymph recurrence of left retroperitoneal lymph nodes.Isolated involvement of distant nodal regions is extremely uncommon.Complex therapy, including a definitive radiotherapy of retroperitoneal para-aortic lymph nodes combined with targeted therapy achieved complete remission in nonregional abdominal lymph recurrence.
Received: January 03, 2021; Accepted: January 26, 2021; Published: January 29, 2021 It has been reported that a so-called clean colon procedure, in which all precancerous lesions, colorectal tubular adenomas / colorectal tubulovillous adenomas, are endoscopically resection treatment is extremely useful for preventing colorectal carcinogenesis and death from colorectal cancer [1-4]. The effectiveness of chemopreventive measures to take the antidiabetic drugs metformin and low-dose aspirin has also been reported [5-7]. Recently, there have been reports suggesting the involvement of intestinal microorganisms such as Fusobacterium nucleatum (F. nucleatum) in colorectal carcinogenesis [8-13], and there is a possibility that a strategy targeting intestinal microorganisms will be taken as future methods for preventing colorectal carcinogenesis. This review describes the prospects for new strategies on colorectal carcinogenesis prevention targeting intestinal microbiome such as F. nucleatum.
in the CNS and therapeutic resistance which are repetitively seen at the time of microtubule-targeting, the use of these drugs is limited [1-4]. The new generation of mitotic drugs aims for the mitotic regulatory machinery which involves the motor proteins, mitotic kinesins, or the Aurora and polo-like kinases and complexes which are expressed only at the time of cell division [2]. Research efforts are intended towards developing superior antimitotic drugs that would not be only more specific in their action but would also lessen the burden of side effects on patients. Also, because cancer cells demonstrate vast phenotypic miscellany they are characteristically responsive to phenotypic screening which would assist in translating the molecular mechanism as a therapeutic approach in treating cancer with familiar cellular phenotypes following the theory of mechanism-informed phenotypic screening.
Pulmonary sclerosing pneumocytoma (PSP) is a rare benign neoplasm, predominantly occurring in middle-aged women. When first reported, PSP was thought to be vascular in origin and named pulmonary sclerosing hemangioma because of its high morphological similarity to cutaneous sclerosing hemangioma. Thanks to electron microscopy and immunofluorescence, it has been defined as being primitive respiratory epithelium-oriented and renamed as PSP [1].
The concepts of cancer etiology have changed over the years, mainly based on molecular epidemiology studies and bioinformatics approaches.Until relatively recently the most accepted theory of cancer etiology has dealt with the accumulation of gene mutations and the consequent cognate proteins dysfunction, but now some authors have argued against the proposed theory.The additional role of noncellular genes in the cause of malignancy, associated to environmental factors and host genetic background, has been proposed and mostly accepted by the scientific community.Some of our data from human populations in Brazil concerning cancer epidemiology, molecular and serological surveys, were conducted looking for the detection of putative oncogenic viruses, as the Human T-cell Lymphotropic virus/ HTLV-1/2, Human Papillomavirus/HPV, the Mouse or Human Mammary Tumor Virus/MMTV, the Human Endogenous Retrovirus/HERVs and the Hepatitis C virus/HCV, in human, healthy and malignized, tissues.Generally, research work around the world suggests that 10 to 20 % of all human cancers are etiologically linked to oncogenic viruses, so if the presence of exogenous or endogenous virus sequences in the human DNA has any significancy in the cancer etiology, it deserves further and continuous research work and discussion.
A 66-year-old male patient with was admitted to hospital with complaints of fatigue and shortness of breath. In the chest X-ray of the patient, homogeneous density increase was observed in the lower zone of the right lung, suggesting pleural effusion and showing Damoiseau's line. In the patient who underwent thoracentesis, pleural fluid in the form of yellow pus and empyema was seen. The pleural fluid biochemistry was in the character of exudate. Thoracic computed tomography (CT) was performed in the patient who underwent closed underwater drainage with tube thoracostomy. Pleural effusion was reaching 8 cm. in the right hemithorax. The size of the spleen was increased, the liver parenchyma was heterogeneous. In the follow-ups, although the pleural effusion and Damoiseau line of the patient were erased, the fluid continued to come out of the drain as a daily empyema; the patient's clinical and laboratory tests were not compatible with empyema. In addition, a possible hematological malignancy was considered due to low Hb, leukocyte, platelet levels, and hepatosplenomegaly. Chylothorax was taken into the differential diagnosis and triglyceride and cholesterol were sent from the pleural fluid. Triglyceride was high in pleural fluid. No malignant cells were seen in pleural fluid cytology. Positron emission tomography (PET)/CT was performed to determine the etiology in the patient who was diagnosed with chylothorax. There were dense hypermetabolic lymphadenopathy masses starting from the level of the 8th thoracic vertebra up to the retrocrural area in the prevertebral area. Spleen sizes were increased and there were intense hypermetabolic involvements. Involvement due to lymphoproliferative diseases was considered in the foreground. Mediastinoscopy was performed. Biopsies were taken from mass in the paraesophageal area (posterior mediastinum). The pathology result of the biopsies was "Diffuse Large B-Cell Lymphoma". The patient was referred to hematology and oncology clinics for treatment and discharged.
A 20 -year-old schoolteacher presented to her GP with the recurrent dystonic movement of the left arm, loss of appetite and weight loss of 6 kilograms in the last three months.She started to feel unstable on her feet and had near fallen.She did not smoke or drink alcohol.Her past medical history was non-contributory.She was not on any regular medication including over counter medications.There was no significant family history.She traveled to India a year before.She spent six months on a mission and enjoyed food and drinks from the hotel.She was well with no symptoms during her trip.She was UpToDate with her immunization.
Hepatic hemangiomas (HHs) are defines as "giant" when are larger than 4 cm.The following case is reviewed due its unusual evolution.A case of 64-year-old woman was found at CT scan to have a "giant" HH (>20 cm in diameter).In 2015 (8 years after initial diagnosis), in the absence of treatments, abdominal CT scan highlighted the initial spontaneous regression of the HH, that progressed over time.Management of giant hemangiomas remains debated.Surgery should be restricted to specific situations, depending on growth pattern, symptom persistence, risk of complications and patient anxiety.Usually HHs remain stable in size over time and only a prolonged clinical and radiological follow-up is advised.The commonly known natural history of HHs in non-cirrhotics do not include decrease in size or regression.Clearly documented cases of spontaneous regression of giant HHs in non-cirrhotic adult patients have not yet been reported.
The article presents a case of a 75-year-old male patient who fell ill with Kaposi's sarcoma at the age of 60.He had small formations in the second stage of sarcoma, which were removed with liquid nitrogen, but the disease passed into the third stage, in which the patient no longer received any treatment of his own free will.The patient is diagnosed with classic Kaposi's sarcoma, which has passed the spotty, popular and tumor stages of the disease over 12 years.Before the use of low doses of verapamil-hydrochloride (40 mg in a tablet), tumor nodes with a diameter of up to 5 cm appeared in the patient's lower extremities, which disappeared after 2-3 months, and new nodes appeared nearby, while there was no pattern in their appearance -disappearance was traced.
Introduction: Immunity of colitis-associated colorectal cancer (CAC) differs fundamentally from that of the sporadic form. The aim of this study was to evaluate whether this difference could potentiate the efficacy of immune-checkpoint inhibitor anti-PD1 against CAC. Methods: CAC tumorigenesis was induced by azoxymethane (AOM) followed by three cycles of dextran sodium sulfate (DSS) in mice. Two weeks after the end of DSS, mice were treated with anti-PD1 antibody (n=9) or with isotype antibody (n=9). The severity of clinical and histological colitis, tumor counts, and infiltration of CD8+ T-lymphocytes and neutrophils were compared. Results: The anti-PD1 antibody did not aggravate the colitis as exemplified by the absence of differences in weight loss (p=0.424) and in the standardized pathological scores (p=1.000) compared to those of the control. On macroscopic examination, the median number of tumors was 24.0 [21.5/31.0] in treated mice and 17.0 [4.0/23.5] in controls (p=0.037). The percentage of tumor tissue within the entire colonic epithelium was significantly higher in treated mice (33.1% [27.2/39.0]) than in controls (15.3% [8.1/25.0]) (p=0.003). The intra-tumoral CD8+ T-lymphocyte density was similar between the two groups (p=0.546). In contrast, CD8+ T-lymphocyte density was significantly higher in non-tumor colonic epithelium in treated mice than in controls (p=0.019). Regarding innate immunity, neutrophil density was similar within the tumors (p=0.864) and augmented in non-tumor colonic epithelium in treated mice compared with controls (p=0.012). Conclusion: Unexpectedly, checkpoint inhibitor anti-PD1 treatment of CAC stimulates tumor proliferation without flaring-up the colitis. *Correspondence to: Eric Ogier-Denis, Laboratory of intestinal inflammation, center of research on inflammation, UMR1149, INSERM, University of Paris, 16 rue Henri Huchard, 75018, France, Tel: +33157277307, Fax: +3315727746, E-mail: eric.ogier-denis@inserm.fr
Lymphedema, one of the most common consequences of breast cancer treatment, associated with the accumulation of fluids with high protein content in the intercellular space except to dysfunction also creates an aesthetic problem for women. In addition, it increases the risk of skin infections and affects the quality of life. Here we report the case of a 37-year-old a female patient diagnosed with breast cancer who underwent left breast mastectomy and left lymph node axillary emptying. Six months after the treatment, the patient developed left-sided lymphedema. Based on the recommendation of the Oncologist decongestive therapy for lymphedema was initiated for 6 weeks with a frequency of 3 times a week. Decongestive therapy included manual lymphatic drainage according to Leduc, pressotherapy, and elastic-compression orthoses. The patient was also educated on exercise therapy with light physiological repetitive arm movements at home, on thoracic and diaphragmatic breathing as they have good decongestive effects. Decongestive Therapy although it does not affect the prevention of lymphedema, gives good results in the management and prevention of lymphatic stasis in breast cancer patients who have undergone surgery. *Correspondence to: Fatjona Kamberi, Research Center of Public Health, Faculty of Public Health, University of Vlore “Ismail Qemali”, Vlore, Albania, E-mail: fatjonakamberi@gmail.com / fatjona.kamberi@univlora.edu.al Received: June 02, 2020; Accepted: June 20, 2020; Published: June 23, 2020 Introduction Lymphedema is one of the most common consequences of breast cancer treatment. One in five women develops secondary lymphedema within the first 2 years after treatment [,]. It is associated with the accumulation of fluids with high protein content in the intercellular space. Clinically, the patient complains of severe sensation in the arm, paresthesia, and difficulty during daily life activities. In addition to dysfunction, lymphedema also creates an aesthetic problem for women, increases the risk of skin infections, and affects the quality of life. Breast cancer is associated with the emptying of axillary lymphatic stasis and radiotherapy. The development of secondary lymphedema is a major challenge for women due to the fact that it is a chronic problem. Decongestive therapy includes manual lymphatic drainage, pressotherapy, and exercise therapy and aims to stimulate lymph circulation and prevent lymphatic stasis [3-5].
Received: January 20, 2020; Accepted: February 05, 2020; Published: February 10, 2020 Kawabata, a Japanese writer, won the Nobel Prize for literature in 1968. Four years later, at age 72, words from his short story “Silence” were quoted in his obituary: “A silent death is an endless word” [1]. That story and my travels to Japan inspired this commentary. Remarkably, the story, while written more than a decade before Kawabata’s protégé took his life in the traditional and dramatic samurai manner, foreshadowed the Nobel laurate’s death. To the chagrin of his readers and fellow citizens, the former suicide apparently triggered Kawabata’s.
Received: February 12, 2020; Accepted: February 22, 2020; Published: February 25, 2020 Prostate cancer is the most common male cancer in the United States and the second leading cause of male cancer death in the United States. African American men have a 60% higher incidence and mortality rate from prostate cancer compared to Caucasian men in North America, indicating that prostate cancer is a major public health problem in this population [1]. The etiology of these racial differences in the clinical manifestation of prostate cancer is not unclear: hormonal, genetic, behavioral and environmental factors have all been implicated [2]. To understand the many factors suspected of contributing to the development of this malignancy, there is a critical need for in vitro models representing primary tumors. However, no suitable in vitro models which accurately reflect the in situ characteristics of malignant epithelium for the study of African American prostate cancer are available. Studies of prostate cancer have been hampered by various factors including (1) restricted access to tissue (2) difficulties in propagating premalignant lesions and primary prostate tumors in vitro and (3) limited availability of prostate cell lines for in vitro studies. To date there is no commercially available pair of nonmalignant and tumor cells derived from the same prostate cancer patient.
