EliasHossain/CancerAbstracts huggingface dataset:
Category: Thyroid_Cancer
Thyroid cancer is the most common endocrine malignancy. While surgery remains the mainstay of the treatment of all different histologies, for differentiated thyroid cancers, radioactive iodine also plays an important role in management. Once tumor becomes radio-iodine refractory, it needs systemic therapy. Earlier, these tumors had very dismal prognosis. However, with the advancement of technology and research, it has become clear now that thyroid cancer cells are driven by various mutations. Targeting these oncogenic drivers by various molecules have proven to be effective therapeutic strategy in thyroid cancer. Besides, as in other solid tumors, immunotherapy is also being evaluated in thyroid cancer. While these new therapeutic approaches have revolutionized the treatment on advanced/metastatic thyroid cancer, there are definite challenges which limit their use in common clinical practice. These challenges include higher treatment cost and lack of testing to identify the driver mutations. Moreover, there is still need for further research in thyroid cancers to identify oncogenic targets and agent to act upon them.
Category: Colon_Cancer
The role of cyclooxygenase-2 (COX-2) in colorectal tumorigenesis in mice was studied by Oshima et al. to determine the effects of COX-2 gene knockouts and a new COX-2 inhibitor. In the study, heterozygous Apcdelta716 knockout mice, a mouse model of human familial adenomatous polyposis (FAP), were either crossed to COX-2 gene knockout mice, or fed chow containing the COX-2-selective inhibitor. Apcdelta716 litter mates were used as positive controls, which developed 652+/-198 (SD) polyps at 10 weeks. Introduction of a COX-2 gene mutation, or feeding with the COX-2-selective inhibitor to the Apcdelta716 knockout mice, reduced the number and size of intestinal polyps dramatically. The results provide direct genetic evidence that COX-2 plays a key role in tumorigenesis, and indicate that COX-2-selective inhibitors can be a new class of therapeutic agents for colorectal polyposis and cancer.
Category: Colon_Cancer
A new mechanism leading to cancer has been delineated in the last two years when genes whose mutations cause susceptibility to hereditary nonpolyposis colorectal cancer, HNPCC, have been mapped, cloned, and characterized. The genes involved belong to a family of DNA mismatch repair genes, and the homozygous effects of their mutations lead to a so-called mutator or replication error phenotype characterized by genome-wide mutations most readily detectable as lengthening or shortening of microsatellite repeats in tumor tissue as compared to normal tissue from the same individual. Germline mutations are inherited in a dominant Mendelian fashion causing the multiorgan cancer susceptibility syndrome misnamed HNPCC. Clinically, the molecular characterization of these mutations in affected individuals now allows genotype-phenotype correlations, and a new view of the natural history of the disease may arise. In at risk individuals, it allows predictive testing for cancer susceptibility, enhanced clinical surveillance with the aim of early cancer detection and cure, and preventive measures.
Category: Lung_Cancer
Among all cancer, lung cancer has the highest rate of mortality in the western world. The persisting grim lung cancer mortality figures argue powerfully for new approaches for controlling this disease such as chemoprevention that has been defined as the use of agents that inhibit or reverse lung carcinogenesis. Carcinogens from cigarette smoke are implicated in about 90% of male and 75-80% of female lung cancer deaths. Confoundingly epidemiologic studies show that only about 15% of heavy smokers will ultimately develop lung cancer. The fact that 85% of heavy smokers will not develop lung cancer points to a variation in individual susceptibility. It also suggests that modulation of susceptibility might be used as a preventive strategy. This review summarizes the outcomes of recent clinical chemoprevention trials and reveals that the chemoprevention approach in lung cancer is still experimental.
Category: Thyroid_Cancer
Although fine-needle aspiration biopsy (FNA) remains the mainstay of the preoperative workup of thyroid nodules, it does not provide a diagnosis in up to 20% of nodules. This group of indeterminate lesions, including lesions with cellular atypia, suspicious cytology, and demonstrating a follicular pattern, provides one of the greatest challenges to researchers in thyroid cancer today. Over the last 2 decades, considerable work has been done to find molecular markers to resolve this diagnostic dilemma. This article explores some of the markers including galectin-3, HBME-1, BRAF, RET/PTC, PAX8-PPARgamma, hTERT, telomerase, miRNA, and microarray and multigene assays. Although no one marker has proven to be a panacea, several combinations of markers have shown great promise as an adjunct to FNA.
Category: Thyroid_Cancer
Thyrotoxicosis with concomitant thyroid cancer is rare and poorly recognized, which may result in delayed diagnosis, inappropriate treatment and even poor prognosis. To provide a comprehensive guidance for clinicians, the etiology, pathogenesis, diagnosis and treatment of this challenging setting were systematically reviewed. According to literatures available, the etiologies of thyrotoxicosis with concomitant thyroid cancer were categorized into Graves' disease with concurrent differentiated thyroid cancer (DTC) or medullary thyroid cancer, Marine-Lenhart Syndrome with coexisting DTC, Plummer's disease with concomitant DTC, amiodarone-induced thyrotoxicosis with concomitant DTC, central hyperthyroidism with coexisting DTC, hyperfunctioning metastases of DTC and others. The underlying causal mechanisms linking thyrotoxicosis and thyroid cancer were elucidated. Medical history, biochemical assessments, radioiodine uptake, anatomic and metabolic imaging and ultrasonography-guided fine-needle aspiration combined with pathological examinations were found to be critical for precise diagnosis. Surgery remains a mainstay in both tumor elimination and control of thyrotoxicosis, while anti-thyroid drugs, beta-blockers, 131I, glucocorticoids, plasmapheresis, somatostatin analogs, dopamine agonists, radiation therapy, chemotherapy and tyrosine kinase inhibitors should also be appropriately utilized as needed.
Category: Colon_Cancer
We report a case of cerebellum metastasis from transverse colon cancer, which had no evidence of recurrence in the thoracoabdominal region by chemotherapy and resection of liver and lung metastases after initial operation. The case is a 71-year-old male. We performed a radical resection of transverse colon cancer (D2) in 2001. The finding was moderately-differentiated adenocarcinoma, se, n1, ly1, v2, H0, P0, M0, stage IIIa. Relapsing tumor, which metastasized to the liver in 3 years, the right lung in 4 years and 8 months and the left lung in 5 years and 11 months after initial operation, were totally resected. Following the partial resection of the left lung, he received a treatment with 12 times of mFOLFOX6 and S-1+PSK. There was a good control observed in the thoracoabdominal region with no metastases for 14 months. However, drift and dizziness developed in April 2008, and cerebellum metastasis was diagnosed by MRI. He underwent a partial resection of cerebellum tumor, radiation therapy and FOLFIRI. He has been alive for 1 year after the treatment of the cerebellum metastasis, and there has been no evidence of recurrence in the thoracoabdominal region in 8 years after initial operation.
Category: Lung_Cancer
The authors give an overview about the novel results and shifting paradigm of lung cancer screening. They also summarize the results of previous and most recent clinical trials, which re-directed the international interest on lung cancer screening.
Category: Colon_Cancer
Pfizer announced plans to acquire Array BioPharma, maker of a BRAF-MEK inhibitor combination that is currently approved for melanoma and could become a first-in-class treatment for colorectal cancer. The $11.4 billion deal also lands Pfizer a small pipeline of other targeted cancer medicines in development and a portfolio of out-licensed medicines with the potential to generate substantial royalties.
Category: Lung_Cancer
After surgical resection of their primary lung cancer, 33 patients were randomized into one of three groups. The first received high-dose methotrexate once per month with citrovorum rescue, for 3 months. The second group were immunized monthly with a homogenate of Freund's complete adjuvant and carefully characterized soluble antigen derived from allogeneic lung cancer cells of appropriate histology, for 3 months. The third group received a combination of methotrexate and immunization monthly, for 3 months. Each patient was monitored immunologically before, during, and after the treatment period, by use of delayed hypersensitivity reactions to recall and cancer antigens, in vitro lymphocyte response to mitogens, and mixed lymphocyte blocking factor activity. The group that received methotrexate showed little change in skin reactivity, a reduction of blocking factor activity, and significant rebound overshoot in in vitro lymphocyte performance. The immunized group showed a tendency to production of blocking factor activity, striking conversion and enhancement of skin reactivity, and little change in in vitro lymphocyte performance. The immunochemotherapy group showed dramatic increases in specific skin reactivity to cancer antigens, up to 2 years after treatment, in vitro lymphocyte rebound overshoot, and reduction of blocking factor activity production. Classic life table analysis of the probability of freedom from metastases in patients with stage-I cancer indicate that the disease-free interval in patients who received methotrexate is longer than in historic and concomitant controls but not as long as in those who received immunization. The best group appear to be those who received combination immunochemotherapy. We emphasize that the small numbers in this pilot study do not yet allow firm conclusions to be made.
Category: Colon_Cancer
Colorectal cancer is the second most common cause of overall cancer mortality in the United States. This article review pertinent clinical and policy issues, details current colorectal cancer screening concepts, summarizes American College of Radiology achievements to date, and outlines projects in the next phase of the effort.
Category: Colon_Cancer
Colon cancer in humans results in considerable morbidity and mortality throughout most of the world. During the twentieth century, there was a rapid rise in colon cancer within modernizing countries that has not been adequately explained, although the role of diet has been widely explored. Previously, we showed that the presence of the endemic Eimeria spp. protozoan in intestinal tissues is associated with regions of low tumorigenesis in the large and small bovine intestine and that an Eimeria surface protein is a potent activator of dendritic cells and a useful immunomodulator, with anti-cancer and anti-viral properties. Therefore, we hypothesize that the persistent presence of such an intestinal protozoan enhances immunosurveillance by elevating the intestinal alert status and that the loss of these organisms could lead to a higher incidence of colon cancer. Preliminary support of this hypothesis derives from the observations that domestic animals, known to maintain this protozoan, have very low colon cancer incidence. We propose that this also may occur in human populations that use human excrement (night soil) as a fertilizer, a practice that serves to complete the life cycle of this type of microbe. We examine some evidence for this hypothesis in Japan's mortality patterns, where we show that colon cancer increased after the cessation of night soil use, but before the change to a western diet. We conclude that this hypothesis, a variation of the hygiene hypothesis, is worth further consideration and continued elaboration.
Category: Lung_Cancer
The observation that carcinogen exposure is strongly associated with the probability of developing pulmonary neoplasms has suggested for many years that acquired somatic mutations play a key role in the genesis of these environmentally induced cancers. With the advent of new techniques in cytogenetics and in the molecular analysis of DNA extracted from lung tumors, it has now become possible to test this hypothesis and to search for candidate genes that may be targeted by the chronic exposure of these environmental insults. Early work in this field, studying lung tumors of different histologic types, appears to implicate several distinct chromosomal loci (at chromosomes 3p, 13q, 17p, and others), suggesting that sequential genetic events occur during the initiation and progression pathways to pulmonary tumorigenesis. Identifying the candidate gene products and understanding the chronology and stringency of mutational events at these loci will be an essential goal to understanding the cellular basis of lung tumors and for developing strategies for the next generation of diagnostic and therapeutic studies.
Category: Lung_Cancer
The relationship between cancer and coagulopathy was suggested by Trousseau nearly 150 years ago. Later, it became more evident that oncologic patients are at a higher risk of experiencing thromboembolic events. This can be due to activation of the coagulation system either by neoplastic cells or by prescribed therapies (chemotherapy or surgical procedures). In fact, these events can constitute the first manifestation of cancer, and their recurrence, despite efficient anticoagulation, has been described. The coagulation system is normally activated in order to provide healing. In the presence of neoplasms, this complex system is activated as a response to multiple stimuli and seems to contribute to cancer progression. Activation of the coagulation system has a greater effect on metastatic foci than on the primary tumor. However, most cancer victims die from complications caused by metastasis, which underscores the importance of this theme. In this area, various mechanisms have been described, creating promising perspectives for future treatments. The current success in using low-molecular-weight heparins against small cell lung cancer is encouraging. Although the knowledge of those mechanisms is relatively incipient, many basic research and clinical studies are underway.
Category: Colon_Cancer
In patients with colon cancer who undergo resection for potential cure, 40% to 60% have advanced locoregional disease and are classified as either stage II or stage III. The role of adjuvant therapy in stage III colon cancer is well defined. The results from the MOSAIC trial (Multicenter International Study of Oxaliplatin/5-Fluorouracil/Leucovorin in the Adjuvant Treatment of Colon Cancer) and the National Surgical Adjuvant Breast and Bowel Project C-07 trial confirm a definite disease-free survival (DFS) benefit with the addition of oxaliplatin to either infusional or bolus 5-fluorouracil/leucovorin (5-FU/LV). The Xeloda in Adjuvant Colon Cancer Therapy (X-ACT) trial showed capecitabine to be of equivalent clinical benefit to bolus 5-FU/LV. However, adjuvant trials with irinotecan, including Cancer and Leukemia Group B (CALGB 89803), the Pan-European Trial in Adjuvant Colorectal Cancer 3 (PETACC-3), and the French ACCORD trial, have not shown a significant DFS advantage. In contrast, in patients with stage II disease, a small survival benefit of 1% to 5% exists with chemotherapy. Perhaps the analysis of molecular markers in combination with high-risk histopathologic features will help increase patient specificity and identify subsets of patients with stage II colon cancer who will derive a survival benefit with adjuvant therapy. The current Intergroup study stratifying stage II patients based on presence of microsatellite instability and loss of heterozygosity 18q allele will help us better understand the risk versus benefit observed.
Category: Lung_Cancer
Tumor markers are defined as substances which are produced by cancer cells or non-cancer cells reactive to cancer cells, and reflect the cancer status, such as its presence, characteristics, and volume. Clinically, many tumor markers are useful not only to assess the presence/absence of cancer, the primary site, histology, stage, and recurrence, but also to monitor the anti-cancer therapy. Tumor markers for lung cancer play only supporting roles because of their limited sensitivity and specificity, but they are clinically essential to daily medical oncology. This review addresses 6 important tumor markers for lung cancer, namely, CEA, SLX, CYFRA, SCC, ProGRP, and NSE.
Category: Colon_Cancer
Colon cancer cells, like other types of cancer cells, undergo the remodeling of the intracellular Ca2+ homeostasis that contributes to cancer cell hallmarks including enhanced cell proliferation, migration, and survival. Colon cancer cells display enhanced store-operated Ca2+ entry (SOCE) compared with their non-cancer counterparts. Colon cancer cells display an abnormal expression of SOCE molecular players including Orai1 and TRPC1 channels, and the stromal interacting molecule (STIM) 1 and 2. Interestingly, upregulation of Orai1 and TRPC1 channels and their contribution to SOCE are associated with cancer malignancy in colon cancer cells. In a specific cellular model of colon cancer, whereas in non-cancer colon cells SOCE is composed of the Ca2+ release activated (CRAC) currents, in colon cancer cells SOCE is composed of CRAC- and cationic, non-selective store operated (SOC) currents. Former SOCs are mediated by TRPC1 channels. Moreover, colon cancer cells also display dysregulation of the expression of 1,4,5-triphosphate receptors (IP3R) that could contribute to the enhanced SOCE. Another important factor underlying the enhanced SOCE is the differential mitochondrial modulation of the CRAC and SOC currents in non-cancer and colon cancer cells. In colon cancer cells, mitochondria take up more Ca2+ that prevent the Ca2+-dependent inactivation of the SOCs, leading to sustained Ca2+ entry. Notably, the inhibition of SOCE in cancer colon cells abolishes their cancer hallmarks. Robust evidence has shown the efficiency of non-steroidal anti-inflammatory drugs (NSAIDs) and difluoromethylornithine (DFMO) to reverse the enhanced cell proliferation, migration, and apoptosis resistance of cancer cells. In colon cancer cells, both NSAIDs and DFMO decrease SOCE, but they target different molecular components of SOCE. NSAIDs decrease the Ca2+ uptake by mitochondria, limiting their ability to prevent the Ca2+-dependent inactivation of the SOCs that underlie SOCE. On the other hand, DFMO inhibits the expression of TRPC1 channels in colon cancer cells, eliminating their contribution to SOCE. The identification of players of SOCE in colon cancer cells may help to better understand the remodeling of the Ca2+ homeostasis in cancer. Importantly, the use of different pharmacological tools that target different SOCE molecular players in colon cancer cells may play a pivotal role in designing better chemoprevention strategies.
Category: Generic
The earliest industrial biotechnology originated in ancient China and developed into a vibrant industry in traditional Chinese liquor, rice wine, soy sauce, and vinegar. It is now a significant component of the Chinese economy valued annually at about 150 billion RMB. Although the production methods had existed and remained basically unchanged for centuries, modern developments in biotechnology and related fields in the last decades have greatly impacted on these industries and led to numerous technological innovations. In this chapter, the main biochemical processes and related technological innovations in traditional Chinese biotechnology are illustrated with recent advances in functional microbiology, microbial ecology, solid-state fermentation, enzymology, chemistry of impact flavor compounds, and improvements made to relevant traditional industrial facilities. Recent biotechnological advances in making Chinese liquor, rice wine, soy sauce, and vinegar are reviewed.
Category: Lung_Cancer
Metastatic tumors of the larynx are rare. The most common tumors metastasizing to the larynx are melanoma and renal cell carcinoma. Bronchogenic carcinoma metastasizing to the larynx has been rarely described. Herein, we report the case of a 49-year-old, chronic smoker, who incidentally had a laryngeal growth detected during flexible bronchoscopy examination for evaluation of suspected lung cancer. Histopathological examination of the laryngeal nodule and the biopsy obtained from the main bronchus growth confirmed the diagnosis of metastatic squamous cell carcinoma to the larynx from primary lung cancer.
Category: Thyroid_Cancer
Cancer risks were studied in 834 thyroid cancer patients given 131I (4,551 MBq, average) and in 1,121 patients treated by other means in Sweden between 1950 and 1975. Record-linkage with the Swedish Cancer Register identified 99 new cancers more than 2 years after 131I therapy [standardised incidence ratio (SIR) = 1.43; 95% confidence interval (CI) 1.17-1.75] vs 122 (SIR = 1.19; 95% CI 0.88-1.42) in patients not receiving 131I. In females treated with 131I overall SIR was 1.45 (95% CI 1.14-1.83) and significantly elevated were noted for tumours of the salivary glands, genital organs, kidney and adrenal gland. No elevated risk of a subsequent breast cancer or leukaemia was noted. SIR did not change over time, arguing against a strong radiation effect of 131I. Organs that were estimated to have received more than 1.0 Gy had together a significantly increased risk of a subsequent cancer following 131I treatment (SIR = 2.59; n = 18). A significant trend was seen for increasing activities of 131I with highest risk for patients exposed to greater than or equal to 3,664 MBq (SIR = 1.80; 95% CI 1.20-2.58). No specific cancer or group of cancers could be convincingly linked to high-dose 131I exposures since SIR did not increase after 10 years of observation. However, upper confidence intervals could not exclude levels of risk that would be predicted based on data from the study of atomic bomb survivors. We conclude that the current practice of extrapolating the effects of high-dose exposures to lower-dose situations is unlikely to seriously underestimate radiation hazards for low LET radiation.
Category: Thyroid_Cancer
Thyroid cancer is an uncommon childhood malignancy that presents primarily in young children or adolescent females and may be related to radiation exposure or genetic predisposition. Gene alterations, such as RET mutation or RET/PTC rearrangement, are not uncommon. Recent studies have lead to an increased understanding of the role of these particular gene alterations in the diagnosis, prognosis, and treatment of thyroid cancer. Surgery remains the mainstay of treatment for thyroid cancer followed by radioactive iodine when appropriate. In patients with MEN2, prophylactic thyroidectomy is recommended, although a delay in the initial diagnosis is common. With early aggressive treatment and long-term follow-up, these patients generally have excellent outcomes. Recent research suggests potential usefulness of novel therapies directed at oncogenic signaling pathways, modulators of growth, angiogenesis inhibitors, immunomodulators, and gene therapy.
Category: Lung_Cancer
The author addresses the attribution of lung cancer to cigarette smoking and the problems of confounding synergistic effects of occupational and other carcinogenic risk factors, as well as the divergent trends of declining smoking rates and increasing rates of lung cancer. He also reviews the existing literature to document associations between lung cancer and occupational exposures. Finally, interventions for prevention of occupational lung cancer are discussed.