ResearchPad - oncology https://www.researchpad.co Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Decyl caffeic acid inhibits the proliferation of colorectal cancer cells in an autophagy-dependent manner <i>in vitro</i> and <i>in vivo</i>]]> https://www.researchpad.co/article/elastic_article_13874 The treatment of human colorectal cancer (CRC) cells through suppressing the abnormal survival signaling pathways has recently become a significant area of focus. In this study, our results demonstrated that decyl caffeic acid (DC), one of the novel caffeic acid derivatives, remarkedly suppressed the growth of CRC cells both in vitro and in vivo. The inhibitory effects of DC on CRC cells were investigated in an in vitro cell model and in vivo using a xenograft mouse model. CRC cells were treated with DC at various dosages (0, 10, 20 and 40 μM), and cell survival, the apoptotic index and the autophagy level were measured using an MTT assay and flow cytometry analysis, respectively. The signaling cascades in CRC were examined by Western blot assay. The anti-cancer effects of DC on tumor growth were examined by using CRC HCT-116 cells implanted in an animal model. Our results indicated that DC differentially suppressed the growth of CRC HT-29 and HCT-116 cells through an enhancement of cell-cycle arrest at the S phase. DC inhibited the expression of cell-cycle regulators, which include cyclin E and cyclin A proteins. The molecular mechanisms of action were correlated to the blockade of the STAT3 and Akt signaling cascades. Strikingly, a high dosage of DC prompted a self-protection action through inducing cell-dependent autophagy in HCT-116 cells. Suppression of autophagy induced cell death in the treatment of DC in HCT-116 cells. DC seemed to inhibit cell proliferation of CRC differentially, and the therapeutic advantage appeared to be autophagy dependent. Moreover, consumption of DC blocked the tumor growth of colorectal adenocarcinoma in an experimental animal model. In conclusion, our results suggested that DC could act as a therapeutic agent through the significant suppression of tumor growth of human CRC cells.

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<![CDATA[<i>In silico</i> analyses identify lncRNAs: WDFY3-AS2, BDNF-AS and AFAP1-AS1 as potential prognostic factors for patients with triple-negative breast tumors]]> https://www.researchpad.co/article/elastic_article_13870 Long non-coding RNAs (lncRNAs) are characterized as having 200 nucleotides or more and not coding any protein, and several been identified as differentially expressed in several human malignancies, including breast cancer.MethodsHere, we evaluated lncRNAs differentially expressed in triple-negative breast cancer (TNBC) from a cDNA microarray data set obtained in a previous study from our group. Using in silico analyses in combination with a review of the current literature, we identify three lncRNAs as potential prognostic factors for TNBC patients.ResultsWe found that the expression of WDFY3-AS2, BDNF-AS, and AFAP1-AS1 was associated with poor survival in patients with TNBCs. WDFY3-AS2 and BDNF-AS are lncRNAs known to play an important role in tumor suppression of different types of cancer, while AFAP1-AS1 exerts oncogenic activity.ConclusionOur findings provided evidence that WDFY3-AS2, BDNF-AS, and AFAP1-AS1 may be potential prognostic factors in TNBC development. ]]> <![CDATA[Low LEF1 expression is a biomarker of early T-cell precursor, an aggressive subtype of T-cell lymphoblastic leukemia]]> https://www.researchpad.co/article/elastic_article_13868 Early T-cell precursor (ETP) is the only subtype of acute T-cell lymphoblastic leukemia (T-ALL) listed in the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia. Patients with ETP tend to have worse disease outcomes. ETP is defined by a series of immune markers. The diagnosis of ETP status can be vague due to the limitation of the current measurement. In this study, we performed unsupervised clustering and supervised prediction to investigate whether a molecular biomarker can be used to identify the ETP status in order to stratify risk groups. We found that the ETP status can be predicted by the expression level of Lymphoid enhancer binding factor 1 (LEF1) with high accuracy (AUC of ROC = 0.957 and 0.933 in two T-ALL cohorts). The patients with ETP subtype have a lower level of LEF1 comparing to the those without ETP. We suggest that incorporating the biomarker LEF1 with traditional immune-phenotyping will improve the diagnosis of ETP.

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<![CDATA[Early budget impact analysis on magnetic seed localization for non-palpable breast cancer surgery]]> https://www.researchpad.co/article/elastic_article_13866 Current localization techniques used in breast conserving surgery for non-palpable tumors show several disadvantages. Magnetic Seed Localization (MSL) is an innovative localization technique aiming to overcome these disadvantages. This study evaluated the expected budget impact of adopting MSL compared to standard of care.MethodsStandard of care with Wire-Guided Localization (WGL) and Radioactive Seed Localization (RSL) use was compared with a future situation gradually adopting MSL next to RSL or WGL from a Dutch national perspective over 5 years (2017–2022). The intervention costs for WGL, RSL and MSL and the implementation costs for RSL and MSL were evaluated using activity-based costing in eight Dutch hospitals. Based on available list prices the price of the magnetic seed was ranged €100-€500.ResultsThe intervention costs for WGL, RSL and MSL were respectively: €2,617, €2,834 and €2,662 per patient and implementation costs were €2,974 and €26,826 for MSL and RSL respectively. For standard of care the budget impact increased from €14.7m to €16.9m. Inclusion of MSL with a seed price of €100 showed a budget impact of €16.7m. Above a price of €178 the budget impact increased for adoption of MSL, rising to €17.6m when priced at €500.ConclusionMSL could be a cost-efficient localization technique in resecting non-palpable tumors in the Netherlands. The online calculation model can inform adoption decisions internationally. When determining retail price of the magnetic seed, cost-effectiveness should be considered. ]]> <![CDATA[Retrospective observational cohort study on innovation in oncology and progress in survival: How far have we gotten in the two decades of treating patients with advanced non-small cell lung cancer as a single population?]]> https://www.researchpad.co/article/elastic_article_13816 We assessed the impact of new antineoplastic agents on the overall survival (OS) of advanced non-small cell lung cancer (aNSCLC) patients followed up until 2012. Multivariate regression models were run for OS (outcome) and four proxies for innovation (exposure): Index (InnovInd, for SEER-Research data 1973–2012) and three levels of aggregation of Mean Medication Vintage, i.e. Overall (MMVOverall), using data aggregated at the State Level (MMVState), and using patient-level data (MMVPatient) using data from the US captured in SEER-Medicare 1991–2012. We derived Hazard ratios (HR) from Royston-Parmar models and odds ratios (OR) from a logistic regression on 1-year OS. Including 164,704 patients (median age 72 years, 56.8% stage IV, 61.8% with no comorbidities, 37.8% with adenocarcinoma, 22.9% with squamous-cell, 6.1% were censored). One-year OS improved from 0.22 in 1973 to 0.39 in 2012, in correlation with InnovInd (r = 0.97). Ten new NSCLC drugs were approved and 28 more used off-label. Regression-models results indicate that therapeutic innovation only marginally reduced the risk of dying (HROverall = 0.98 [0.98–0.98], HRMMV-Patient = 0.98 [0.97–0.98], and HRMMV-State = 0.98 [0.98–0.98], and slightly improved 1-year survival (ORMMV-Overall = 1.05 95%CI [1.04–1.05]). These results were validated with data from the Swedish National Health Data registers. Until 2013, aNSCLC patients were treated undifferentiated and the introduction of innovative therapies had statistically significant, albeit modest, effects on survival. Most treatments used off-guidelines highlight the high unmet need; however new advancements in treatment may further improve survival.

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<![CDATA[The COVID-19 Pandemic and its Impact on the Cardio-Oncology Population]]> https://www.researchpad.co/article/elastic_article_13340 The novel Coronavirus (2019-nCoV, COVID-19) is historically one of the most severe acute respiratory syndromes and pandemics to affect the globe in the twenty-first century. Originating in Wuhan, the virus rapidly spread and impacted subsets of populations with initial unclear risk factors contributing to worsening morbidity and mortality. Patients with diagnosis of cancer and undergoing treatment further represent a population at risk for worsening cardiopulmonary outcomes. This review explores specific risk factors, diagnoses, and treatment options that impact cardio-oncologic patients with COVID-19.Recent FindingsMultiple studies globally, including Italy, China, and the USA, have documented severe outcomes. Cancer patients are at increased risk of cardiac injury which itself is a risk factor for mortality. Additionally, elderly cancer patients undergoing recent anti-cancer treatment may be at greater risk for sustaining worse outcomes, although data remains suboptimal in this population. Major gaps remain regarding risk associated with type of cancer and type of anti-cancer treatment, as well as the layered risk of cardiovascular disease and cancer. Immunomodulatory therapies used to treat cytokine release syndrome secondary to anti-cancer therapies, as well as other agents being traditionally used to treat cardiovascular and cancer disease states, are being investigated for treatment of COVID-19.SummaryHypertension, cardiovascular disease, diabetes, and cancer have been associated with more severe COVID-19 infection and worse outcomes. Patients undergoing anti-cancer therapy or those who have suffered from coronavirus infection may develop long-standing changes, not limited to pulmonary fibrosis, hyperlipidemia, and worsening atherosclerosis. Those undergoing anti-cancer therapy are at theoretically increased susceptibility for infection, with type of cancer not necessarily dictating outcome. A review of the literature of patients with cardiovascular and/or cancer disease is presented, as well as proposed strategies to attenuate risk regarding treatment, management, and surveillance in this vulnerable population. ]]> <![CDATA[Downregulation of miR-22 Contributes to Epithelial-Mesenchymal Transition in Osteosarcoma by Targeting Twist1]]> https://www.researchpad.co/article/elastic_article_13089 The epithelial-mesenchymal transition (EMT) is a vital step in osteosarcoma (OS) progression toward metastasis, but the specific molecular events governing this process are incompletely characterized, with miRNAs having increasingly been found to regulate the EMT. In this study, We assessed levels of miR-22 and its target, Twist1, via real-time PCR (qRT-PCR). We further used functional proliferation assays, measures of cell morphology, and western blotting to assess the functional relevance of miR-22 in OS and confirmed Twist1 as a miR-22 target via luciferase reporter assay. We observed a significant decrease in miR-22 levels in OS tumor samples relative to normal tissue, with such downregulating being significantly associated with tumor histological grade. When overexpressed, miR-22 impaired OS cell proliferation and EMT progression. We found Twist1 to be a direct miR-22 target, with levels of miR-22 and Twist1 mRNA being inversely correlated in patient samples. When overexpressed, miR-22 suppressed Twist1 translation and thereby attenuated the EMT in OS cells. These results clearly demonstrate that miR-22 can regulate the EMT in OS cells via targeting Twist1, thus highlighting a potentially novel pathway that can be therapeutically targeted in order to treat OS.

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<![CDATA[Precision Medicine and the Role of Biomarkers of Radiotherapy Response in Breast Cancer]]> https://www.researchpad.co/article/elastic_article_13039 Radiotherapy remains an important treatment modality in nearly two thirds of all cancers, including the primary curative or palliative treatment of breast cancer. Unfortunately, largely due to tumor heterogeneity, tumor radiotherapy response rates can vary significantly, even between patients diagnosed with the same tumor type. Although in recent years significant technological advances have been made in the way radiation can be precisely delivered to tumors, it is proving more difficult to personalize radiotherapy regimens based on cancer biology. Biomarkers that provide prognostic or predictive information regarding a tumor's intrinsic radiosensitivity or its response to treatment could prove valuable in helping to personalize radiation dosing, enabling clinicians to make decisions between different treatment options whilst avoiding radiation-induced toxicity in patients unlikely to gain therapeutic benefit. Studies have investigated numerous ways in which both patient and tumor radiosensitivities can be assessed. Tumor molecular profiling has been used to develop radiosensitivity gene signatures, while the assessment of specific intracellular or secreted proteins, including circulating tumor cells, exosomes and DNA, has been performed to identify prognostic or predictive biomarkers of radiation response. Finally, the investigation of biomarkers related to radiation-induced toxicity could provide another means by which radiotherapy could become personalized. In this review, we discuss studies that have used these methods to identify or develop prognostic/predictive signatures of radiosensitivity, and how such assays could be used in the future as a means of providing personalized radiotherapy.

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<![CDATA[IGF-1 Interacted With Obesity in Prognosis Prediction in HER2-Positive Breast Cancer Patients]]> https://www.researchpad.co/article/elastic_article_13036 Purpose: Dysmetabolism and high circulating insulin-like growth factor 1 (IGF-1) would increase breast cancer risk, but its association with survival in HER2+ breast cancer patients has not been well-studied. Herein, we aim to evaluate the prognostic value of IGF-1 and metabolic abnormalities in HER2+ population.

Patients and Methods: HER2+ breast cancer patients treated in Ruijin Hospital between November 2012 and June 2017 were retrospectively analyzed. Median value of circulating IGF-1 was adopted to classify low or high IGF-1 group. Metabolic syndrome (MetS) was defined using AHA/NHLBI criteria. Overweight was defined by body mass index (BMI) ≥ 24.0 kg/m2 in Chinese population.

Results: Overall, 679 patients were included and 209 had synchronous MetS. High IGF-1 level was more common in pre/peri-menopausal women (P < 0.001) and high IGFBP-3 patients (P < 0.001). After a median follow-up of 36 months, 52 patients had disease recurrences. IGF-1 level was not associated with recurrence-free survival (RFS, P = 0.620) in the whole population. However, exploratory subgroup analysis found that BMI and IGF-1 interacted in predicting RFS (P = 0.009). For non-overweight patients, high IGF-1 showed a superior 4-years RFS (91.1 vs. 85.0%; HR 0.53, 95% CI 0.27–1.00, P = 0.049) compared with patients with low IGF-1 level. In contrast, for overweight patients, high IGF-1 was associated with an impaired 4-years RFS (88.3 vs. 95.7%, HR 3.20, 95% CI 1.00–10.21, P = 0.038). Furthermore, high IGF-1 level was independently associated with better OS in the whole (HR 0.26, 95% CI 0.08–0.82, P = 0.044) as well as non-overweight population (HR 0.15, 95% CI 0.03–0.68, P = 0.005).

Conclusions: IGF-1 level was not associated with RFS in HER2+ breast cancer patients. However, IGF-1 and BMI had significant interaction in disease outcome prediction in HER2+ patients. High IGF-1 was protective in non-overweight patients, but risk factor for those overweight, which deserves further evaluation.

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<![CDATA[The predictive value of PRDM2 in solid tumor: a systematic review and meta-analysis]]> https://www.researchpad.co/article/elastic_article_12811 Many studies have reported the presence of Positive Regulatory/Su(var)3-9, Enhancer-of-zeste and Trithorax Domain 2 (PRDM2) downregulation in cancer. However, its potential as a diagnostic biomarker is still unclear. Hence, a systematic review and meta-analysis were conducted to address this issue.IntroductionAs of 2018, cancer has become the second leading cause of death worldwide. Thus, cancer control is exceptionally vital in reducing mortality. One such example is through early diagnosis of cancer using tumor biomarkers. Having a function as a tumor suppressor gene (TSG), PRDM2 has been linked with carcinogenesis in several solid tumor. This study aims to assess the relationship between PRDM2 downregulation and solid tumor, its relationship with clinicopathological data, and its potential as a diagnostic biomarker. This study also aims to evaluate the quality of the studies, data reliability and confidence in cumulative evidence.Materials & MethodsA protocol of this study is registered at the International Prospective Register of Systematic Reviews (PROSPERO) with the following registration number: CRD42019132156. PRISMA was used as a guideline to conduct this review. A comprehensive electronic search was performed from inception to June 2019 in Pubmed, Cochrane Library, ProQuest, EBSCO and ScienceDirect. Studies were screened and included studies were identified based on the criteria made. Finally, data synthesis and quality assessment were conducted.ResultsThere is a significant relationship between PRDM2 downregulation with solid tumor (RR 4.29, 95% CI [2.58–7.13], P < 0.00001). The overall sensitivity and specificity of PRDM2 downregulation in solid tumors is 84% (95% CI [39–98%]) and 86% (95% CI [71–94%]), respectively. There is a low risk of bias for the studies used. TSA results suggested the presence of marked imprecision. The overall quality of evidence for this study is very low.DiscussionWe present the first meta-analysis that investigated the potential of PRDM2 downregulation as a diagnostic biomarker in solid tumor. In line with previous studies, our results demonstrated that PRDM2 downregulation occurs in solid tumor. A major source of limitation in this study is the small number of studies.ConclusionsOur review suggested that PRDM2 is downregulated in solid tumor. The relationship between PRDM2 downregulation and clinicopathological data is still inconclusive. Although the sensitivity and specificity of PRDM2 downregulation are imprecise, its high values, in addition to the evidence that suggested PRDM2 downregulation in solid tumor, hinted that it might still have a potential to be used as a diagnostic biomarker. In order to further strengthen these findings, more research regarding PRDM2 in solid tumors are encouraged. ]]> <![CDATA[Psychometric properties of self-reported financial toxicity measures in cancer survivors: a systematic review protocol using COSMIN methodology]]> https://www.researchpad.co/article/elastic_article_12548 Due to the higher costs associated with advancements in cancer treatment and longer duration of cancer survivorship, increasing financial toxicity has become a great threat to survivors, caregivers and public healthcare systems. Since accurate and reproducible measures are prerequisites for robust results, choosing an acceptable measure with strong psychometric properties to assess financial toxicity is essential. However, a description of the psychometric properties of existing measures is still lacking. The aim of this study is to apply COnsensus-based Standards for the selection of health Measurement INstruments (COSMIN) methodology to systematically review the content and structural validity of patient-reported outcome measures (PROMs) of financial toxicity for cancer survivors.Methods and analysisPubMed/Medline, Medline (Ovid), Embase (Ovid), CINAHL (EBSCO), Web of Science, ProQuest Dissertations and Theses, and Cochrane Library (Wiley) will be comprehensively searched from database inception to 15 November 2019. Studies that report the measurement properties of PROMs assessing financial toxicity for cancer survivors will be included. The evaluation of measurement properties, data extraction and data synthesis will be conducted according to the COSMIN methodology.Ethics and disseminationNo individual data are involved in this systematic review. The results will be disseminated to a clinical audience and policy-makers though peer-reviewed journals and conferences and will support researchers in choosing the best measure to evaluate the financial toxicity of cancer survivors. ]]> <![CDATA[Metastatic Neuroendocrine Carcinoma Presenting with Bilateral Axillary Lymphadenopathy]]> https://www.researchpad.co/article/elastic_article_11597 Metastatic, high-grade neuroendocrine carcinomas are frequently associated with small cell lung cancer (SCLC), classically spreading to the liver, bone, lung, and brain. Though SCLCs most commonly present as large masses interfering with the airway, this malignancy may appear initially as a benign mass at a distant site. This case profiles a 64-year-old woman who presented with bilateral breast masses that were identified as metastases of poorly differentiated, high-grade neuroendocrine SCLC through mammogram, ultrasound, CT, and core biopsy. Accurately identifying etiology of a breast malignancy is critical to therapeutic planning, as disparate treatment guidelines and disease courses exist for primary breast cancer and SCLC.

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<![CDATA[Cryosurgery Versus Primary Androgen Deprivation Therapy for Locally Recurrent Prostate Cancer After Primary Radiotherapy: A Propensity-Matched Survival Analysis]]> https://www.researchpad.co/article/elastic_article_11574 Background

Optimal management of isolated local recurrence of prostate cancer after primary radiotherapy remains to be defined. Up-front androgen deprivation therapy (ADT) is widely used but may adversely affect the quality of life and is essentially a palliative treatment. Local salvage carries a different side-effect profile and is potentially curative, but it has not been compared to ADT.

Materials and methods

We conducted a propensity-matched analysis of cohorts of men treated with either whole gland cryotherapy (CRYO) or primary ADT following the diagnosis of locally recurrent prostate cancer. Our specific objectives were to compare overall survival (OS) and prostate cancer-specific mortality (PCSM) between CRYO vs. ADT.

Results

After a one-to-one matching, 169 patients from each cohort were included in comparisons. Median follow-up time was 6.7 years (ADT) vs. 18 years (CRYO). The 10-year PCSM was 18.5% (ADT) vs. 16.2% (CRYO), which was not statistically different [hazard ratioo (HR): 0.69, 95% CI: 0.36-1.34, p=0.27]. The median OS was 12.3 years (CRYO) versus 10.2 years (ADT) (HR: 0.63, 95% CI: 0.42-0.95, p=0.03).

Conclusions

While PCSM was similar between the two strategies, CRYO was associated with a longer OS compared to primary ADT. Given the retrospective nature of the trial, these results should be considered hypothesis-generating, and phase III trials comparing these two options are required to further explore these findings.

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<![CDATA[Administration of lower doses of radium-224 to ankylosing spondylitis patients results in no evidence of significant overall detriment]]> https://www.researchpad.co/article/elastic_article_11232 The use of low doses of radium-224 (224Ra) chloride for the treatment of ankylosing spondylitis was stopped following the discovery that patients treated with it had a higher than control incidence of leukaemia and other cancers. This was so even though the treatment resulted in decreased pain and increased mobility–both of which are associated with decreased mortality. It was decided to re-analyze the epidemiological data looking at all causes of death. The risk of leukaemia, solid cancer, death from non-cancer causes and from all causes in a study populations of men that received either the typical dose of 5.6 to 11.1 MBq of 224Ra, any dose of 224Ra or no radium were compared using the Cox proportional hazard model. For patients that received the typical dose of 224Ra agreed with the excess cancer was similar to that reported in previous studies. In contrast, these patients were less likely to die from non-cancer diseases and from all causes of death than the control patients. No excess mortality was also found in the population of all males that received the radionuclide. It is concluded that 224Ra treatment administered at low doses to patients with ankylosing spondylitis did not impact mortality from all causes. The study demonstrates the need to consider all causes of death and longevity when assessing health impacts following irradiation.

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<![CDATA[A modified arginine-depleting enzyme NEI-01 inhibits growth of pancreatic cancer cells]]> https://www.researchpad.co/article/elastic_article_11227 Arginine deprivation cancer therapy targets certain types of malignancies with positive result in many studies and clinical trials. NEI-01 was designed as a novel arginine-depleting enzyme comprising an albumin binding domain capable of binding to human serum albumin to lengthen its half-life. In the present work, NEI-01 is shown to bind to serum albumin from various species, including mice, rat and human. Single intraperitoneal administration of NEI-01 to mice reduced plasma arginine to undetectable level for at least 9 days. Treatment of NEI-01 specifically inhibited cell viability of MIA PaCa-2 and PANC-1 cancer cell lines, which were ASS1 negative. Using a human pancreatic mouse xenograft model, NEI-01 treatment significantly reduced tumor volume and weight. Our data provides proof of principle for a cancer treatment strategy using NEI-01.

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<![CDATA[SMARCB1/INI1-Deficient Extrarenal Rhabdoid Tumor: A Case Report of a Rare and Aggressive Soft Tissue Sarcoma]]> https://www.researchpad.co/article/elastic_article_10708 Malignant SMARCB1/INI1-deficient extrarenal rhabdoid tumors are aggressive tumors that are extremely rare in adults. A 56-year-old male presented with the chief complaints of unilateral lower abdominal and pelvic pain. He underwent urgent surgical intervention and mass resection with tissue sampling. After pathology confirmed the diagnosis, systemic chemotherapy with vincristine, doxorubicin plus ifosfamide, and mesna was administered. Following treatment, he experienced a durable and long-lasting response to therapy for this aggressive and rare soft tissue sarcoma. To date, the patient remains in complete remission following the cessation of chemotherapy. Malignant SMARCB1/INI1-deficient extrarenal rhabdoid tumors are aggressive neoplasms that are extremely rare in adults. We report a rare case of such a tumor and review the literature for its molecular, clinical, and imaging features.

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<![CDATA[Coronavirus Disease 2019 (COVID-19) in Cancer Patients]]> https://www.researchpad.co/article/elastic_article_10705 The Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become the most talked-about clinical entity in early 2020. As an infection that spreads easily and has a significant mortality rate, it has caused global panic rarely seen before. Many of the measures taken by governments worldwide will have long-lasting impacts on the wellbeing of the population at large. It has been widely reported that the most vulnerable patients have been most negatively affected by SARS-CoV-2 (COVID-19). In this study, we have tried to search the currently available data on the outcomes of infected cancer patients. Most of the data points to the very challenging nature of treating such patients. Their overall outcomes seem to be worse than in the general population, and it may be difficult to differentiate which potential complications are a result of the primary oncologic disease versus the infection. Management presents its own set of challenges, including but not limited to, deciding whether postponing cancer treatment until the infection resolves is going to benefit the patient and how to organize all aspects of patient care when social contact is as limited as it is for patients newly diagnosed with COVID-19. We believe that as more data becomes available, it is going to be necessary to publish detailed guidelines on how to approach this unique clinical challenge.

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<![CDATA[Breast Cancer Metastasis Masquerading as a Primary Gynecological / Colonic Malignancy: A Rare Diagnostic Conundrum]]> https://www.researchpad.co/article/elastic_article_10540 Breast cancer is the most common malignancy affecting women. Metastatic involvement of the gastrointestinal (GI) tract secondary to a primary breast malignancy is rare. Here, we describe the case of a 60-year-old woman with a history of right lobular breast cancer (diagnosed and treated five years prior to presentation) who presented with fatigue, generalized abdominal pain, distension, weight loss, and vomiting. Her initial imaging was suspicious for a primary gynecological malignancy; however, subsequent workup showed a colonic mass. Total colonoscopy revealed colon metastases, and an immunohistochemical profile favored invasive lobular carcinoma of breast. Most cases of gastrointestinal metastases from breast cancer have lobular histology; however, colonic involvement is rare.

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<![CDATA[Complete Molecular Response in Chronic Myeloid Leukemia After Six Months of Imatinib: A Single Center Experience]]> https://www.researchpad.co/article/elastic_article_10506 Introduction: The hallmark of chronic myeloid leukemia (CML) is the development of the fusion gene, BCR-ABL which has unopposed tyrosine kinase activity. The first tyrosine kinase inhibitor (TKI) imatinib is claimed to have superior efficacy and side effect profile as compared to traditional treatment options. This study was conducted to see our patients’ molecular response to imatinib treatment. The objective of this study was to determine the frequency of complete molecular response in patients after six months of imatinib therapy.

Methods: A descriptive case series was designed and conducted in Oncology department, Jinnah hospital Lahore (May-November 2016). Newly diagnosed patients of CML aged between 20 and 65 years were enrolled. They were prescribed 400 mg imatinib daily and complete molecular response was assessed after six months of treatment.

Results: Mean age was 39.76 ± 9.072 years. Some 66 of them were males while 69 were females. Some 40 patients (29.6%) were found to be in complete molecular response after six months of imatinib therapy.

Conclusion: Imatinib at a dose of 400 mg/day is optimal as the primary therapy for CML.

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<![CDATA[Discoid Lupus Erythematosus Lesions Associated with Systemic Fluorouracil Agents: A Case Report and Review]]> https://www.researchpad.co/article/elastic_article_10497 Systemic fluorouracil agents include not only 5-fluorouracil (5FU), but also capecitabine, tegafur, and uracil/tegafur (UFT). Systemic lupus erythematosus (SLE), subacute cutaneous lupus erythematosus (SCLE), and discoid lupus erythematosus (DLE) are subtypes of lupus erythematosus; drug-induced lupus erythematosus can also present in each of these subtypes. This report describes the case of a 65-year-old woman with systemic 5FU-induced DLE. Fluorouracil agent-induced DLE lesions occurring after initiating treatment with either systemic 5FU or its prodrugs have been described in 19 individuals (Including the woman in this report) in the literature: tegafur (10 patients), UFT (six patients), systemic 5FU (two patients), and capecitabine (one patient). The mean duration before the appearance of the DLE lesions on sun-exposed areas was 232 days after beginning the fluorouracil agent; however, the much earlier (three weeks) appearance of the DLE lesions after starting systemic 5FU in the women described in this report may have occurred since there was no delay associated with the conversion of a precursor drug to 5FU. Within two months (mean: 36 days) after stopping the fluorouracil agent, the DLE lesions resolved in 95% of the patients. Laboratory studies were only performed on some of the patients. None of the patients tested had antibodies to Ro/Sjogren’s syndrome A (Ro/SSA) and La/Sjogren’s syndrome B (La/SSB). The antinuclear antibody (ANA) titer was elevated in 71% of the tested individuals and decreased in all of the patients who were evaluated after the causative drug was discontinued. The pathogenesis for fluorouracil agent drug-induced DLE remains to be definitively established.

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