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(searched for: doi:10.1097/coc.0b013e3181917158)
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J. Ristau, M. Thiel, S. Katayama, I. Schlampp, K. Lang, M. F. Häfner, K. Herfarth, J. Debus,
Published: 1 February 2021
Radiation Oncology, Volume 16, pp 1-9; https://doi.org/10.1186/s13014-021-01749-x

Abstract:
Background Radiation therapy and chemoradiation therapy play a major role in the definitive management of esophageal cancer. Survival in esophageal cancer patients is still relatively poor, mostly due to high rates of local recurrence and distant metastases. It is hypothesized that dose escalation in radiotherapy could improve outcomes. Therefore, this retrospective analysis aimed to investigate the outcomes and toxicity in patients treated with local dose escalation by means of using simultaneous integrated boost concepts. Methods Between 2012 and 2018, 101 patients with esophageal carcinoma were analyzed in this monocentric, retrospective study. All patients received definitive chemoradiation or radiation therapy alone as intensity modulated radiotherapy. The prescribed dose was 50.4 Gy in 28 fractions to the primary tumor and the elective lymph nodes as well as a simultaneous integrated boost (SIB) with 58.8 Gy to macroscopic tumor and lymph node metastases. Endpoints were overall survival (OS), progression free survival (PFS), local control rate (LCR) and toxicity. Results 60 patients (59.4%) received chemoradiation, 41 patients (40.6%) radiotherapy alone. The median follow up was 17 months (range 0–75 months). OS, PFS and LCR were at 63.9%, 53.9% and 59.9% after 1 year and 37.6%, 34.5% and 36.1%, respectively after 3 years. 16 patients (15.8%) in total developed a locoregional recurrence within the field of radiation. In 48 patients (47.5%) at least one grade III° (CTCAE) toxicity was documented during radiotherapy, mostly dysphagia (36 pat., 75%). One patient suffered from a grade IV° pneumonia. Conclusion This retrospective analysis demonstrates that a SIB concept in definitive (chemo)radiation therapy is safe and feasible, showing acceptable outcomes in this patient cohort. Considering that this cohort mainly consists of elderly patients not eligible for chemotherapy in many cases, we emphasize the aspect of SIB radiation therapy as potential partial compensation for omitted simultaneous chemotherapy. Prospective studies are needed for validation.
Sabrina M Saeed, Samer Naffouje, Rutika Mehta, Sarah E Hoffe, Jacques P Fontaine, Gregory Y Lauwers, Parth Shah, Jessica Frakes,
Diseases of the Esophagus, Volume 34; https://doi.org/10.1093/dote/doaa099

Abstract:
Background Esophageal squamous cell carcinoma (ESCC) has been linked to superior pathologic treatment response compared to esophageal adenocarcinoma (EAC) after neoadjuvant chemoradiation. However, the impact of histology on survival remains unclear. It has been suggested, based on epidemiologic similarities, that distal EAC should be grouped with gastric cancers as an entity distinct from distal ESCC, but there is little data to support this recommendation. We therefore aim to compare pathologic treatment response (PTR) and overall survival (OS) in patients with distal EAC versus distal ESCC. Methods This retrospective cohort study included patients who underwent esophagectomy for distal esophageal malignancy. Histologic sub-groups were matched (1:1) using a propensity-score matching approach. Pre-operative clinical parameters, oncologic outcomes and survival were compared between groups. Results 1031 distal EC patients, with a median age of 64.4 years and a male preponderance (86.5%), underwent esophagectomy at our institution between 1999 and 2019. 939 (91.1%) patients had a diagnosis of EAC and 92 (8.9%) had ESCC. A higher proportion of ESCC patients were female (26.1% vs. 12.1%; P < 0.01) and non-white (12.0% vs. 3.8%; P < 0.01). Propensity-score sub-analysis identified 75 matched pairs. Rates of pathologic complete response (58.0% vs. 48.9%; P = 0.67) and OS (43.0 vs. 52.0 months; P = 0.808) were not significantly different between matched groups. Conclusions Although traditionally known to have a better overall PTR compared to EAC, ESCC patients in our large series did not show any improvement in PTR or OS. Treatment recommendations for patients with EAC and ESCC should consider tumor location in addition to histology.
, Dhanpat Jain
Annals of the New York Academy of Sciences, Volume 1482, pp 163-176; https://doi.org/10.1111/nyas.14462

The publisher has not yet granted permission to display this abstract.
, Lawrence F. Borges
The SAGES Manual of Foregut Surgery pp 329-338; https://doi.org/10.1007/978-3-319-96122-4_26

The publisher has not yet granted permission to display this abstract.
Hui Qin, Yunyun Li, Hongyan Zhang, Feng Wang, Hong-Liu He, Xue Bai, Shan-Shan Li
Published: 1 March 2019
OncoTargets and Therapy, pp 1917-1927; https://doi.org/10.2147/ott.s190145

Abstract:
Background: The MYBL2 gene, a highly conserved member of the Myb transcription-factor family, has been implicated in the genesis and progression of many types of tumors. Methods: We analyzed the expression of MYBL2 and Ki67 in tissue samples of esophageal squamous-cell carcinoma (ESCC) patients by immunohistochemistry. We further analyzed the effect of MYBL2 on cell proliferation and DNA replication using a CCK8 assay, 5-ethynyl- 2'-deoxyuridine–retention assay, flow-cytometry analysis, real-time quantitative PCR, Western blot, and a xenograft model of ESCC cells in nude mice. Results: MYBL2 expression was significantly higher in ESCC tissue when compared to the adjacent normal tissue (P=0.007). MYBL2 was found to be positively correlated with Ki67 (γ=0.286, P=0.003). Furthermore, Kaplan–Meier curves indicated that MYBL2 expression in ESCC tissue was associated with poor patient outcome (P<0.001), with MYBL2-positive patients who exhibited high Ki67 expression in ESCC tissue showing the worst prognosis for overall survival (P=0.003). Our in vitro results showed that downregulation of MYBL2 in ESCC cell lines inhibited cell proliferation and DNA replication (P<0.05 for both). We also found that loss of MYBL2 caused a reduction in levels of cell cycle-related G2/M proteins CDK1 and cyclin B1 in ESCC cells. In contrast, overexpression of MYBL2 caused an increase in these proteins. In vivo, we found that in nude mice that received cells knocked down for MYBL2, tumor growth was inhibited in comparison to the group that received control cells (P<0.05). Conclusion: MYBL2 overexpression induces tumor proliferation in ESCC cells by regulating cell-cycle at the S and G2/M phase. Therefore, MYBL2 may serve as a novel prognostic biomarker in ESCC patients.
Douglas Z. Liou, Leah M. Backhus, Natalie S. Lui, ,
The Journal of Thoracic and Cardiovascular Surgery, Volume 155, pp 2697-2707; https://doi.org/10.1016/j.jtcvs.2017.12.136

The publisher has not yet granted permission to display this abstract.
, Mathieu Laversanne, Linda Morris Brown, Susan S Devesa,
American Journal of Gastroenterology, Volume 112, pp 1247-1255; https://doi.org/10.1038/ajg.2017.155

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, Wenle Tan, Zhiqiang Ling, , Mingming Shao, , Yingying Luo, Yanjie Zhao, Yun Liu, Xiancong Huang, et al.
Published: 26 May 2017
Nature Communications, Volume 8; https://doi.org/10.1038/ncomms15290

Abstract:
Approximately half of the world’s 500,000 new oesophageal squamous-cell carcinoma (ESCC) cases each year occur in China. Here, we show whole-genome sequencing of DNA and RNA in 94 Chinese individuals with ESCC. We identify six mutational signatures (E1–E6), and Signature E4 is unique in ESCC linked to alcohol intake and genetic variants in alcohol-metabolizing enzymes. We discover significantly recurrent mutations in 20 protein-coding genes, 4 long non-coding RNAs and 10 untranslational regions. Functional analyses show six genes that have recurrent copy-number variants in three squamous-cell carcinomas (oesophageal, head and neck and lung) significantly promote cancer cell proliferation, migration and invasion. The most frequently affected genes by structural variation are LRP1B and TTC28. The aberrant cell cycle and PI3K-AKT pathways seem critical in ESCC. These results establish a comprehensive genomic landscape of ESCC and provide potential targets for precision treatment and prevention of the cancer.
, Patrick Michl
Published: 7 April 2017
Digestion, Volume 95, pp 253-261; https://doi.org/10.1159/000464130

Abstract:
Esophageal cancer represents a heterogeneous malignancy mostly diagnosed in advanced stages. Worldwide, squamous cell carcinomas (SCCs) continue to be the most prevalent subtype; however, in the Western countries, the incidence of adenocarcinomas is increasing and will exceed that of SCC in the near future. During the last decade, several landmark trials contributed to a better understanding of the disease and emphasized the importance of multimodal treatment protocols.
Published: 1 August 2016
Thoracic Surgery Clinics, Volume 26, pp 295-304; https://doi.org/10.1016/j.thorsurg.2016.04.006

The publisher has not yet granted permission to display this abstract.
Hai-De Qin, , Yuan-Bin Chen, Shao-Yi Huang, Wen-Qiong Xue, Fang-Fang Li, Xiao-Song Ge, De-Qing Liu, Qiuyin Cai, Jirong Long, et al.
The American Journal of Human Genetics, Volume 98, pp 709-727; https://doi.org/10.1016/j.ajhg.2016.02.021

Abstract:
The genetic mechanisms underlying the poor prognosis of esophageal squamous cell carcinoma (ESCC) are not well understood. Here, we report somatic mutations found in ESCC from sequencing 10 whole-genome and 57 whole-exome matched tumor-normal sample pairs. Among the identified genes, we characterized mutations in VANGL1 and showed that they accelerated cell growth in vitro. We also found that five other genes, including three coding genes (SHANK2, MYBL2, FADD) and two non-coding genes (miR-4707-5p, PCAT1), were involved in somatic copy-number alterations (SCNAs) or structural variants (SVs). A survival analysis based on the expression profiles of 321 individuals with ESCC indicated that these genes were significantly associated with poorer survival. Subsequently, we performed functional studies, which showed that miR-4707-5p and MYBL2 promoted proliferation and metastasis. Together, our results shed light on somatic mutations and genomic events that contribute to ESCC tumorigenesis and prognosis and might suggest therapeutic targets.
, Thomas R. Mccarty, John W. Birk
Journal of Gastroenterology and Hepatology, Volume 31, pp 1141-1146; https://doi.org/10.1111/jgh.13289

The publisher has not yet granted permission to display this abstract.
, Luise Meurer, Antônio Barros Lopes, Luis C.M. Antunes, Sara Vanazzi, Renato B. Fagundes
Applied Immunohistochemistry & Molecular Morphology, Volume 22, pp 669-673; https://doi.org/10.1097/pai.0000000000000011

Abstract:
Squamous cell carcinoma of the esophagus is a lethal cancer and carries a poor prognosis because of late diagnosis. Identification of molecular markers may aid early diagnosis. We assessed the expression of CDKN2A/RB1 in the esophageal mucosa and its association with the histology. Esophageal biopsies were collected from 38 patients with no esophageal lesion (group 1), from iodine-negative areas of 108 alcoholics/smokers (group 2), and from tumor and nontumor areas in 41 patients with squamous cell carcinoma (group 3). The histologic diagnosis was compared with immunoexpression of CDKN2A/RB1. In group 1, histology showed normal mucosa/mild esophagitis and no expression of CDKN2A/RB1. In groups 2 and 3, the diagnosis was: normal mucosa (38.4%), esophagitis (44.4%), dysplasia and carcinoma in situ (2.8%), and carcinoma (14.3%). The immunoexpression of CDKN2A/RB1 increased in a stepwise manner from the normal mucosa, to esophagitis, dysplasia/carcinoma in situ, and carcinoma (P<0.01). CDKN2A/RB1 was not expressed in the esophageal mucosa of patients without risk factors. p16/pRb expression increased in a stepwise manner, according to the severity of histologic lesions, in biopsies from patients exposed to risk factors or with carcinoma. Esophageal mucosa exposed to risk factors with the expression of those proteins may be at risk for malignant transformation.
Journal of Thoracic Disease, Volume 6; https://doi.org/10.3978/j.issn.2072-1439.2014.03.11

Abstract:
Survival of esophageal cancer is improving but remains poor. Esophageal cancer stage is based on depth of tumor invasion, involvement of regional lymph nodes, and the presence or absence of metastatic disease. Appropriate work-up is critical to identify accurate pre-treatment staging so that both under-treatment and unnecessary treatment is avoided. Treatment strategy should follow guideline recommendations, and generally should be developed after multidisciplinary evaluation.
Yoshifumi Baba
World Journal of Gastrointestinal Oncology, Volume 6, pp 121-8; https://doi.org/10.4251/wjgo.v6.i5.121

Abstract:
Squamous cell carcinoma and adenocarcinoma are types of esophageal cancer, one of the most aggressive malignant diseases. Since both histological types present entirely different diseases with different epidemiology, pathogenesis and tumor biology, separate therapeutic strategies should be developed against each type. While surgical resection remains the dominant therapeutic intervention for patients with operable esophageal squamous cell carcinoma (ESCC), alternative strategies are actively sought to reduce the frequency of post-operative local or distant disease recurrence. Such strategies are particularly sought in the preoperative setting. Currently, the optimal management of resectable ESCC differs widely between Western and Asian countries (such as Japan). While Western countries focus on neoadjuvant or definitive chemoradiotherapy, neoadjuvant chemotherapy followed by surgery is the standard treatment in Japan. Importantly, each country and region has established its own therapeutic strategy from the results of local randomized control trials. This review discusses the current knowledge, available data and information regarding neoadjuvant treatment for operable ESCC.
Zhensheng Wang, Michael Goodman, Nabil Saba, Bassel F. El-Rayes
Published: 20 August 2013
Cancer, Volume 119, pp 4020-4027; https://doi.org/10.1002/cncr.28313

Abstract:
BACKGROUND The objective of this study was assess differences in the incidence, late‐stage diagnosis, and prognosis of squamous cell carcinoma of the esophagus (SCCE), adenocarcinoma of the esophagus (AE), and adenocarcinoma of the gastric cardia (AGC) in metropolitan, urban, and rural areas in the United States. METHODS The authors identified 29,527 patients with SCCE, AE, or AGC who were reported to the Surveillance, Epidemiology, and End Results Program between 2004 and 2009. Incidence estimates for each malignancy were compared across metropolitan, urban, and rural areas. Multivariable logistic regression models were applied to evaluate the association between residential setting and late (distant‐stage) diagnosis, and the results were reported as adjusted odds ratios and 95% confidence intervals (CIs). Cox proportional hazard models were used to examine the association between residential setting and cause‐specific survival. RESULTS When residential setting was analyzed using metropolitan population centers as the reference category, the incidence of AE was higher in urban areas (rate ratio [RR], 1.13; 95% CI, 1.06‐1.20) and rural areas (RR, 1.15; 95% CI, 1.05‐1.25), whereas the incidence of SCCE was lower in rural areas (RR, 0.80; 95% CI, 0.70‐0.91). Rural patients were less likely to be diagnosed with stage IV AE compared with patients residing in metropolitan areas (odds ratio, 0.79; 95% CI, 0.65‐0.97). No differences in prognosis were observed when patients from large metropolitan centers were compared with their rural counterparts. CONCLUSIONS The current findings indicated that preconceptions regarding disparities in the time of diagnosis and survival between patients from metropolitan and rural areas in the United States are either unwarranted or out of date, at least with respect to gastroesophageal cancers. Cancer 2013;119:4020–4027. © 2013 American Cancer Society.
, Renato A. Luna,
Seminars in Thoracic and Cardiovascular Surgery, Volume 24, pp 275-287; https://doi.org/10.1053/j.semtcvs.2012.11.001

The publisher has not yet granted permission to display this abstract.
, Bruce D. Greenwald
Published: 17 January 2013
Digestive Diseases and Sciences, Volume 58, pp 1477-1485; https://doi.org/10.1007/s10620-012-2554-0

The publisher has not yet granted permission to display this abstract.
Radiation Oncology (London, England), Volume 7, pp 60-60; https://doi.org/10.1186/1748-717X-7-60

Abstract:
Treatment options for oesophageal cancer have changed considerably over the last decades with the introduction of multimodal treatment concepts dominating the progress in the field. However, it remains unclear in how far the documented scientific progress influenced and changed the daily routine practice. Since most patients with oesophageal cancer generally suffer from reduced overall health conditions it is uncertain how high the proportion of aggressive treatments is and whether outcomes are improved substantially. In order to gain insight into this we performed a retrospective analysis of patients treated at a larger tertiary referral centre over time course of 25 years. Data of all patients diagnosed with squamous cell carcinoma (SCC) and adenocarcinoma (AC) of the oesophagus, treated between 1983 and 2007 in the department of radiation oncology of the LMU, were obtained. The primary endpoint of the data collection was overall survival (calculated from the date of diagnosis until death or last follow up). Changes in basic clinical characteristics, treatment approach and the effect on survival were analysed after dividing the cohort into five subsequent time periods (I-V) with 5 years each. In a second analysis any pattern of change regarding the use of radio(chemo)therapy (R(C)T) with and without surgery was determined. In total, 503 patients with SCC (78.5%) and AC (18.9%) of the oesophagus were identified. The average age was 60 years (range 35-91 years). 56.5% of the patients were diagnose with advanced UICC stages III-IV. R(C)T was applied to 353 (70.2%) patients; R(C)T+ surgery was performed in 134 (26.6%) patients, 63.8% of all received chemotherapy (platinum-based 5.8%, 5-fluorouracil (5-FU)12.1%, 42.3% 5-FU and mitomycin C (MMC)). The median follow-up period was 4.3 years. The median overall survival was 21.4 months. Over the time, patients were older, the formal tumour stage was more advanced, the incidence of AC was higher and the intensified treatment had a higher prevalence. However there was only a trend for an improved OS over the years with no difference between RCT with or without surgery (p = 0.09). The use of radiation doses over 54 Gy and the addition of chemotherapy (p = 0.002) were associated with improved OS. Although more complex treatment protocols were introduced into clinical routine, only a minor progress in OS rates was detectable. Main predictors of outcome in this cohort was the addition of chemotherapy. The addition of surgery to radio-chemotherapy may only be of value for very limited patient groups.
Published: 26 May 2011
Radiation Oncology, Volume 6, pp 55-55; https://doi.org/10.1186/1748-717x-6-55

Abstract:
Since the 1980s major advances in surgery, radiotherapy and chemotherapy have established multimodal approaches as curative treatment options for oesophageal cancer. In addition the introduction of functional imaging modalities such as PET-CT created new opportunities for a more adequate patient selection and therapy response assessment. The majority of oesophageal carcinomas are represented by two histologies: squamous cell carcinoma and adenocarcinoma. In recent years an epidemiological shift towards the latter was observed. From a surgical point of view, adenocarcinomas, which are usually located in the distal third of the oesophagus, may be treated with a transhiatal resection, whereas squamous cell carcinomas, which are typically found in the middle and the upper third, require a transthoracic approach. Since overall survival after surgery alone is poor, multimodality approaches have been developed. At least for patients with locally advanced tumors, surgery alone can no longer be advocated as routine treatment. Nowadays, scientific interest is focused on tumor response to induction radiochemotherapy. A neoadjuvant approach includes the early and accurate assessment of clinical response, optimally performed by repeated PET-CT imaging and endoscopic ultrasound, which may permit early adaption of the therapeutic concept. Patients with SCC that show clinical response by PET CT are considered to have a better prognosis, regardless of whether surgery will be performed or not. In non-responding patients salvage surgery improves survival, especially if complete resection is achieved.
Annals of Oncology, Volume 21; https://doi.org/10.1093/annonc/mdq294

Abstract:
Due to the poor prognosis of patients after unimodal therapy like surgical resection or radiotherapy multidisciplinary treatment is regarded as standard of care in localized esophageal cancer. Within the last decade phase III trials investigating the curative potential of radiochemotherapy alone have challenged surgery to be an indispensible part of curative therapy. Nevertheless, surgical resection does play an important role in the multidisciplinary treatment. But its role is limited to subgroups of patients with a distinct clinical situation. Today it appears that particularly patients with adenocarcinomas of the lower esophagus and esophagogastric junction and those patients with squamous cell carcinomas not responding to induction chemo- or radiochemotherapy benefit from surgery. Patient selection according to their individual operative risk is most important to guide multidisciplinary therapy. Early molecular or diagnostic markers to predict response to chemo- or radiotherapy and also recurrence despite complete surgical resection are urgently needed.
, Michael Bergqvist, Roger Tell, Stefan Bergström, Johan Lennartsson
Expert Opinion on Therapeutic Targets, Volume 14, pp 317-328; https://doi.org/10.1517/14728221003621278

Abstract:
Oesophageal carcinoma has a poor prognosis with a 5-year overall survival rate of only 10 - 20%. The disease is often diagnosed at a late stage, when dissemination may already have occurred, contributing to the poor prognosis. However, recent developments in targeted therapy now offer new possibilities in the treatment arsenal. Heat shock protein 90 (Hsp90) has been demonstrated to protect oncogenic variants of signalling molecules from degradation, thus promoting cell growth and survival. Hsp90 has been found to be abundantly expressed in oesophageal cancer and may serve as a therapeutic target in the treatment of this disease. We have summarised available data concerning the role of Hsp90 in oesophageal carcinoma as well as available information on other tumour types. To be able to elaborate on the molecular mechanisms of action of Hsp90 and discuss state-of-the-art of clinical trials involving Hsp90 inhibitors in malignancies, with a special emphasis on oesophageal cancer. Preclinical studies on Hsp90 inhibition in oesophageal cancer are promising and it is anticipated that in the near future clinical trials with Hsp90 inhibitors will be initiated also for oesophageal cancer, using the experience from other trials.
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