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Purpose This article examines ways COVID-19 health surveillance and algorithmic decision-making (“ADM”) are creating and exacerbating workplace inequalities that impact post-treatment cancer survivors. Cancer survivors’ ability to exercise their right to work often is limited by prejudice and health concerns. While cancer survivors can ostensibly elect not to disclose to their employers when they are receiving treatments or if they have a history of treatment, the use of ADM increases the chances that employers will learn of their situation regardless of their preferences. Moreover, absent significant change, inequalities may persist or even expand. Methods We analyze how COVID-19 health surveillance is creating an unprecedented amount of health data on all people. These data are increasingly collected and used by employers as part of COVID-19 regulatory interventions. Results The increase in data, combined with the health and economic crisis, means algorithm-driven health inequalities will be experienced by a larger percentage of the population. Post-treatment cancer survivors, as for people with disabilities generally, are at greater risk of experiencing negative outcomes from algorithmic health discrimination. Conclusions Updated and revised workplace policy and practice requirements, as well as collaboration across impacted groups, are critical in helping to control the inequalities that flow from the interaction between COVID-19, ADM, and the experience of cancer survivorship in the workplace. Implications for Cancer Survivors The interaction among COVID-19, health surveillance, and ADM increases exposure to algorithmic health discrimination in the workplace.

Although patients with early localized prostate cancer can survive longer, castration-resistant prostate cancer (CRPC) has gradually emerged with the use of androgen deprivation therapy (ADT). N-Myc and TEM8 play a vital role in the progression of several cancer types. However, the underlying mechanism of how N-Myc and TEM8 promote the progression of prostate cancer remains unclear. In this study, the expression of N-Myc and TEM8 was detected in benign prostatic hyperplasia (BPH) and prostate cancer (PCa) tissues by immunohistochemistry (IHC). LNCaP cell lines were maintained in RPMI 1640 medium supplemented with 10% charcoal-stripped fetal bovine serum. Subsequently, R language software was used to verify our results. Tubule formation assay of human umbilical vein endothelial cell (HUVEC) was conducted to examine the effect of N-Myc and TEM8 overexpression on angiogenesis in prostate cancer cells. IHC results showed a positive correlation between the expression of N-Myc and TEM8 in prostate cancer tissues. Further analysis showed that N-Myc and TEM8 were associated with clinicopathological features and poor prognosis in prostate cancer patients. Moreover, the overexpression of N-Myc and TEM8 promoted proliferation of prostate cancer cells and angiogenesis. Additionally, N-Myc and TEM8 overexpression was associated with therapeutic resistance. We further found that N-Myc promoted angiogenesis and therapeutic resistance in prostate cancer via TEM8. Hence, targeting N-Myc/TEM8 pathway in prostate cancer would be a novel therapeutic strategy to enhance the treatment of prostate cancer patients.

Although the etiology of most childhood cancers remains elusive, pediatric oncologists find themselves in the paradoxical situation of having effective therapy at hand for about 50% of all malignancies that afflict children. Thus, we are curing leukemia and osteogenic sarcoma before we have a clue as to the cause. That statement isn’t entirely accurate because we are now aware of a number of associated genetic conditions, immune deficiency states (Kersey et al., 1973), chromosomal abnormalities, congenital malformations (Bolande, 1977), and environmental events that may predispose a child to cancer or significantly increase the risk of developing a malignancy. Foremost on the list of predisposing causes are such diverse disorders as (1) aniridia-Wilms* tumor syndrome; (2) chromosomal instability syndromes (Fanconi1s anemia, Bloom’s syndrome, ataxia-telangiectasia) and leukemia; (3) 21-tri-somy and leukemia; (4) immune deficiency diseases (severe combined immune deficiency disease (SCID), Wiskott-Aldrich syndrome, ataxia-telangiectasia and lymphoma; and (5) multimodality therapy (alkylating agents and radiation therapy) in Hodgkin’s disease or non-Hodgkin’s lymphoma followed by a second malignant neoplasm, acute non-lymphocytic leukemia.

Collision tumor is the occurrence of two histologically and morphologically distinct tumors within the same organ with no histological admixture. Collision tumors of the thyroid are extremely rare constituting

Oral therapies have highly modified cancer patient management and changed hospital practises. We introduce a specific Oral Therapy Centre and retrospectively review information prospectively recorded by co-ordination nurses (CNs) (the DICTO programme). We describe the roles played by CNs in the management of oral cancer therapies at Limoges Dupuytren Hospital between May 2015 and June 2018. All cancers, irrespective of stage or whether oral general chemotherapy or targeted therapy was prescribed, are included. We followed up 287 patients of median age 67 years (range 26–89 years). Of these, 76% had metastases and 44% were on first-line therapy. The vast majority (88%) of their first CN contacts occurred just after physician consultation and lasted an average of 60 min. As part of follow-up, the CNs made 2719 calls (average 10 min) to patients to educate them and to verify compliance and drug tolerance. They also received 833 calls from patients (70%) or their relatives or health professionals (30%) seeking advice on management of side effects. In addition to the initial appointments, 1069 non-scheduled follow-up visits were made to assess side effects (49.2%). The CNs devoted 5 h to each patient over 3 months of treatment (i.e. 25 min/day) and, also organised scheduled hospitalisations in the department of oncology for 51% of patients. We show the interest and real-life work in a specific oral therapy centre within oncology department with the role of CNs to facilitate the global health care of the patients. Electronic supplementary material The online version of this article (10.1007/s12032-020-01393-7) contains supplementary material, which is available to authorized users.

Gastric cancer is an important disease due to its high mortality. Despite the decline in frequency, most cases are discovered late in its course, and most of the cancer patients die within a few years of diagnosis. In addition to Helicobacter pylori gastritis, gastrin is considered an important factor in the development of this disease, and thus, cholecystokinin-B receptor (CCKBR) becomes of interest. The aim of our study was to explore whether CCKBR is expressed in stomach cancers. Thirty-seven tumors from 19 men and 18 women diagnosed with either adenocarcinoma or neuroendocrine neoplasm (NENs) were included in this study. The tumors were classified into 29 adenocarcinomas and eight NENs. Immunohistochemistry with antibodies against chromogranin A (CgA), synaptophysin and CCKBR, and in situ hybridization with probes against CgA, CCKBR and histidine decarboxylase were used to further explore these tumors. Thirty-three (89%) of the tumors expressed CCKBR protein, whereas only 20 (54%) of all tumors expressed CCKBR mRNA. Of the 20 tumors expressing CCKBR mRNA, eight were NENs and 12 were adenocarcinoma. The highest amount of CCKBR was expressed in NEN. Interestingly, a high degree of co-expression of CCKBR and CgA was observed when the two markers were examined together with in situ hybridization. In conclusion, we found that all eight NENs expressed CCKBR and neuroendocrine markers in a majority of tumor cells. The same markers were also expressed in a proportion of adenocarcinomas supporting the view that gastrin is important in the development of gastric cancer. © The Author(s) 2017. Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/).

India has one of the highest incidences of oral squamous cell carcinoma (OSCC), with 75,000–80,000 new cases a year. The outcome in early oral cancer is better, but a significant proportion (12–14%) of these patients still relapses and dies due to locoregional or distant recurrences. Several clinicopathological and molecular factors have been used to prognosticate and predict outcomes in these patients of OSCC. The present study aims to validate Brandwein Gensler (BG) risk predictive model in surgically treated OSCC patients in a tertiary care centre in North India. All oral cavity cancer patients, treated in the Department of Surgical Oncology, King George’s Medical University, between 2013 and 2017, were reviewed. Patients with histologically diagnosed OSCC, aged > 18 years undergoing primary surgical resection were included in the study. The final histopathological evaluation was done by a dedicated pathologist to categorize patients according to BG model risk categories. This model comprises of three factors, lymphocytic host response, perineural invasion and worst pattern of invasion, scored by the method described by Brandwein Gensler et al. The sum of these scores is used to define low, moderate and high risk categories. The study, conducted during 2013–2017, included 149 patients. Median age was 45 years (range 25–75 years). Tobacco use was noted in 143 patients. Buccal mucosa was the most common site (51%). Surgical margins were clear (> 5 mm) in 97.9% cases. Postoperative radiotherapy was given in 47.7% patients. Locoregional recurrences (LRR) (primary site and neck) were documented in 17 of the 149 patients (11.4%). There was no synchronous or metachronous distant metastasis noted in any of the study patients. Six patients had disease specific mortality. Among the 17 patients with LRR, majority (11) belonged to the high risk category of the BG risk model. Adjuvant radiotherapy had been administered in 10 of these 11 recurrent patients belonging to the high risk category. The Brandwein Gensler risk model is predictive of locoregional recurrences (p = 0.02) for OSCC undergoing primary surgery. It can be used to devise strategies to prevent recurrences or identification of recurrences at an earlier point for salvage. The benefit of further escalation of adjuvant therapy in the high risk category needs further studies, as 90% patients in this group recurred despite complete adjuvant treatment.

Depth of invasion (DOI) and tumour thickness (TT) are known prognostic indicators in oral squamous cell carcinoma (OSCC), but varying definitions have been used by pathologists for reporting. The American Joint Committee on Cancer (AJCC) has proposed adoption of a uniform definition of DOI and incorporated this measurement in the revised TNM staging (8th edition); however, unambiguous DOI determination can be a challenge in clinical practice. We reviewed archived slides of 95 cases of T1/T2N0 OSCC and listed the challenges in accurate DOI measurement with pictographical documentation. The impacts of DOI and TT on disease-free survival (DFS) were also assessed. The mean DOI and TT was 5.89 mm and 7.32 mm respectively. Challenge in horizon estimation for DOI measurement was experienced in 75/95 cases (78.9%). The most common challenges were lack of adjacent uninvolved mucosa in sections or presence only on one side, rounded/convoluted nature of the tumour surface for tongue and polypoidal tumours, and angulation of adjacent mucosa for alveolar or lip tumours. In cases with very thin epithelium, DOI was equal to TT. In spite of the challenges, Kaplan–Meier analysis showed DOI > 5 mm significantly predicted poorer DFS while TT did not. We recommend various guidelines to help improve consistency in measuring DOI and recording of TT in ambiguous cases for accurate staging of OSCC.

Tobacco smoking is associated with adverse health effects among people living with HIV (PLWH), including a higher risk of cancer and cardiovascular problems. Further, there is evidence that PLWH are two to three times more likely to smoke than the general population. The aim of this study was to examine the association between tobacco smoking and biomarkers of HIV disease progression, including unsuppressed viral load (viral load >200 copies/mL) and low CD4 cell count (

Failure to comply with treatment recommendations is very common in patients, but still poorly recognised by doctors. The current practice of using oral therapy on a large scale has been increasingly adopted for cancer patients. Chronic myeloid leukaemia (CML) is just such an example, where the introduction of taking new oral medications, the tyrosine kinase BCR-ABL inhibitors (TKI), has now revolutionised the treatment. The aim of our study was to assess treatment adherence in a group of Polish CML patients (a survey was conducted on 140 patient aged ≥18 years) treated with oral TKI (imatinib, dasatinib and nilotinib) taking into account the following variables: gender, age, education, place of residence, family circumstances and duration of therapy. In addition, we evaluated whether there is a relationship between how patients perceive their level of adherence to treatment recommendations with how subjectively the required dosage regimen was followed. Half the patients admitted to skipping at least one drug dose during the entire course of treatment and 39% did so within their last treatment month. Patients were also found to overestimate their own adherence assessment; around 60% of those missing at least 1 drug dose within the last treatment month believed they ‘always’ followed recommendations. The study demonstrated that adherence deteriorates over time. Furthermore, patients aged >65 years and patients suffering at least one comorbid disease had better adherence (p

Human brain tissue contains various alcohol dehydrogenase (ADH) isoenzymes and possess also aldehyde dehydrogenase (ALDH) activity. In our last experiments we have shown that ADH and ALDH are present also in the brain tumour cells. Moreover the activities of total ADH and class I isoenzymes were significantly higher in cancer tissue than healthy cells. It can suggests that these changes may be reflected by enzyme activity in the serum of patients with brain cancer. Serum samples were taken for routine biochemical investigation from 62 patients suffering from brain cancer (36 glioblastoma, 26 meningioma). For the measurement of the activity of class I and II ADH isoenzymes and ALDH activity, the fluorometric methods were used. The total ADH activity and activity of class III and IV isoenzymes were measured by the photometric method. A statistically significant increase of class I alcohol dehydrogenase isoenzymes was found in the sera of patients with brain cancer. The median activity of this class isoenzyme in the patients group increased about 24 % in the comparison to the control level. The total alcohol dehydrogenase activity was also significantly higher (26 %) among patients with brain tumour than healthy ones. The activities of other tested ADH isoenzymes and total ALDH were unchanged. The increase of the activity of total ADH and class I alcohol dehydrogenase isoenzyme in the sera of patients with brain cancer seems to be caused by the release of this isoenzyme from tumour’s cells.

Previous studies of pancreatic ductal adenocarcinoma (PDAC) have demonstrated that the addition of tumor grade to the 7th American Joint Committee on Cancer (AJCC) staging can provide improved prognostication and that the recently proposed 8th edition AJCC staging exhibited superior reproducibility to the 7th edition in resectable PDAC. Thus, we aimed to combine tumor grade and 8th AJCC stage to develop a refined staging scheme for resectable PDAC. We analyzed 7719 patients with resectable PDAC from the 2004-2012 Surveillance, Epidemiology, and End Results database. We performed recursive partitioning analysis (RPA) to objectively incorporate tumor grade with 8th AJCC stage into a novel staging system. The performance of the proposed RPA staging was assessed against the 8th AJCC staging in terms of discriminatory ability and prognostic homogeneity. For each 8th AJCC stage, survival was significantly worse for high-grade versus low-grade tumors. RPA divided resectable PDAC into five stages: RPA-IA (low-grade T1N0), RPA-IB (high-grade T1N0 or low-grade T2N0), RPA-IIA (high-grade T2N0 or low-grade T3N0/T1-T3N1), RPA-IIB (high-grade T3N0/T1-T3N1 or low-grade T1-T3N2), and RPA-III (high-grade T1-T3N2; median survival: 42, 26, 19, 15, and 12 months, respectively; P

Studies have shown that cancer requires two conditions for tumor progression: cancer cell proliferation and an environment permissive to and conditioned by malignancy. Chemotherapy aims to control the number and proliferation of cancer cells, but it does not effectively control the two best-known conditions of the tumor-permissive environment: neoangiogenesis and tolerogenic immunity. Many malignant diseases exhibit poor outcomes after treatment with chemotherapy. Therefore, we investigated the potential benefits of adding an induction regimen of antiangiogenesis and antitumor immunity to chemotherapy in poor outcome disease. In a prospective, randomized trial, we included patients with advanced, unresectable pancreatic adenocarcinomas, non-small cell lung cancer, or prostate cancer. Two groups of each primary condition were compared: group 1 (G1), n = 30, was treated with the standard chemotherapy and used as a control, and group 2 (G2), n = 30, was treated with chemotherapy plus an induction regimen of antiangiogenesis and antitumor immunity. This induction regimen included a low dose of metronomic cyclophosphamide, a high dose of Cox-2 inhibitor, granulocyte colony-stimulating factor, a sulfhydryl (SH) donor, and a hemoderivative that contained autologous tumor antigens released from patient tumors into the blood. After treatment, the G2 group demonstrated significantly longer survival, lower blood level of neoangiogenesis and immune-tolerance mediators, and higher blood levels of antiangiogenesis and antitumor immunity mediators compared with the G1 group. Toxicity and quality of life were not significantly different between the groups. In conclusion, in several advanced malignancies of different primary localizations, an increase in survival was observed by adding an induction regimen of antiangiogenesis and antitumor immunity to standard chemotherapy.

BH3 mimetics have been proposed as new anticancer therapeutics. They target anti-apoptotic Bcl-2 proteins, up-regulation of which has been implicated in the resistance of many cancer cells, particularly leukemia and lymphoma cells, to apoptosis. Using probabilistic computational modeling of the mitochondrial pathway of apoptosis, verified by single-cell experimental observations, we develop a model of Bcl-2 inhibition of apoptosis. Our results clarify how Bcl-2 imparts its anti-apoptotic role by increasing the time-to-death and cell-to-cell variability. We also show that although the commitment to death is highly impacted by differences in protein levels at the time of stimulation, inherent stochastic fluctuations in apoptotic signaling are sufficient to induce cell-to-cell variability and to allow single cells to escape death. This study suggests that intrinsic cell-to-cell stochastic variability in apoptotic signaling is sufficient to cause fractional killing of cancer cells after exposure to BH3 mimetics. This is an unanticipated facet of cancer chemoresistance., 11 pages, In press

The present study was designed to explore the cross talk between fatty acid synthase (FASN) and HER2 (ErbB2) in ovarian cancer. A total of 60 ovarian cancer patients and 15 normal ovarian tissues were enrolled. Tissue array was conducted by using a tissue microarray instrument. Immunohistochemistry was performed to quantify the expressions of HER2 and FASN. The FASN was detected to be distributed in the cell cytoplasm and was significantly correlated with cancer grade (p = 0.000) and FIGO staging (p = 0.000). Patients with FASN overexpression in ovarian cancer tend to have a worse overall survival rate (p = 0.000). HER2 was also stained to be distributed in the cell cytoplasm associated with higher expression in high-grade cancer. It was also disclosed that FASN expression level is not correlated with HER2 status in ovarian cancer. These results for the first time indicated that a cross talk in FASN and HER2 expressions might be associated with prognosis in malignant ovarian cancer.

The aim of the study was to define biological subtypes of breast cancer that have the propensity to metastasize to the leptomeninges and to assess factors influencing survival from detection of leptomeningeal metastatis (LM). One hundred and eighteen consecutive breast cancer patients with LM were treated in one institution, between the years 1999 and 2009; 40.5 % of patients had triple-negative subtype, 37.5 % had luminal A subtype and 22 % had HER2-positive subtypes (luminal B and HER2). Of patients with LM, 35 % had lobular cancer. Median survival from the detection of LM was 18 weeks, and 1-year survival was 16 %. Cox multivariate analysis revealed that performance status and systemic treatment statistically significantly influenced survival of patients with LM. Triple-negative biological subtype and lobular histological type of breast cancer had the propensity to metastasize to the leptomeninges. Performance status and systemic treatment ordered after detection of LM statistically significantly influenced survival.

Tumor depth of invasion (DOI) is a histologic feature that consistently correlates with lymph node metastasis; however, there are many difficulties with accurately assessing DOI. The aim of this study was to identify a simpler and more reproducible method of determining DOI, by using skeletal muscle invasion as a surrogate marker of depth. Oral tongue squamous cell carcinoma American Joint Committee on Cancer (AJCC) stage T1 cases were identified in the Emory University Department of Pathology database. 61 cases, with a minimum of 2 years of follow-up, were included in the study. Cases were examined histologically to assess muscle invasion and DOI. The two methods of measurement were analyzed to determine the positive predictive value (PPV) of DOI or muscle invasion for both nodal disease and local recurrence. Cases with muscle invasion had a 23.3% PPV of occult lymph node metastasis. Cases with DOI of greater than 3 mm had a 29.7% PPV of occult lymph node metastasis. Cases with muscle invasion had a 43.7% PPV of local tumor recurrence. Cases with maximum DOI of greater than 3 mm had a 40.4% PPV of tumor recurrence. Although the PPV of muscle invasion in regards to nodal status was slightly less than DOI, it represents a more easily reproducible parameter which could guide surgeons in determining if the case warrants an elective neck dissection in a cN0 (clinically negative) neck. Interestingly, the PPV of local recurrence was higher with muscle invasion than DOI, and may represent an important indicator for extent of resection.

The aim of this study was to describe the clinical features of 18 cases of metastatic tumors to the oral cavity. The files of patients seen between 1992 and 2009 with oral (soft tissue and jawbones) metastatic lesions were reviewed. Clinical features, including gender, age, site of the primary tumor, site of metastatic tumor and treatment were evaluated. Patients were 11 males and 7 females, with mean age of 64.6 years. In males, most primary tumors originated in the lungs. In females, the lung and breast were the most common sites of the primary tumors. The mandible was the main site for the development of the metastatic lesions and the most common histologic type was adenocarcinoma. Treatment modalities included radiotherapy, chemotherapy and surgical resection. Metastatic lesions should be considered in the differential diagnosis of oral lesions, particularly when a previous history of cancer is present.