ABSTRACTObjectivesThe study evaluated the impact of lifestyle and environmental exposure on the etiology of multiple myeloma (MM).MethodsA multicenter case–control study was conducted in 20 hematology centers and in 5 outpatient clinics in Poland. The questionnaire on exposure to potential risk factors including sociodemographic data, lifestyle, and environmental factors was completed.ResultsA total of 274 patients with newly diagnosed MM and 208 patients from primary healthcare centers in the control group were enrolled in the study. Regarding lifestyle, sports practiced systematically for at least half a year play a protective role in the development of myeloma (OR = 0.40, 95% CI, 0.28–0.58, p < 0.001). Among environmental factors harmful exposures that increase the likelihood of the development of MM include pesticides (OR = 3.29, p < 0.001), asphalt (OR = 2.42, p = 0.026), coal dust (OR = 2.27, p = 0.004), organic vapors (OR = 2.11, p = 0.001), metal dust (OR = 2.07, p = 0.023), exhaust fumes (OR = 2.03, p < 0.01), and chemicals (OR = 1.80, p < 0.01).ConclusionsThe pathogenesis of MM is complex with the impact of modifiable factors. Lifestyle, with physical activity, seems to play a key role.

This study evaluates the usefulness of serum KL-6, SP-D and TGF-β1 levels in assessing lung impairment and predicting interstitial lung disease (ILD) short-term progression in patients with interstitial pneumonia with autoimmune features (IPAF). A total of 24 patients with IPAF, 21 with connective tissue disease-associated ILD (CTD-ILD) and 23 with CTD without ILD were followed for 1 year. Serum levels of KL-6, SP-D and TGF-β1 were measured and their associations with disease severity and progression were analysed. KL-6, SP-D and TGF-β1 levels were significantly higher in IPAF and CTD-ILD patients compared to CTD without ILD (p < 0.0001, p = 0.0005 and p = 0.0001, respectively). KL-6 (r = 0.45, p = 0.002) and SP-D (r = 0.35, p = 0.02) levels correlated with lung involvement in HRCT in the ILD group. In IPAF, KL-6 levels correlated with pulmonary function tests (FVC%, TLCO%, and 6MWD) and SpO2, while SP-D correlated with 6MWD and SpO2. In CTD-ILD, KL-6 and SP-D levels were positively correlated with BAL cell count (KL-6: r = 0.58, p = 0.04; SP-D: r = 0.63, and p = 0.02). KL-6 also showed a negative correlation with the time since symptom onset (r = −0.51, p = 0.02). No significant associations were found between the baseline biomarker levels and ILD progression risk. KL-6 and SP-D may serve as potential biomarkers for assessing lung impairment in IPAF, though their predictive value for short-term prognosis remains uncertain.

Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is a common leukemia characterized by clonal expansion of mature CD5+/CD23 + B cells in the blood, bone marrow (BM) and lymphoid tissues. CLL can undergo extramedullary and extranodal infiltration, with one study noting an incidence of only 0.3 per 100,000 people, and in 17.6

Despite advances in multiple myeloma (MM) treatment, drug resistance remains a clinical challenge. We aimed to develop a prognostic model for bortezomib resistance based on miRNA expression profiling. The study included 40 previously untreated MM patients receiving bortezomib-based regimens (20 treatment-sensitive, 20 resistant). Pretreatment venous blood samples were analyzed for miRNA expression. Differential expression analysis revealed upregulated miR-27b-3p (FC 1.45, p = 0.017) and let-7b-5p (FC 1.44, p = 0.025) in the resistant group. Univariate analysis identified let-7b-5p (OR 3.17, 95%CI: 1.19-11.4, p = 0.04) and miR-27b-3p (OR 4.73, 95%CI: 1.4-26.6, p = 0.036) as risk factors for resistance. The final multivariate model included miR-27b-3p (OR 23.1, 95% CI: 2.8-452, p = 0.015), let-7b-5p (OR 4.38, 95% CI: 1.28-22.2, p = 0.038), and miR-103a-3p (OR 15.3, 95% CI: 1.33-351, p = 0.049). These miRNAs may serve as biomarkers of treatment response in MM. However, external validation is necessary to confirm the clinical utility of our model.

Introduction: MRD2STOP is a prospective trial evaluating maintenance therapy cessation guided by measurable residual disease (MRD) negativity by next generation sequencing (NGS, clonoSEQ) in multiple myeloma (MM). We have previously reported that the estimated 3-year MRD-free survival (defined as death, progression, or MRD 10-6 resurgence) among patients with MRD < 10-6 at the time of discontinuation was 68% and was further improved to 78% when using a novel MRD < 10-7 cutoff (Derman et al. ASCO 2024). These results suggest that disease re-emergence can occur in patients achieving the deepest levels of MRD negativity. Clonotypic peptide mass spectrometry (MS), which has a limit of detection 1000x more sensitive than serum immunofixation and involves monoclonal protein (M-protein) de novo sequencing and peptide quantification to accomplish highly sensitive blood-based monitoring of a patient's M-protein over time. In this analysis, we assessed clonotypic peptide MS status among patients in the MRD2STOP cohort. Method: Clonotypic peptide MS was performed on peripheral blood in a subset of patients enrolled into the MRD2STOP trial, who had high-disease burden samples available (M-protein > 2 g/L) for patient. Eligibility for maintenance cessation required patients to be in a stringent complete response, with PET negativity and MRD < 10-6 as assessed by clonoSEQ (Adaptive Biotechnologies). Patient high-disease burden serum samples were digested with several combinations of proteolytic enzymes to permit sequencing of the M-protein heavy and light chain. Clonotypic peptides specific to the patient's complementarity-determining regions (CDR) were selected for quantification by MS using a bioinformatics algorithm and compared to RNA sequencing data. Clonotypic peptide quantification by MS was performed using M-InSight® (Sebia/Corgenix) on available tracking peripheral blood samples, typically at 6-month intervals. Results: To date, 11 patients had high-tumor burden samples enabling identification of clonotypic peptides; in 10 of the 11 cases, at least one of the clonotypic peptides predicted by clonoSEQ matched a clonotypic peptide identified by MS. An M-protein was detectable by clonotypic peptide MS at time zero in all 11 patients despite no detectable disease by serum immunofixation in 11/11 (100%), MRD < 10-6 in 11/11 (100%), and MRD <10-7 in 8/11 (73%). The median M-protein concentration at time zero was 0.0029 g/L (range 0.0000001 g/L - 0.03 g/L). At a median follow-up of 31.6 months from maintenance discontinuation, there were 4 MRD 10-6 resurgence events, including 2 progression events. Of the 4 patients with disease re-emergence, 3 occurred at 12 months and one occurred at 24 months. The 12-month rate of disease re-emergence from maintenance cessation was 33% and increased to 44% at 24 months. The median time zero MS M-protein concentration among those with disease re-emergence was 0.0035 g/L vs 0.00002 g/L for those without re-emergence. In follow-up from maintenance cessation, the MS M-protein concentration increased from baseline in 6 patients; of these 6 cases, MRD 10-6 resurgence at the 12-month mark occurred in 3 patients including 2 patients who had disease progression. There was a logfold increase in M-protein concentration at least 6 months prior to disease progression in both cases. No patient with stable or decreasing M-protein concentration in follow-up experienced disease progression though one had MRD 10-6 resurgence. Conclusion: Despite undetectable disease in the bone marrow at the 10-6 or even 10-7 threshold, trace M-proteins were still detectable in the blood by clonotypic peptide MS indicating the potential presence of MRD. The significance of MS M-protein kinetics over time requires additional evaluation to confirm this observation. In the search to identify cures in MM, clonotypic peptide MS may serve as a key marker for better defining the absence of disease in MM.

Introduction: Survival outcomes have improved dramatically for patients (pts) with multiple myeloma (MM), though cumulative exposure to therapies is associated with increased risk for second hematologic malignancies. Clonal hematopoiesis (CH) can be a precursor lesion for MM therapy-related leukemia (Saygin, Blood Cancer Discov 2024). Incidence of CH in MM pts prior to autologous stem cell transplant (ASCT) was reported at 22% with an allelic frequency (AF) cut-off >1%. (Mouhieddine, Nature Commun 2020). It is unclear if cessation of therapy can reverse the progression of CH and reduce the risk for leukemia. We hypothesize that discontinuation of therapy can lead to regression of CH clones in MM, and aim to identify patients whose risk for secondary leukemia may be reduced by treatment discontinuation. Methods: We studied prospective samples from pts in the MRD2STOP trial, in which pts with MM who achieved flow cytometric and next-generation sequencing (NGS)-based measurable residual disease (MRD)-negativity discontinued maintenance therapy (Derman ASCO 2024). DNA was extracted from CD138-depleted bone marrow cells obtained at baseline (prior to discontinuation of MM therapy), and at 12- and 24-months follow-up. DNA was sequenced with a hybrid capture-based targeted gene panel at a high depth of 2000x coverage for 22 genes and 95% of CH mutations found in the general population. The assay reaches an AF sensitivity of 0.01%. Results: A total of 95 samples from 38 individual pts were analyzed. Median age was 65 years (range, 39-84), 50% were female. Patients were 71% White, 18% Black, 5% Hispanic, 3% Asian and 3% more than one race; 34% had high-risk MM by cytogenetics. 97% of patients received one prior line of therapy prior to discontinuation. Induction therapy was a quadruplet regimen in 45%, triplet regimen in 53%, and doublet regimen in 2%. After induction, 61% received ASCT, and 13% received multi-drug post-transplant consolidation prior to maintenance therapy. Most (95%) patients received lenalidomide maintenance, and average duration of consolidation and/or maintenance therapy prior to discontinuation was 44 months (range, 13-90). Using an AF cut-off of 0.1%, we identified CH mutations in 97% of pts at baseline with the following distribution of mutated genes: TP53 (83%), DNMT3A (33%), SF3B1 (13%), IDH1 (13%), ASXL1 (11%), GNAS (11%), KRAS (11%), NRAS (8%), TET2 (5%), JAK2 (3%), PPM1D (3%), SRSF2 (3%). Among all pts, 29% had one, 39% had two, 24% had three and 3% had four mutations in CH-associated genes in their marrow. Using an AF cut-off of 1%, 42% of pts had CH clones. The frequency of CH with TP53 clones at AF >1% was 21% (8 out of 38). Therefore, the median AF of TP53 clones (0.18%, range 0.1%-14.5%) was significantly smaller than DNMT3A (0.33%, range 0.1%-13.8%) and ASXL1 (6.4%, range 0.1%-23.6%) clones, but comparable to other mutated genes. There were no significant correlations between age, gender, ASCT status, or duration of treatment and the frequency of mutated genes. In assessment of serial samples with a baseline AF cutoff of 0.1%, the size of TP53-mutant CH clones was stable after treatment discontinuation with median AF of 0.18% at baseline, 0.17% at 12 months (p=0.40), and 0.2% at 24 months post-discontinuation (p=0. 79). Four patients with TP53-mutant clones AF >1% at baseline demonstrated clonal regression over time, and one demonstrated progression. Other CH clones showed similar patterns of stability over 24 months, but clonal regressions (DNMT3A, ASXL1, KRAS in 1 pt each) and expansions (ASXL1 in 2 pts) were seen in some cases. One patient in this cohort developed therapy-related acute lymphoblastic leukemia two years after lenalidomide withdrawal, but no driver mutations were identified in the ALL clone. Conclusions: In summary, we demonstrated a high prevalence of CH in MM patients prior to therapy discontinuation. This included a disproportionately high frequency of TP53-mutant CH, but not the traditional age-related CH (i.e., DNMT3A, TET2, ASXL1), in MM pts who were exposed to current standard of care therapies. These CH clones remained stable even after treatment was discontinued, and more patients will be added to further assess the clonal evolution of TP53 CH. Longer follow up is needed to determine the full impact of these findings on risk for therapy related leukemia.

Introduction Epidemiologic observations and genetic studies suggest an inherited susceptibility to multiple myeloma (MM) occurs in some patients. Several candidate genes for hereditary MM risk have been identified, but the prevalence of pathogenic/likely pathogenic (P/LP) germline variants in genes associated with hereditary cancer syndromes and related disorders remains understudied. One ASH abstract estimated 8.8% of patients with MM carry P/LP variants in hereditary cancer genes (Thibaud, ASH 2021). Considering the postulated role of immune stimulation in MM pathogenesis, we hypothesized that additional variants associated with immunological disorders and/or hereditary hematopoietic disorders may also be important for MM predisposition. Therefore, we determined the prevalence of P/LP variants in genes related to hereditary cancer, hematopoietic, and immune syndromes in a large, multi-institutional cohort of MM patients, the CoMMpass dataset. Methods DNA was extracted from non-tumor tissue (peripheral blood), and whole exome sequencing (WES) was performed. After alignment and duplicate calling, the GVCF workflow by GATK4.4 was used to call germline variants using HaplotypeCaller. Single nucleotide polymorphisms (SNPs) and insertions/deletions (indels) were quality filtered based on GATK Best Practices. Filtered variants were functionally annotated using Funcotator's curated germline data source. The resulting variants were manually validated, and pathogenicity was determined using the ClinVar database. Clinical characteristics were obtained from the IA22 CoMMpass dataset. The study group and intragroup associations were examined using the Chi-square or Fisher's exact test. The Kaplan-Meier method and Cox proportional hazards models were used for univariate and multivariate survival analyses. When applicable, the Bonferroni method was applied to adjust for multiple testing. Survival was compared using the log-rank test. Stepwise selection was used to determine the optimal multivariate model. Results We identified 137 P/LP germline variants in 130 patients out of 972 included in this analysis (13.4%). Six patients carried two P/LP variants, and one patient carried three different variants. TNFRSF13B was the most commonly mutated gene (24 patients, 2.5%), followed by MUTYH (21 patients, 2.2%), APC (9 patients, 1.0%), TTR (8 patients, 1.0%), and CHEK2 (8 patients, 1.0%). The median age of the 130 patients with germline MM predisposition was 63 years (range: 32-86), compared to 63 (27-89) in other patients (p=0.9). There were no differences between the groups in terms of sex (46% female vs 38%, p=0.15), race (78% White, 15% Black vs 76% and 17%, p=0.49), or family history of cancer (62% vs 55%, p=0.21). In terms of disease characteristics, 71% of patients with germline MM predisposition had at least one high-risk cytogenetic abnormality by FISH-seq [del(17p), amp(1q), del(1p), t(4:14), t(14:16), t(14:20)], compared to 61% of patients without germline predisposition (p=0.04). ISS stage III disease was present in 25% of patients with germline MM predisposition and in 27% of the remaining patients (p=0.6). Patients with P/LP variants had significantly better progression-free survival (PFS) after first-line therapy, with a median of 49.1 months vs 35.0 months [HR=0.73 (95%CI: 0.57-0.94), p=0.01]. This PFS benefit remained significant in multivariable analysis [HR=0.69 (0.53-0.89), p=0.005] after adjusting for cytogenetic risk [HR=1.52 (1.27-1.83), p<0.001], ISS stage III [HR=1.62 (1.34-1.94), p<0.001], and use of first-line ASCT [HR=0.43 (0.36-0.51), p<0.001]. There were no differences in overall survival between the two groups [median not reached in both groups, HR=0.82 (0.6-1.13), p=0.2]. Conclusions We found 13.4% of patients with MM carried P/LP germline variants when analyzed with an extended panel of genes. This is higher than prior reports. We identified TNFRSF13B, which causes hereditary immunodeficiency, as the most frequently mutated gene in this cohort of patients. Presence of P/LP variants was associated with a significant PFS benefit. Further studies are needed to better elucidate the impact of these P/LP germline variants on myeloma biology, treatment response, and prognosis.

Multiple myeloma (MM) is a hematological malignancy characterized by the clonal proliferation of plasma cells in the bone marrow (BM) microenvironment. Despite the progress made in treatment, some MM patients still die within the first year of diagnosis. Numerous studies investigating microRNA (miRNA) expression patterns suggest they may be good prognostic markers. The primary aim of this study was to analyze the expression of selected miRNAs in the serum of MM patients who were later treated with bortezomib-based regimens, and to determine their potential to predict early mortality. The study was conducted in 70 prospectively recruited patients with newly diagnosed MM admitted to the Department of Hematology of the Copernicus Memorial Hospital, Lodz (Poland) between 2017 and 2021. Among them, 17 patients experienced death within 12 months of diagnosis. The expression of 31 selected miRNAs was determined using a miRCURY LNA miRNA Custom PCR Panel. The obtained clinical data included patient characteristics on diagnosis, treatment regimen, response to treatment, and follow-up. Differential expression analysis found two miRNAs to be significantly downregulated in the early mortality group: hsa-miR-328-3p (fold change—FC: 0.72, p = 0.0342) and hsa-miR-409-3p (FC: 0.49, p = 0.0357). Univariate and multivariate logistic regression analyses were performed to assess the early mortality rate. The final model consisted of hsa-miR-409-3p, hsa-miR-328-3p, age, and R-ISS 3. It yielded an area under the curve (AUC) of 0.863 (95%CI: 0.761–0.965) with 88.2% sensitivity and 77.5% specificity. Further external validation of our model is needed to confirm its clinical value.

Introduction: Despite several studies, the impact of coronavirus disease 2019 on patients with multiple myeloma remains uncertain. Material and methods: We performed a survey that covered the period of the first and second waves of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic in 23 centers inseven countries. Out of 352 patients with myeloma and SARS-CoV-2, 23% died. Results: Logistic regression showed a lower risk of death among patients treated with proteasome inhibitor and a higher risk of death for those who had a severe or a very severe course of disease.

Multiple myeloma (MM) is a hematological malignancy characterized by the clonal proliferation of plasma cells in the bone marrow (BM) microenvironment. Despite the progress made in treatment, some MM patients still die within the first year of diagnosis. Numerous studies investigating microRNA (miRNA) expression patterns suggest they may be good prognostic markers. The primary aim of this study was to analyze the expression of selected miRNAs in the serum of MM patients subsequently treated with bortezomib-based regimens and determine their potential to predict early mortality. The study was conducted in 69 prospectively-recruited patients with newly-diagnosed MM admitted to the Department of Hematology of the Copernicus Memorial Hospital, Lodz (Poland) between 2017 and 2021. Among them, 17 patients experienced death within 12 months of diagnosis. The expression of 31 selected miRNAs was determined using miRCURY LNA miRNA Custom PCR Panel. The obtained clinical data included patient characteristics on diagnosis, treatment regimen, response to treatment, and follow-up. Differential expression analysis found two miRNAs to be significantly downregulated in the early mortality group: hsa-miR-328-3p (fold change- FC: 0.72, p=0.0342) and hsa-miR-409-3p (FC: 0.49, p=0.0357). Univariate and multivariate logistic regression analyses were performed to assess the early mortality rate. The final model consisted of hsa-miR-409-3p, hsa-miR-328-3p, age and R-ISS 3. It yielded an area under the curve (AUC) of 0.863 (95%CI: 0.761-0.965) with 88.2% sensitivity and 77.5% specificity. Further external validation of our model is necessary to confirm its clinical value.

Introduction: Acute lymphoblastic leukemia (ALL) is one of the most commonly occurring cancers among children with one of the highest survival rates, thanks to its very strict treatment protocol. In this paper, the impact of delays in treatment during the induction phase was assessed. Material and methods: Retrospective single center analysis of 127 patients treated between years 2003 and 2015 was performed. Patients were categorized by their respective gender, age, leukemia variant, risk group and chemotherapy protocol used. The delays were measured using protocol milestones as reference points. The associations between treatment delay intervals and event-free survival (PFS) or overall survival (OS) were evaluated using Kaplan-Meier curves and univariate Cox proportional hazards regression models. Results: Delays in treatment which occurred before the 8th day were associated with a 30% increase in the risk of death ( p < 0.01) and a 33% increase in the risk of relapse or death ( p < 0.01). The influence of delays after the 8 th day was statistically insignificant. Delays were proven to have the most influence on outcome in the high-risk group, especially before the 8 th day. Conclusions: The ALL treatment protocols should be strictly followed as any delay may lead to worse patients' survival.

Multiple myeloma (MM) is a common malignant hematological malignancy. Recently, interest has grown in the role of non-coding regions in disease pathogenesis. MicroRNAs (miRNAs) are small non-coding RNAs containing 19-25 bases that play a crucial role in messenger RNA silencing and post-transcriptional regulation of gene expression. Several miRNAs demonstrate markedly dysregulated expression in MM, suggesting that they may act as both tumor suppressors and oncogenes. microRNAs are also reportedly involved in the regulation of other epigenetic mechanisms of gene expression. Additionally, some miRNAs have been associated with drug resistance, and therefore a further exploration of their activity may lead to its reversal. Moreover, miRNA expression patterns in either MM cells or serum exosomes have been shown to be good prognostic markers. This review describes the roles of miRNAs in MM and examines their potential to predict MM prognosis and play a role in novel therapeutic strategies.

Multiple myeloma (MM) is a genetically complex disease that results from a multistep transformation of normal to malignant plasma cells in the bone marrow. However, the molecular mechanisms responsible for the initiation and heterogeneous evolution of MM remain largely unknown. A fundamental step needed to understand the oncogenesis of MM and its response to therapy is the identification of driver mutations. The introduction of gene expression profiling (GEP) in MM is an important step in elucidating the molecular heterogeneity of MM and its clinical relevance. Since some mutations in myeloma occur in non-coding regions, studies based on the analysis of mRNA provide more comprehensive information on the oncogenic pathways and mechanisms relevant to MM biology. In this review, we discuss the role of gene expression profiling in understanding the biology of multiple myeloma together with the clinical manifestation of the disease, as well as its impact on treatment decisions and future directions.

Purpose of review This article provides a brief update on the recommended diagnosis and treatment strategies for patients with the classic form of hairy cell leukemia (HCL) and HCL variant (HCLv). Recent findings HCL is a chronic B-cell malignancy with multiple treatment options. In recent years, many novel drugs have been assessed for HCL treatment with promising results. The investigated nonchemotherapy options include moxetumomab pasudotox, which targets CD22; vemurafenib or dabrafenib, which target the BRAFV600E protein; trametinib, which targets mitogen-activated protein kinase enzyme; and ibrutinib, which targets Bruton tyrosine kinase. Summary Purine analogs significantly improve survival in patients with HCL. However, patients often relapse, require multiple treatments, and may become refractory. The introduction of novel agents has expanded the spectrum of therapy possibilities in those patients. In the coming years, they will assist standard therapy for patients with HCL who may currently have suboptimal results.

Ibrutinib and idelalisib, B-cell receptor (BCR) signaling pathway inhibitors, have been recently approved for use against relapsed/refractory chronic lymphocytic leukemia (CLL). To assess the efficacy and safety of BCR pathway inhibitors in relapsed/refractory CLL, we conducted a systematic review and meta-analysis of five randomized controlled trials (1866 patients). Our study demonstrated that BCR pathway inhibitors significantly prolonged progression-free survival (PFS; pooled HR=0.24; 95%CI: 0.19-0.30) and overall survival (HR=0.58; 0.46-0.73) compared with control treatment. BCR pathway inhibitors increased the probability of response (RR=3.54; 95%CI: 1.69-7.41) and decreased the risk of progression (RR=0.21, 95%CI: 0.13-0.34). However, BCR pathway inhibitors increased the risk of grade 3 and 4 adverse events (AEs; RR=1.25; 95%CI: 1.08-1.44) and serious AEs (RR=1.32; 95% CI: 1.17-1.50). AEs causing discontinuation (RR=1.26; 95% CI: 0.88-1.81) or death (RR=1.06; 95% CI: 0.72-1.57) were not significantly increased. No statistically significant difference in any aspect of meta-analysis was noted between ibrutinib and idelalisib.

UNLABELLEDThe aim of the study was to assess patients' awareness of the prevention and treatment of colorectal cancer.MATERIAL AND METHODSPatients diagnosed with colorectal cancer, hospitalised at the Department of General and Colorectal Surgery of the Medical University in Łódź during the period from January 2015 to April 2015, were asked to complete a questionnaire concerning their families' medical case record, factors predisposing them to the development of colorectal cancer, the tests applied in diagnostics, and the treatment process. The questionnaire comprised 42 closed-ended questions with one correct answer. A statistical analysis of all answers was carried out.RESULTSThe study group consisted of 30 men and 20 women aged 27-94 years old. A strong, statistically significant negative correlation between a patient's age and his/her awareness of the prevention and treatment of colorectal cancer was noted (p<0.001; r= -0.51). The study demonstrated a statistically significant relationship between the occurrence of neoplasms in a patient's family (p=0.009) or, more specifically, the occurrence of colorectal cancer (p=0.008), and the awareness of the prevention programme. The women's group was characterised by statistically significantly greater awareness of colonoscopy as a screening examination (p=0.004).CONCLUSIONSPatients need more information on colorectal cancer, its risk factors, prevention, the treatment process, and postoperative care. Lack of awareness of the colorectal cancer issue can be one of the major factors contributing to the high incidence of this disease.

Medical nutrition therapy has a pivotal role in the management of chronic gastrointestinal disorders, like chronic pancreatitis, inflammatory bowel diseases (Leśniowski-Crohn's disease and ulcerative colitis) or irritable bowel syndrome. The aim of this study is to develop, deploy and evaluate an interactive application for Windows and Android operating systems, which could serve as a digital diet diary and as an analysis and a prediction tool both for the patient and the doctor. The software is gathering details about patients' diet and associated fettle in order to estimate fettle change after future meals, specifically for an individual patient. In this paper we have described the process of idea development and application design, feasibility assessment using a phone survey, a preliminary evaluation on 6 healthy individuals and early results of a clinical trial, which is still an ongoing study. Results suggest that applied approximative approach (Shepard's method of 6-dimensional metric interpolation) has a potential to predict the fettle accurately; as shown in leave-one-out cross-validation (LOOCV).