Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association
Second Cancer Risk Heightened After Appendiceal Adenocarcinoma Diagnosis
Adults with primary primary appendiceal adenocarcinoma face a higher risk of developing a second primary cancer, including colorectal and prostate cancers.
Adults with appendiceal adenocarcinoma have a higher risk of developing a second primary cancer, including colorectal and prostate cancers.
Among adult patients in the United States diagnosed with a first primary appendiceal adenocarcinoma, researchers found that one in every 13 will be diagnosed with a second primary cancer within 10 years.
The study, presented at the 2025 Gastrointestinal Cancers Symposium, also revealed that patients with appendiceal adenocarcinoma have an additional 12% excess incidence in secondary primary cancers and double the excess incidence in secondary primary colorectal cancers compared with the general population.
Furthermore, the study underscores the importance of implementing robust cancer prevention and early detection strategies for individuals diagnosed with appendiceal adenocarcinoma. These strategies, which include interventions such as colonoscopy screening and genetic testing, are identified as a critical clinical priority, according to the study.
"Incidence rates of rare appendiceal cancers are increasing across the United States. Although this is suggestive of a growing population of appendiceal cancer survivors over time, the risk of second primary cancers specific to patients with a first primary appendiceal adenocarcinoma remains unknown," Dr. Andreana N Holowatyj, an assistant professor of medicine in the Division of Epidemiology and Cancer Biology at Vanderbilt University Medical Center and Vanderbilt-Ingram Cancer Center, in Nashville, Tennessee, and co-authors wrote in the abstract of their presentation.
Glossary:Cumulative incidence: total new cases.
Standardized incidence ratios: compare disease rates.
Pseudomyxoma peritonei: rare abdominal tumor.
Fine and Gray methods: analyze survival with competing risks.
Holowatyj also serves as research director and co-director of the Research Immersion Course at the Vanderbilt University School of Medicine.
The cumulative incidence of second primary cancer was 7.5% and 11.7, at 10 and 20 years after appendiceal adenocarcinoma diagnosis, respectively. The cumulative incidence was significantly different between sexes and age at the diagnosis of appendiceal adenocarcinoma.
For instance, at a 10-year post-diagnosis, the cumulative incidence of second primary cancer for females was 6.4% and for males was 8.8%. The overall standardized incidence ratios (SIRs) for any second primary cancer were 1.12, which as the study states, corresponds to an excess of 14.8 cancers per 10,000 person-years. SIRs for common types of second primary cancers included: 1.07 for prostate cancer, 2.12 for colorectal cancer, 0.91 for female breast cancer, 0.81 for lung cancer and 1.2 for melanoma.
During the trial, a total of 5,827 adults diagnosed with a first primary appendiceal adenocarcinoma (mean age 58 years) were identified during the trial period. Of those identified, 418 developed a second primary cancer (51.8% female). The most common types of second primary cancer were prostate cancer (17.7%), colorectal cancer (14.4%), female breast cancer (10.5%), lung cancer (8.4%) and melanoma (6%).
Appendiceal cancer originates in the appendix, a small pouch in the abdomen, with two main types: epithelial and neuroendocrine. Epithelial cancers may produce mucin, causing pseudomyxoma peritonei, while neuroendocrine tumors arise from enterochromaffin cells. Cancer may spread within the abdomen or, less commonly, through lymph nodes to other areas.
A population-based study was conducted using data from the Surveillance, Epidemiology, and End Results (SEER) Program, evaluating adults (18 or more years) diagnosed with first primary appendiceal adenocarcinoma from 1992 to 2021. Cumulative incidence of second primary cancer, defined as any primary cancer occurring three or more months after appendiceal adenocarcinoma, was estimated using Fine and Gray methods to account for the competing risk of death. SIRs were calculated to compare the observed number of second cancers with the expected number, based on age-, sex- and race-specific incidence rates in the general population.
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Researcher Talks Lung Cancers At UW
Lung cancer expert Triparna Sen delivered a seminar in the Cancer Biology Seminar Series at the University of Wisconsin Jan. 22. The seminars are hosted weekly by the McArdle Laboratory for Cancer Research at the Health Sciences Learning Center.
Sen's lab at the Icahn School of Medicine at Mount Sinai Hospital focuses on lung cancer research broadly. During the seminar Wednesday, Sen spoke about three distinct topics, spanning specific cancer types to cancers that change what cells they are.
Sen started the seminar by speaking about the effects of oncogenes in adenocarcinoma, a cancer in the cells lining the lungs. Oncogenes are genes related to the development of cancer either through their mutation or inability to function.
Sen focused on genes that prevented ferroptosis, a process in which a cell dies through the accumulation of toxins in the cell. Cancer cells can inhibit ferroptosis by increasing the presence of proteins that prevent toxin accumulation.
Gene knockouts are the inactivation of genes typically through mutations. The mutations render the created proteins nonfunctional. Certain gene knockouts prevent treatments that induce ferroptosis in cancer cells from being effective.
In these cancer variants, Sen's lab found that inhibiting SCD1 — a protein that maintains the balance of saturated to unsaturated fatty acids in cells — was able to decrease the size of tumors in mice for some time.
Sen then pivoted to small-cell lung cancers and her teams' research on cancers with two gene knockouts that make them resistant to other treatments and the immune system. By knocking out an additional two genes, Sen's lab saw improvement in the immune response to the tumors.
The last subject Sen spoke about was cancers which transformed cell types.
During treatment with tyrosine kinase inhibitors, a subset of adenocarcinomas transformed into small-cell cancers. After transformation, analyses conducted by Sen's lab showed these cancers shared hallmarks of certain gene mutations but not at the expected level. This led Sen to suspect epigenetic inhibitions in the transformed cancers without mutations.
Epigenetics is the process in which gene transcription is modified by factors outside of what is in the genetic code. The genes silenced by mutations in some transformed cancers were epigenetically silenced in those without mutations.
The method of transformation between cell types is unclear. Sen theorized the deregulation of certain pathways allowed new cancer cells to develop into either the original or different but related cells. In this case, glandular epithelial cells — the cancerous cells in adenocarcinomas — differentiated into cancerous small cells.
Jazz Pharmaceuticals asked Sen's lab to conduct trials with lurbinectedin, a drug designed to attack transformed small cell carcinomas. When paired with osimertinib, a TKI, tumors shrunk significantly and for an extended period compared to either drug on its own in human trials.
Following the conclusion of Sen's seminar, the National Institute of Health suspended communications, research and grant meetings. Sen's lab receives a portion of its funding through an R01 Chartered Study Section grant from the National Cancer Institute, an agency of the NIH.
Role Of CDKN2A And MTF1 In Lung Adenocarcinoma Prognosis
Photo Credit: netocoh
The following is a summary of "Biological characterization and clinical significance of cuproptosis-related genes in lung adenocarcinoma," published in the January 2025 issue of Pulmonology by Li et al.
Lung cancer, distinguished by high morbidity and mortality rates and a poor prognosis, presents a significant clinical challenge, with cuproptosis emerging as a novel cell death mechanism.
Researchers conducted a retrospective study to analyze the biological characteristics and clinical significance of genes related to cuproptosis in lung adenocarcinoma (LUAD) and to explore the molecular mechanisms underlying its occurrence and progression.
They targeted 10 cuproptosis-related genes identified in prior studies and used datasets from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) databases to find differential genes. Data analysis was performed using R package, Cytoscape, TISDB, cBioPortal, STRING, CancerSEA, and Disgenet. Immunohistochemistry validation was carried out for further detection.
The results showed that CDKN2A and MTF1 were cuproptosis-associated differential genes in LUAD, with differential expression across immune subtypes and the expressions were correlated with various LUAD functional states, CDKN2A was negatively linked to LUAD survival prognosis.
Investigators concluded that CDKN2A and MTF1 were associated with LUAD diagnosis, with CDKN2A demonstrating a negative correlation with patient survival and prognosis, suggesting its potential utility as a biomarker for early diagnosis and prognostic assessment in LUAD.
Source: bmcpulmmed.Biomedcentral.Com/articles/10.1186/s12890-025-03477-4
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