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Related Concept Videos

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Treatment Resistent Cancers02:56

Treatment Resistent Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.

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SWI/SNF complex alterations predict immunotherapy response in bladder cancer.

Jian Zhang1, Yapeng Wang1, Qian Yan1

  • 1Department of Urology, Daping Hospital, Army Medical University, Chongqing, China.

Frontiers in Immunology
|December 24, 2025
PubMed
Summary

SWI/SNF alterations in urothelial bladder cancer (UBC) predict better response to immunotherapy. These genetic changes create an inflamed tumor microenvironment, improving patient survival and guiding precision treatment strategies.

Keywords:
SWI/SNFbladder cancerimmune checkpoint inhibitorsmachine-learningprediction model

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Area of Science:

  • Oncology
  • Genetics
  • Immunotherapy

Background:

  • Immune checkpoint inhibitors (ICIs) have transformed urothelial bladder cancer (UBC) treatment, but only benefit a subset of patients.
  • The role of SWItch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex alterations in UBC and their impact on ICI response are not well understood.

Purpose of the Study:

  • To investigate the frequency and functional significance of SWI/SNF gene mutations in UBC.
  • To evaluate SWI/SNF alterations as predictive biomarkers for response to immune checkpoint blockade therapy.

Main Methods:

  • Analysis of tumor specimens from 49 patients and integration with five public cohorts (2,280 cases).
  • Somatic alteration identification via sequencing and transcriptomic profiling via RNA sequencing.
  • Survival analysis, immune landscape characterization, and machine-learning-based prognostic modeling.

Main Results:

  • SWI/SNF alterations were found in 42.8% of UBC cases, notably in ARID1A, ARID1B, ARID2, SMARCA4, and PBRM1.
  • SWI/SNF-mutant tumors exhibited higher tumor mutational burden, increased neoantigen load, and an immune-inflamed microenvironment.
  • These tumors showed significantly improved overall survival with ICI treatment (p < 0.05), with genotype-specific models demonstrating strong prognostic discrimination.

Conclusions:

  • SWI/SNF alterations represent a key biomarker for stratifying UBC patients who respond to immunotherapy.
  • Developed genotype-specific prognostic models offer a practical framework for optimizing precision immunotherapy in UBC.