Cancer immunotherapy uses the body’s immune system to combat cancer, marking a significant advancement in treatment. This review traces its evolution from the late 19th century to its current status. It began with William Coley’s pioneering work using bacterial toxins to stimulate the immune system against cancer cells, establishing the foundational concept of immunotherapy. In the mid-20th century, cytokine therapies like interferons and interleukins emerged, demonstrating that altering the immune response could reduce tumors and highlighting the complex interplay between cancer and the immune system. The discovery of immune checkpoints, regulatory pathways that prevent autoimmunity but are exploited by cancer cells to evade detection, was a pivotal development. Another major breakthrough is CAR-T cell therapy, which involves modifying a patient’s T cells to target cancer-specific antigens. This personalized treatment has shown remarkable success in certain blood cancers. Additionally, cancer vaccines aim to trigger immune responses against tumor-specific or associated antigens, and while challenging, ongoing research is improving their efficacy. The historical progression of cancer immunotherapy, from Coley’s toxins to modern innovations like checkpoint inhibitors and CAR-T cell therapy, underscores its transformative impact on cancer treatment. As research delves deeper into the immune system’s complexities, immunotherapy is poised to become even more crucial in oncology, offering renewed hope to patients globally.

Cancer immunotherapy uses the body’s immune system to combat cancer, marking a significant advancement in treatment. This review traces its evolution from the late 19th century to its current status. It began with William Coley’s pioneering work using bacterial toxins to stimulate the immune system against cancer cells, establishing the foundational concept of immunotherapy. In the mid-20th century, cytokine therapies like interferons and interleukins emerged, demonstrating that altering the immune response could reduce tumors and highlighting the complex interplay between cancer and the immune system. The discovery of immune checkpoints, regulatory pathways that prevent autoimmunity but are exploited by cancer cells to evade detection, was a pivotal development. Another major breakthrough is CAR-T cell therapy, which involves modifying a patient’s T cells to target cancer-specific antigens. This personalized treatment has shown remarkable success in certain blood cancers. Additionally, cancer vaccines aim to trigger immune responses against tumor-specific or associated antigens, and while challenging, ongoing research is improving their efficacy. The historical progression of cancer immunotherapy, from Coley’s toxins to modern innovations like checkpoint inhibitors and CAR-T cell therapy, underscores its transformative impact on cancer treatment. As research delves deeper into the immune system’s complexities, immunotherapy is poised to become even more crucial in oncology, offering renewed hope to patients globally.

Cancer immunotherapy uses the body’s immune system to combat cancer, marking a significant advancement in treatment. This review traces its evolution from the late 19th century to its current status. It began with William Coley’s pioneering work using bacterial toxins to stimulate the immune system against cancer cells, establishing the foundational concept of immunotherapy. In the mid-20th century, cytokine therapies like interferons and interleukins emerged, demonstrating that altering the immune response could reduce tumors and highlighting the complex interplay between cancer and the immune system. The discovery of immune checkpoints, regulatory pathways that prevent autoimmunity but are exploited by cancer cells to evade detection, was a pivotal development. Another major breakthrough is CAR-T cell therapy, which involves modifying a patient’s T cells to target cancer-specific antigens. This personalized treatment has shown remarkable success in certain blood cancers. Additionally, cancer vaccines aim to trigger immune responses against tumor-specific or associated antigens, and while challenging, ongoing research is improving their efficacy. The historical progression of cancer immunotherapy, from Coley’s toxins to modern innovations like checkpoint inhibitors and CAR-T cell therapy, underscores its transformative impact on cancer treatment. As research delves deeper into the immune system’s complexities, immunotherapy is poised to become even more crucial in oncology, offering renewed hope to patients globally.

Cancer immunotherapy uses the body’s immune system to combat cancer, marking a significant advancement in treatment. This review traces its evolution from the late 19th century to its current status. It began with William Coley’s pioneering work using bacterial toxins to stimulate the immune system against cancer cells, establishing the foundational concept of immunotherapy. In the mid-20th century, cytokine therapies like interferons and interleukins emerged, demonstrating that altering the immune response could reduce tumors and highlighting the complex interplay between cancer and the immune system. The discovery of immune checkpoints, regulatory pathways that prevent autoimmunity but are exploited by cancer cells to evade detection, was a pivotal development. Another major breakthrough is CAR-T cell therapy, which involves modifying a patient’s T cells to target cancer-specific antigens. This personalized treatment has shown remarkable success in certain blood cancers. Additionally, cancer vaccines aim to trigger immune responses against tumor-specific or associated antigens, and while challenging, ongoing research is improving their efficacy. The historical progression of cancer immunotherapy, from Coley’s toxins to modern innovations like checkpoint inhibitors and CAR-T cell therapy, underscores its transformative impact on cancer treatment. As research delves deeper into the immune system’s complexities, immunotherapy is poised to become even more crucial in oncology, offering renewed hope to patients globally.

Purpose: Endometrial cancer (EC) ranks as one of the most prevalent gynecological malignancies globally. The presence and role of stromal tumor-infiltrating lymphocytes (TILs) in the tumor microenvironment have garnered interest due to their prognostic and therapeutic potential. This study aimed to evaluate the association between stromal TILs and various clinicopathological parameters in EC. Methods: A prospective study was conducted which included 30 histologically confirmed cases of endometrial carcinoma. Specimens collected from January 2023 to June 2024 were processed for routine histopathological examination and immunohistochemistry for CD3 and CD20 markers. TILs were quantified as per the International Immuno-Oncology Biomarker Working Group guidelines and categorized into low (<20%) and high (≥20%) TILs. Results: The study comprised 30 female patients, predominantly aged 51 to 60 years. Most tumors were of the endometrioid subtype (93.3%). High TILs were significantly associated with early tumor stage, lower grade, lesser myometrial invasion, and absence of nodal involvement on univariate analysis and with lower tumor stage and grade on multivariate analysis. No significant association was found between TILs and age, lymphovascular, or perineural invasion. Conclusion The findings suggest that high TIL infiltration correlates with favorable tumor characteristics, potentially serving as a prognostic marker for early and less aggressive EC. High TILs were associated with better tumor stage, grade, and reduced nodal involvement, indicating their protective role in tumor progression. However, the lack of association with certain parameters calls for further investigation into the functional state of TILs and their interactions within the tumor microenvironment.

Purpose: Breast cancer subtypes are delineated by human epidermal growth factor receptor 2 (HER2) expression, pivotal in treatment selection. HER2-positive tumors typically respond to targeted therapies, whereas HER2-negative tumors lack HER2 overexpression. However, a subset exhibits low HER2 expression without amplification, termed HER2 low breast cancer. Despite being distinct, its clinicopathological characteristics and therapeutic implications remain less understood. Methods: A retrospective cohort study was conducted on histologically confirmed breast cancer cases from January 2022 to December 2023. Clinicopathological data including age, tumor size, nodal involvement, and hormone receptor status were collected. Immunohistochemistry categorized tumors into luminal, triple-negative, and HER2-enriched subtypes. HER2 expression was re-evaluated, classifying tumors into HER2 low and HER2-negative based on staining intensity and amplification status. Statistical analysis was performed using SPSS software. Results: Seventy female patients with breast cancer were included, exhibiting diverse clinicopathological features. HER2 low tumors (40%) were significantly associated with higher tumor stage (P=0.03), nodal involvement (P=0.01), and positive androgen receptor expression (P=0.01). Subgroup analysis revealed HER2 low hormone receptor-positive cases (78.6%) were associated with higher tumor stage (P=0.01) and nodal involvement (P=0.01), while HER2 low triple-negative cases (21.4%) demonstrated distinct characteristics such as higher histological grade (P=0.02). Conclusion This study underscores the complexity of HER2 low breast cancer and its implications for clinical management, emphasizing the need for personalized treatment strategies. It provides insights into the clinicopathological parameters of HER2 low breast cancers, highlighting their diverse characteristics and clinical implications.

Purpose: Endometrial cancer is one of the most common gynecological cancers worldwide, with rising incidence rates. Despite therapeutic advances, it remains a significant cause of cancer-related deaths. Tumor budding (TB), characterized by single cells or small clusters at the invasive tumor front, is a recognized prognostic marker in several cancers but is less studied in endometrial cancer. Methods: This prospective cohort study included 30 patients with endometrial cancer who underwent surgical resection from January 2022 to June 2023. Formalin-fixed, paraffin-embedded tissue blocks were reviewed by two blinded pathologists. TB at the invasive front was assessed using hematoxylin and eosin staining. Clinical and pathological parameters, including age, histological type, grade, stage, myometrial invasion, lymphovascular space invasion, and nodal involvement, were recorded. Fisher’s exact and chi-square tests were used for statistical analyses. Results: Most patients (60%) were aged 51–60 years, with 93.3% diagnosed with endometrioid adenocarcinoma. Tumors were graded as 40% grade 1, 43.3% grade 2, and 16.7% grade 3. Staging showed 36.7% FIGO IA, 36.7% IB, 16.7% II, and 10% III. TB was classified as low (70%), intermediate (23.3%), and high (6.7%). Higher TB levels were significantly associated with higher tumor grade (P=0.03), advanced stage (P=0.02), and nodal involvement (P=0.01). Conclusion TB correlates with adverse features in endometrial cancer, including higher grade, advanced stage, and nodal involvement. These findings underscore TB’s potential as a prognostic marker, warranting validation in larger studies and exploration of its molecular basis to guide personalized treatments.

Purpose: Endometrial cancer (EC) ranks as one of the most prevalent gynecological malignancies globally. The presence and role of stromal tumor-infiltrating lymphocytes (TILs) in the tumor microenvironment have garnered interest due to their prognostic and therapeutic potential. This study aimed to evaluate the association between stromal TILs and various clinicopathological parameters in EC. Methods: A prospective study was conducted which included 30 histologically confirmed cases of endometrial carcinoma. Specimens collected from January 2023 to June 2024 were processed for routine histopathological examination and immunohistochemistry for CD3 and CD20 markers. TILs were quantified as per the International Immuno-Oncology Biomarker Working Group guidelines and categorized into low (<20%) and high (≥20%) TILs. Results: The study comprised 30 female patients, predominantly aged 51 to 60 years. Most tumors were of the endometrioid subtype (93.3%). High TILs were significantly associated with early tumor stage, lower grade, lesser myometrial invasion, and absence of nodal involvement on univariate analysis and with lower tumor stage and grade on multivariate analysis. No significant association was found between TILs and age, lymphovascular, or perineural invasion. Conclusion The findings suggest that high TIL infiltration correlates with favorable tumor characteristics, potentially serving as a prognostic marker for early and less aggressive EC. High TILs were associated with better tumor stage, grade, and reduced nodal involvement, indicating their protective role in tumor progression. However, the lack of association with certain parameters calls for further investigation into the functional state of TILs and their interactions within the tumor microenvironment.

Purpose: Breast cancer subtypes are delineated by human epidermal growth factor receptor 2 (HER2) expression, pivotal in treatment selection. HER2-positive tumors typically respond to targeted therapies, whereas HER2-negative tumors lack HER2 overexpression. However, a subset exhibits low HER2 expression without amplification, termed HER2 low breast cancer. Despite being distinct, its clinicopathological characteristics and therapeutic implications remain less understood. Methods: A retrospective cohort study was conducted on histologically confirmed breast cancer cases from January 2022 to December 2023. Clinicopathological data including age, tumor size, nodal involvement, and hormone receptor status were collected. Immunohistochemistry categorized tumors into luminal, triple-negative, and HER2-enriched subtypes. HER2 expression was re-evaluated, classifying tumors into HER2 low and HER2-negative based on staining intensity and amplification status. Statistical analysis was performed using SPSS software. Results: Seventy female patients with breast cancer were included, exhibiting diverse clinicopathological features. HER2 low tumors (40%) were significantly associated with higher tumor stage (P=0.03), nodal involvement (P=0.01), and positive androgen receptor expression (P=0.01). Subgroup analysis revealed HER2 low hormone receptor-positive cases (78.6%) were associated with higher tumor stage (P=0.01) and nodal involvement (P=0.01), while HER2 low triple-negative cases (21.4%) demonstrated distinct characteristics such as higher histological grade (P=0.02). Conclusion This study underscores the complexity of HER2 low breast cancer and its implications for clinical management, emphasizing the need for personalized treatment strategies. It provides insights into the clinicopathological parameters of HER2 low breast cancers, highlighting their diverse characteristics and clinical implications.

Purpose: Endometrial cancer is one of the most common gynecological cancers worldwide, with rising incidence rates. Despite therapeutic advances, it remains a significant cause of cancer-related deaths. Tumor budding (TB), characterized by single cells or small clusters at the invasive tumor front, is a recognized prognostic marker in several cancers but is less studied in endometrial cancer. Methods: This prospective cohort study included 30 patients with endometrial cancer who underwent surgical resection from January 2022 to June 2023. Formalin-fixed, paraffin-embedded tissue blocks were reviewed by two blinded pathologists. TB at the invasive front was assessed using hematoxylin and eosin staining. Clinical and pathological parameters, including age, histological type, grade, stage, myometrial invasion, lymphovascular space invasion, and nodal involvement, were recorded. Fisher’s exact and chi-square tests were used for statistical analyses. Results: Most patients (60%) were aged 51–60 years, with 93.3% diagnosed with endometrioid adenocarcinoma. Tumors were graded as 40% grade 1, 43.3% grade 2, and 16.7% grade 3. Staging showed 36.7% FIGO IA, 36.7% IB, 16.7% II, and 10% III. TB was classified as low (70%), intermediate (23.3%), and high (6.7%). Higher TB levels were significantly associated with higher tumor grade (P=0.03), advanced stage (P=0.02), and nodal involvement (P=0.01). Conclusion TB correlates with adverse features in endometrial cancer, including higher grade, advanced stage, and nodal involvement. These findings underscore TB’s potential as a prognostic marker, warranting validation in larger studies and exploration of its molecular basis to guide personalized treatments.