Cervical Squamous Cell Carcinoma

1. Disease Information

1.1 Definition and current understanding

Cervical squamous cell carcinoma (CSCC) is the most common histologic subtype of cervical cancer, arising from squamous epithelium of the cervix and strongly linked to persistent high‑risk human papillomavirus (hrHPV) infection. CSCC accounts for ~85% of cervical cancers in a recent clinical review spanning 2018–2025, consistent with long‑standing epidemiology. (nagdev2026advancesinscreening pages 1-2)

1.2 Key identifiers and classification

A structured summary of identifiers and nomenclature supported by retrieved sources is provided in the embedded artifact.

Table: This table summarizes the key identifiers, classification concepts, and nomenclature for cervical squamous cell carcinoma supported by the retrieved evidence. It highlights where formal identifiers were not explicitly found and preserves WHO 2020 terminology relevant for pathology reporting.

Key classification concept: The WHO 2020 classification emphasizes reporting cervical squamous carcinomas as HPV‑associated versus HPV‑independent, using p16 immunohistochemistry (IHC) block‑type positivity as a surrogate marker for HPV association; when classification cannot be established, “squamous cell carcinoma, NOS” is acceptable. (hohn20212020whoclassification pages 2-4, hohn20212020whoclassification pages 1-2)

1.3 Synonyms/alternative names

Common terms in the retrieved literature include “cervical SCC” and “cervical squamous cell carcinoma (CSCC).” (nagdev2026advancesinscreening pages 1-2)

1.4 Evidence provenance (aggregated vs patient-level)

Most disease-level facts in this report derive from aggregated resources (GBD analyses, guideline consortia, and narrative/systematic reviews). (ma2025globalregionaland pages 2-3, fischerova2024theroleof pages 1-2, zhou2025globalcervicalcancer pages 1-2)

2. Etiology

2.1 Primary causal factors

Persistent infection with hrHPV is the dominant etiologic driver of cervical cancer: one 2024 screening-focused review states “over 95% of cervical cancers are attributable to HPV.” (goldstein2024thefutureof pages 1-2)

HPV16 and HPV18 contribute the majority of cases globally: estimates in retrieved sources include ~70% (review) and ~71% (global screening review). (nagdev2026advancesinscreening pages 1-2, goldstein2024thefutureof pages 1-2)

2.2 Risk factors (human epidemiology)

A concise, quantitative risk-factor table (restricted to effects explicitly present in retrieved evidence) is embedded below.

Table: This table summarizes the main etiologic drivers, established risk cofactors, and protective/preventive measures for cervical squamous cell carcinoma using only quantitative findings explicitly available in the retrieved evidence. It is useful for quickly separating causal HPV biology from modifiable cofactors and current WHO-aligned prevention strategies.

Smoking: A 2023 systematic review/meta‑analysis (109 studies) reported pooled RR 1.70 (95% CI 1.53–1.88) for invasive cervical cancer in current vs never smokers, and RR 1.13 (95% CI 1.02–1.24) for former vs never smokers, with dose–response and risk reduction after cessation (risk approaching never smokers after ~15–16.5 years). (malevolti2023doseriskrelationshipsbetween pages 1-2, malevolti2023doseriskrelationshipsbetween pages 5-6)

HIV/immunosuppression: A 2026 epidemiology review reports “several‑fold increases in incidence among HIV‑positive women,” supporting HIV as a major cofactor that accelerates HPV persistence/progression. (jouya2026cervicalcancerepidemiology pages 12-13)

Reproductive/sexual cofactors: Early sexual debut, multiple partners, and high parity are cited as important cofactors in a 2026 epidemiology review. (jouya2026cervicalcancerepidemiology pages 12-13)

2.3 Protective factors

HPV vaccination is the major primary preventive factor within the WHO elimination framework (targets described below). (zhou2025globalcervicalcancer pages 1-2)

Smoking cessation is protective: dose–response meta-analysis indicates risk declines with time since quitting and approximates never-smoker risk after ~15–16.5 years. (malevolti2023doseriskrelationshipsbetween pages 5-6, malevolti2023doseriskrelationshipsbetween pages 6-7)

2.4 Gene–environment interactions

Direct quantitative gene–environment interaction estimates were not identified in the retrieved sources during this tool session. Mechanistically, HPV-driven oncogenesis interacts with host immune status (e.g., HIV) and tobacco exposure, consistent with multi-factorial progression models discussed in reviews. (jouya2026cervicalcancerepidemiology pages 12-13, malevolti2023doseriskrelationshipsbetween pages 1-2)

3. Phenotypes (clinical presentation)

3.1 Common phenotypes (signs/symptoms)

Recent guideline and clinical review materials in the retrieved set describe typical presenting features including abnormal vaginal bleeding/discharge and pelvic pain (not always CSCC‑specific but common across cervical cancer). (nagdev2026advancesinscreening pages 1-2)

3.2 Suggested HPO terms (not exhaustive)

Because structured phenotype-frequency estimates were not retrieved in this session, the following HPO terms are suggested as standard mappings (frequency requires additional sourcing): - Abnormal uterine bleeding / postcoital bleeding: HP:0000132 (Abnormality of menstruation) or HP:0000858 (Menorrhagia) depending on context. - Vaginal discharge: HP:0000146 (Vaginal discharge). - Pelvic pain: HP:0002027 (Abdominal pain) / pelvic pain term where available in HPO. - Anemia (from bleeding): HP:0001903 (Anemia).

3.3 Quality-of-life impact

Direct QoL instrument values specific to CSCC were not extracted from the retrieved evidence in this session; however, guideline and review sources emphasize substantial morbidity in advanced disease and the importance of palliative care access. (zhou2025globalcervicalcancer pages 1-2)

4. Genetic / Molecular Information

4.1 Somatic driver landscape (high-level)

OpenTargets disease–target associations for “cervical squamous cell carcinoma” highlight recurrently implicated cancer genes including PIK3CA, FBXW7, KMT2C, EP300, KMT2D, MAPK1, TP53, PTEN, STK11, NOTCH1, ERBB2, among others. This provides a curated pointer to commonly altered pathways in CSCC but is not itself a sequencing cohort analysis. (OpenTargets Search: cervical squamous cell carcinoma)

4.2 HPV-associated vs HPV-independent molecular patterns

A 2024 national guideline summary reports that HPV-associated cervical SCC is the dominant category (~90–95%), while HPV-independent SCC constitutes a minority (~5–7%) and is often associated with abnormal p53 staining and distinct molecular associations (e.g., KRAS, ARID1A, PTEN). (sznurkowski2024thepolishsociety pages 2-3)

4.3 Epigenetics

WHO 2020 discussions note p16 as a surrogate and acknowledge false negatives (e.g., p16 hypermethylation in a small fraction of CIN3), but systematic CSCC epigenomic signatures were not comprehensively extracted in this session. (hohn20212020whoclassification pages 6-8)

4.4 Pathogenic variants (germline)

No germline causal variant set (ClinVar/ClinGen-style) was retrieved for CSCC in this session; CSCC is typically infection-driven with predominantly somatic alterations. (goldstein2024thefutureof pages 1-2)

5. Environmental Information

5.1 Lifestyle/environmental contributors

Smoking is a robust, quantitatively supported risk factor with dose–response effects (RRs above). (malevolti2023doseriskrelationshipsbetween pages 5-6, malevolti2023doseriskrelationshipsbetween pages 1-2)

5.2 Infectious agents

High-risk HPV is the central infectious cause; HPV16/18 dominate global attribution fractions. (goldstein2024thefutureof pages 1-2, nagdev2026advancesinscreening pages 1-2)

6. Mechanism / Pathophysiology

6.1 Causal chain (HPV to CSCC)

A mechanistic review of HPV-associated lower genital tract cancers describes HPV oncoprotein-driven immune evasion, including upregulation of PD‑1/PD‑L1 axis and other checkpoint pathways (IDO1, LAG3, TIM3/Galectin‑9, TIGIT), providing a link from viral oncogenesis to an immunosuppressive tumor microenvironment and therapeutic vulnerability to checkpoint blockade. (zafar2025advancesandchallenges pages 7-8, zafar2025advancesandchallenges pages 20-21)

6.2 Immune microenvironment and checkpoint biology

HPV16 E6 has been described as promoting PD‑L1 expression via a miR‑143/HIF‑1α pathway; HPV-positive cervical cancer cells can also influence exosomal PD‑L1 expression by fibroblasts via CXCL10/CXCR3 and JAK‑STAT signaling, supporting multi-cell mechanisms for immune escape. (zafar2025advancesandchallenges pages 20-21)

6.3 Spatial transcriptomics: metabolic states and oncogenic regulators (2024 primary study)

A 2024 Journal of Translational Medicine study used spatial transcriptomics integrated with scRNA‑seq and TCGA analyses to map hypermetabolic versus hypometabolic regions in CSCC and identify regulatory factors. (zhou2024spatialtranscriptomicsreveals pages 1-2, zhou2024spatialtranscriptomicsreveals pages 9-12)

Key reported findings include: - Leading edge regions were characterized as uniformly hypermetabolic, whereas tumor core contained mixed hyper‑ and hypometabolic spots. (zhou2024spatialtranscriptomicsreveals pages 9-12) - APP was identified as a signaling molecule released by cancer cells with higher expression in hypermetabolic regions, and APP expression correlated with transcription factor TRPS1; functional knockdowns reduced proliferation/migration/invasion in vitro. (zhou2024spatialtranscriptomicsreveals pages 1-2, zhou2024spatialtranscriptomicsreveals pages 14-17) - Immune context differed by region, with PD‑L1 and IDO1 elevated in tumor center in one excerpted analysis, consistent with immune suppression. (zhou2024spatialtranscriptomicsreveals pages 14-17, zhou2024spatialtranscriptomicsreveals pages 6-9)

Visual evidence from the same study illustrating spatial hyper/hypometabolic regions and TRPS1/APP expression patterns is available in retrieved figure crops. (zhou2024spatialtranscriptomicsreveals media 5eccae45, zhou2024spatialtranscriptomicsreveals media 8e0f5cba, zhou2024spatialtranscriptomicsreveals media c108e719, zhou2024spatialtranscriptomicsreveals media f3ff4cda)

6.4 Suggested ontology mappings

GO biological processes (examples): - GO:0006915 (apoptotic process) - GO:0007049 (cell cycle) - GO:0006955 (immune response) - GO:0006096 (glycolytic process) / GO:0006119 (oxidative phosphorylation)

Cell Ontology (CL) cell types (examples): - CL:0000066 (epithelial cell) - CL:0000236 (B cell) - CL:0000623 (natural killer cell) - CL:0000904 (macrophage) - CL:0000451 (dendritic cell)

These ontology suggestions reflect mechanisms described in immune/multi‑omics sources, though specific term-to-claim mappings require additional structured curation beyond retrieved text. (zafar2025advancesandchallenges pages 20-21, zhou2024spatialtranscriptomicsreveals pages 14-17)

7. Anatomical Structures Affected

7.1 Organ and tissue level

Primary site is the cervix uteri, involving squamous epithelium (outer surface). (nagdev2026advancesinscreening pages 1-2)

Suggested UBERON terms (examples): - UBERON:0000002 (uterine cervix) - UBERON:0000458 (epithelium)

7.2 Subcellular/localization (GO-CC suggestions)

• GO:0005634 (nucleus) for transcriptional regulators (e.g., TRPS1)
• GO:0005886 (plasma membrane) for receptor/ligand interactions

8. Temporal Development (natural history)

The natural history from HPV infection through precancer to invasive carcinoma is described as well characterized in recent reviews, supporting screening and prevention paradigms. (nagdev2026advancesinscreening pages 1-2)

(Explicit quantitative transition probabilities and CIN stage durations were not extracted in the retrieved evidence during this session.)

9. Inheritance and Population

9.1 Epidemiology (recent global statistics)

Global incidence and mortality estimates reported in the retrieved sources include: - 2022: 661,021 new cases and 348,189 deaths (global elimination progress analysis). (zhou2025globalcervicalcancer pages 1-2) - GLOBOCAN 2022 (as cited in a 2026 clinical review): 662,000 new cases and 349,000 deaths, with mortality rate 7.1 per 100,000. (nagdev2026advancesinscreening pages 1-2) - 2021 (GBD-based estimates): 667,000 incident cases and 297,000 deaths; ~7.44 million DALYs attributed to cervical cancer. (ma2025globalregionaland pages 2-3)

Health inequities are substantial: one 2026 review states that over 80% of cervical cancer deaths occur in low-HDI settings. (jouya2026cervicalcancerepidemiology pages 12-13)

9.2 Inheritance pattern

CSCC is predominantly infection-associated and not typically inherited as a Mendelian disorder in the retrieved sources. (goldstein2024thefutureof pages 1-2)

10. Diagnostics

10.1 Screening and diagnostic pathway (current practice and developments)

Recent screening developments include primary HPV testing, HPV self‑sampling, and molecular triage strategies (DNA methylation assays, dual-stain cytology), as summarized in a 2024 review on the future of cervical screening. (goldstein2024thefutureof pages 1-2)

10.2 Pathology / biomarkers

WHO 2020 recommends distinguishing HPV-associated from HPV-independent squamous carcinomas and identifies p16 block staining as a reliable (imperfect) surrogate for HPV association; when uncertain, SCC NOS is acceptable. (hohn20212020whoclassification pages 2-4)

10.3 Imaging/staging (2023 guideline update summarized in 2024)

The ESGO/ESTRO/ESP imaging update (2023) recommends: - Pelvic MRI or expert transvaginal/transrectal ultrasound for local tumor delineation and assessing invasion. (fischerova2024theroleof pages 1-2) - Contrast-enhanced CT or 18F‑FDG PET/CT for extrapelvic spread in locally advanced disease or when suspicious nodes are present. (fischerova2024theroleof pages 1-2)

MRI is emphasized as modality of choice for local staging; PET/CT is valuable for nodal/distant disease detection but less optimal for local staging due to soft tissue limitations. (fischerova2024theroleof pages 7-8)

11. Outcome / Prognosis

11.1 Prognostic biomarkers and microenvironment

Spatial transcriptomics evidence suggests that elevated APP and TRPS1 correlate with poorer survival in TCGA CSCC cohort (p-values reported) and promote aggressive phenotypes in vitro, supporting their candidacy as prognostic/biological markers. (zhou2024spatialtranscriptomicsreveals pages 14-17)

11.2 Advanced disease outcomes and unmet need

A 2024 review on advanced/recurrent cervical cancer notes poor prognosis historically and summarizes improved outcomes with immunotherapy-based regimens. (zafar2025advancesandchallenges pages 7-8)

(Registry-derived 5‑year survival stratified by stage/histology was not retrieved in this session.)

12. Treatment

12.1 Standard local therapy (curative intent)

A mechanistic/clinical review notes standard local therapy for cervical cancer includes pelvic external beam radiotherapy (EBRT) with concurrent platinum-based chemotherapy and brachytherapy. (zafar2025advancesandchallenges pages 7-8)

12.2 Systemic therapy—immune checkpoint inhibitors (advanced/recurrent/metastatic)

Evidence extracted from an immunotherapy review includes: - KEYNOTE‑826 (pembrolizumab + chemotherapy ± bevacizumab): reported hazard ratio for death ~0.64 (36% reduction in risk of death) and survival prolongation by 12.1 months in the cited review excerpt. (dey2025immunotherapyincervical pages 7-8) - EMPOWER‑Cervical 1 (cemiplimab vs chemotherapy after platinum): median OS 12 vs 8.5 months; ORR 16.4% vs 6.3% in the cited review excerpt. (dey2025immunotherapyincervical pages 7-8)

A separate checkpoint-focused review reports pembrolizumab median OS 28.6 vs 16.5 months (trial context described) and reiterates cemiplimab OS 12 vs 8.5 months. (zafar2025advancesandchallenges pages 7-8)

12.3 Treatment-related toxicity (high level)

The immunotherapy review notes increased toxicities with combination regimens (e.g., anemia, neuropathy) and highlights immune-related adverse events as clinically relevant. (dey2025immunotherapyincervical pages 7-8)

12.4 Suggested MAXO mappings (examples)

• MAXO:0000058 (radiotherapy)
• MAXO:0000010 (chemotherapy)
• MAXO term for immune checkpoint inhibitor therapy (e.g., “immune checkpoint inhibitor therapy”)—exact MAXO ID not retrieved in this session.

13. Prevention

13.1 WHO elimination strategy and targets

A 2025 global elimination analysis summarizes WHO’s 90–70–90 strategy by 2030: - 90% of girls vaccinated by age 15, - 70% of women screened with high-performance tests by ages 35 and 45, - 90% of women with cervical disease treated. (zhou2025globalcervicalcancer pages 1-2)

The elimination threshold is defined as <4 new cases per 100,000 women per year. (zhou2025globalcervicalcancer pages 1-2)

13.2 Screening technology modernization (2024)

Emerging modalities include rapid low-cost HPV testing, self-sampling, DNA methylation assays, and AI-assisted digital colposcopy interpretation, as summarized in a 2024 screening review. (goldstein2024thefutureof pages 1-2)

14. Other Species / Natural Disease

No cross-species naturally occurring CSCC analog with comparable HPV-driven etiology was retrieved in this session. Comparative HPV-associated squamous carcinomas across lower genital tract sites are discussed broadly in HPV-related reviews, but not as a dedicated veterinary natural disease section. (zafar2025advancesandchallenges pages 7-8)

15. Model Organisms

Specific in vivo model organism systems (e.g., HPV transgenic mouse models), organoids, or PDX resources were not retrieved in this session. The spatial transcriptomics CSCC work used human FFPE tumors integrated with scRNA-seq and in vitro functional assays (HeLa knockdowns), which constitutes a human tissue + cell line translational model rather than an animal model. (zhou2024spatialtranscriptomicsreveals pages 14-17, zhou2024spatialtranscriptomicsreveals pages 1-2)

Recent developments (2023–2024 highlights)

1. Spatial transcriptomics in CSCC (2024): identification of spatially resolved metabolic states and regulators (APP/TRPS1), with supporting figure evidence for regional metabolic patterns and gene expression. (zhou2024spatialtranscriptomicsreveals pages 1-2, zhou2024spatialtranscriptomicsreveals pages 14-17, zhou2024spatialtranscriptomicsreveals media 5eccae45, zhou2024spatialtranscriptomicsreveals media f3ff4cda)
2. Updated European imaging recommendations (2023 update, published 2024): stronger operational role for expert ultrasound and MRI in local staging and PET/CT or CECT for extrapelvic evaluation in higher-risk scenarios. (fischerova2024theroleof pages 1-2, fischerova2024theroleof pages 7-8)
3. Smoking risk quantification updated meta-analysis (2023): robust pooled RRs and cessation timelines relevant to prevention counseling. (malevolti2023doseriskrelationshipsbetween pages 1-2, malevolti2023doseriskrelationshipsbetween pages 5-6)
4. Screening innovation synthesis (2024): primary HPV testing, self-sampling, methylation triage, dual stain cytology, and AI-enabled tools highlighted as near-term implementation candidates. (goldstein2024thefutureof pages 1-2)

Embedded figure evidence (spatial transcriptomics)

The following retrieved figure crops from the 2024 CSCC spatial transcriptomics study support claims about metabolic regions and APP/TRPS1 spatial patterns: hyper/hypometabolic region maps and TRPS1/APP spatial expression panels. (zhou2024spatialtranscriptomicsreveals media 5eccae45, zhou2024spatialtranscriptomicsreveals media 8e0f5cba, zhou2024spatialtranscriptomicsreveals media c108e719, zhou2024spatialtranscriptomicsreveals media f3ff4cda)

Key gaps (not found in retrieved sources in this session)

• MONDO and MeSH unique identifiers for CSCC (codes not explicitly captured in retrieved texts). (OpenTargets Search: cervical squamous cell carcinoma)
• Detailed phenotype frequencies mapped to HPO and validated QoL instrument statistics specific to CSCC.
• Comprehensive germline variant catalog and population allele frequencies.
• Dedicated model organism summaries (HPV transgenic mice, organoids, PDX) with citations.

These gaps reflect limitations of the retrieved document set rather than absence of knowledge in the broader literature.

References

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2. (OpenTargets Search: cervical squamous cell carcinoma): Open Targets Query (cervical squamous cell carcinoma, 39 results). Buniello, A. et al. (2025). Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery. Nucleic Acids Research.

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4. (hohn20212020whoclassification pages 2-4): Anne Kathrin Höhn, Christine E. Brambs, Grit Gesine Ruth Hiller, Doris May, Elisa Schmoeckel, and Lars-Christian Horn. 2020 who classification of female genital tumors. Geburtshilfe und Frauenheilkunde, 81:1145-1153, Oct 2021. URL: https://doi.org/10.1055/a-1545-4279, doi:10.1055/a-1545-4279. This article has 495 citations and is from a peer-reviewed journal.

5. (sznurkowski2024thepolishsociety pages 3-4): Jacek J. Sznurkowski, Lubomir Bodnar, Łukasz Szylberg, Agnieszka Zołciak-Siwinska, Anna Dańska-Bidzińska, Dagmara Klasa-Mazurkiewicz, Agnieszka Rychlik, Artur Kowalik, Joanna Streb, Mariusz Bidziński, and Włodzimierz Sawicki. The polish society of gynecological oncology guidelines for the diagnosis and treatment of cervical cancer (v2024.0). Journal of Clinical Medicine, 13:4351, Jul 2024. URL: https://doi.org/10.3390/jcm13154351, doi:10.3390/jcm13154351. This article has 10 citations.

6. (hohn20212020whoclassification pages 4-6): Anne Kathrin Höhn, Christine E. Brambs, Grit Gesine Ruth Hiller, Doris May, Elisa Schmoeckel, and Lars-Christian Horn. 2020 who classification of female genital tumors. Geburtshilfe und Frauenheilkunde, 81:1145-1153, Oct 2021. URL: https://doi.org/10.1055/a-1545-4279, doi:10.1055/a-1545-4279. This article has 495 citations and is from a peer-reviewed journal.

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12. (goldstein2024thefutureof pages 1-2): Amelia R Goldstein, Mallory Gersh, Gabriela Skovronsky, and Chailee Moss. The future of cervical cancer screening. International Journal of Women's Health, 16:1715-1731, Oct 2024. URL: https://doi.org/10.2147/ijwh.s474571, doi:10.2147/ijwh.s474571. This article has 43 citations and is from a peer-reviewed journal.

13. (malevolti2023doseriskrelationshipsbetween pages 5-6): Maria Chiara Malevolti, Alessandra Lugo, Marco Scala, Silvano Gallus, Giuseppe Gorini, Alessio Lachi, and Giulia Carreras. Dose-risk relationships between cigarette smoking and cervical cancer: a systematic review and meta-analysis. European Journal of Cancer Prevention, 32:171-183, Nov 2023. URL: https://doi.org/10.1097/cej.0000000000000773, doi:10.1097/cej.0000000000000773. This article has 50 citations and is from a peer-reviewed journal.

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15. (malevolti2023doseriskrelationshipsbetween pages 6-7): Maria Chiara Malevolti, Alessandra Lugo, Marco Scala, Silvano Gallus, Giuseppe Gorini, Alessio Lachi, and Giulia Carreras. Dose-risk relationships between cigarette smoking and cervical cancer: a systematic review and meta-analysis. European Journal of Cancer Prevention, 32:171-183, Nov 2023. URL: https://doi.org/10.1097/cej.0000000000000773, doi:10.1097/cej.0000000000000773. This article has 50 citations and is from a peer-reviewed journal.

16. (jouya2026cervicalcancerepidemiology pages 12-13): Sara Jouya, Zahra Shahabinia, Afrooz Mazidimoradi, Leila Allahqoli, Hamid Salehiniya, and Do-Youn Lee. Cervical cancer epidemiology: global incidence, mortality, survival, risk factors, and equity in hpv screening and vaccination. Journal of Clinical Medicine, 15:1079, Jan 2026. URL: https://doi.org/10.3390/jcm15031079, doi:10.3390/jcm15031079. This article has 4 citations.

17. (shao2026globaltrendsand pages 1-2): Dongxuan Shao, Ping Wu, Huici Jiang, and Zhijie Wang. Global trends and future projections of cervical cancer burden: an integrated analysis of gbd 2021, un population and who hpv vaccination data. Frontiers in Public Health, Jan 2026. URL: https://doi.org/10.3389/fpubh.2026.1702186, doi:10.3389/fpubh.2026.1702186. This article has 3 citations.

18. (hohn20212020whoclassification pages 6-8): Anne Kathrin Höhn, Christine E. Brambs, Grit Gesine Ruth Hiller, Doris May, Elisa Schmoeckel, and Lars-Christian Horn. 2020 who classification of female genital tumors. Geburtshilfe und Frauenheilkunde, 81:1145-1153, Oct 2021. URL: https://doi.org/10.1055/a-1545-4279, doi:10.1055/a-1545-4279. This article has 495 citations and is from a peer-reviewed journal.

19. (zafar2025advancesandchallenges pages 7-8): Marhama Zafar, Narjes Sweis, Hitesh Kapoor, and Gerald Gantt. Advances and challenges in the treatment of hpv-associated lower genital tract cancers by immune checkpoint blockers: insights from basic and clinical science. Cancers, 17:1260, Apr 2025. URL: https://doi.org/10.3390/cancers17081260, doi:10.3390/cancers17081260. This article has 3 citations.

20. (zafar2025advancesandchallenges pages 20-21): Marhama Zafar, Narjes Sweis, Hitesh Kapoor, and Gerald Gantt. Advances and challenges in the treatment of hpv-associated lower genital tract cancers by immune checkpoint blockers: insights from basic and clinical science. Cancers, 17:1260, Apr 2025. URL: https://doi.org/10.3390/cancers17081260, doi:10.3390/cancers17081260. This article has 3 citations.

21. (zhou2024spatialtranscriptomicsreveals pages 1-2): Limin Zhou, Jiejie Liu, Peipei Yao, Xing Liu, Fei Chen, Yu Chen, Li Zhou, Chao Shen, You Zhou, Xin Du, and Junbo Hu. Spatial transcriptomics reveals unique metabolic profile and key oncogenic regulators of cervical squamous cell carcinoma. Journal of Translational Medicine, Dec 2024. URL: https://doi.org/10.1186/s12967-024-06011-y, doi:10.1186/s12967-024-06011-y. This article has 8 citations and is from a peer-reviewed journal.

22. (zhou2024spatialtranscriptomicsreveals pages 9-12): Limin Zhou, Jiejie Liu, Peipei Yao, Xing Liu, Fei Chen, Yu Chen, Li Zhou, Chao Shen, You Zhou, Xin Du, and Junbo Hu. Spatial transcriptomics reveals unique metabolic profile and key oncogenic regulators of cervical squamous cell carcinoma. Journal of Translational Medicine, Dec 2024. URL: https://doi.org/10.1186/s12967-024-06011-y, doi:10.1186/s12967-024-06011-y. This article has 8 citations and is from a peer-reviewed journal.

23. (zhou2024spatialtranscriptomicsreveals pages 14-17): Limin Zhou, Jiejie Liu, Peipei Yao, Xing Liu, Fei Chen, Yu Chen, Li Zhou, Chao Shen, You Zhou, Xin Du, and Junbo Hu. Spatial transcriptomics reveals unique metabolic profile and key oncogenic regulators of cervical squamous cell carcinoma. Journal of Translational Medicine, Dec 2024. URL: https://doi.org/10.1186/s12967-024-06011-y, doi:10.1186/s12967-024-06011-y. This article has 8 citations and is from a peer-reviewed journal.

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