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Background:
Communication

STK11 Mutated Lung Adenocarcinoma: A Molecular and Clinicopathologic Study

by
Jeffrey Jean
1,2,
William D. Wallace
1 and
Guang-Qian Xiao
1,*
1
Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA
2
Labcorp, Buffalo, NY 14203, USA
*
Author to whom correspondence should be addressed.
J. Mol. Pathol. 2025, 6(4), 28; https://doi.org/10.3390/jmp6040028
Submission received: 23 September 2025 / Revised: 5 November 2025 / Accepted: 12 November 2025 / Published: 17 November 2025
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Abstract

Targetable gene alterations have become increasingly important in the treatment of cancers. Thirty STK11-mutated lung cancers from 199 cases with molecular profiling performed during 2016–2024 were studied for clinical, morphologic, immunohistochemical (IHC) and molecular features. Of the 30 STK11-mutated lung cancers, 29 were lung adenocarcinomas (LADCs) and 1 was large cell neuroendocrine carcinoma (LCNEC). STK11 mutation was not found in other subtypes of lung cancers. Of the 29 STK11-mutated LADCs, 6 (21%) were mucinous and 23 (79%) were non-mucinous. Of the 19 non-mucinous LADCs with sufficient material for IHC, 9 (47%) displayed acinar/papillary/lepidic patterns, 8 (42%) were poorly differentiated (solid/trabecular/basaloid/complex glandular), and 2 (11%) had mixed solid and acinar patterns. The most common concurrent altered genes were KRAS (52%), followed by TP53 (38%), KEAP1 (34%), and DNA repair genes (BRCA2/ATM) (21%). A total of 6/15 (40%) LADCs with a KRAS mutation presented with mucinous morphology. Concurrent EGFR, ROS, or ALK alterations with STK11 mutation were rare or non-existent. Of the 3 LADCs with SMARCA4 deficiency, 2 were mucinous and 1 had basaloid/adenoid cystic-like features. All the cases were microsatellite stable (MSS). The majority (55%) had low TMB (<10). Most (86%) had PD-L1 TPS 0 or <5%. Among the 14 non-mucinous LADCs with IHC performed, 5 (36%) were TTF-1-negative and all displayed poorly differentiated morphology. Overall, 8/10 (80%) of poorly differentiated components in non-mucinous LADCs were negative for TTF-1. In contrast, all LADCs with better differentiated patterns (acini/papillary/lepidic) were positive for TTF-1. The majority (14/21, 67%) of patients with available follow-up presented with metastasis.

1. Introduction

Adenocarcinoma is the most common malignancy in the lung. Lung adenocarcinoma (LADC) can be further subclassified into mucinous and non-mucinous subtypes. Smoking is the most common risk factor for lung cancers [1], including LADC. With the advancement of molecular techniques and cancer research, targetable gene alterations have become increasingly important in the treatment of cancers. For example, EGFR-targeted therapy has become a cornerstone in the management of advanced LADCs [2,3].
Serine/threonine kinase 11 (STK11), encoding liver kinase B1 (LKB1), is a tumor suppressor gene [4,5]. Germline loss-of-function mutation in STK11 gives rise to Peutz-Jeghers syndrome [5,6], which is associated with a substantially increased lifetime risk of many cancers [5,7]. In the sporadic setting, STK11 mutations have also been found in a subset of LADCs [5,8,9,10]. Although STK11-mutated lung cancers have been sporadically studied, many aspects, including histopathologic features, remain to be elucidated.
In clinical pathology practice, differentiation of primary lung carcinoma versus metastatic adenocarcinoma mainly relies on immunohistochemical (IHC) marker study, in particular, TTF-1 and Napsin A expression in LADC [11]. TTF-1 is reported to be positive in ~90% non-mucinous LADC [12,13]. Whereas, for mucinous LADC, TTF-1 is often negative [14]. The TTF-1/Napsin A-negative non-mucinous LADCs have, so far, not been well characterized.
The aim of this study is to investigate the histomorphologic, IHC, clinical, and molecular features of STK11-mutated LADCs.

2. Materials and Methods

Clinical Cases and Tissue Samples
This study was approved by the USC Institutional Review Board (HS-24-00234). A total of 199 cases of primary and metastatic lung cancers from needle biopsy or resection specimens accessioned at our institution from 2016 to 2024 with comprehensive molecular profiling were found. STK11 mutation was identified in 30 cases (29 LADCs and 1 large cell neuroendocrine carcinoma (LCNEC)). The lung origin and adenocarcinoma subtype were confirmed by clinical and imaging studies, IHC (TTF-1/Napsin A), and/or mucicarmine stain. Other IHC markers (e.g., p40, CK7) commonly used in the workup for lung cancer and markers for exclusion of metastasis of non-lung origin were also performed when appropriate. Neuroendocrine carcinoma was confirmed by neuroendocrine markers (synaptophysin/chromogranin/CD56/INSM1).
Clinical and Pathologic Assessment
Given that the vast majority of STK11-mutated lung cancers were LADCs, this study mainly focused on STK11-mutated LADCs. All the 29 STK11-mutated LADCs were reviewed for their molecular features, IHC profile, and, when tissue was available for review, blindly by two pathologists for their morphologic growth patterns (defined by WHO). Patients’ demographic information, smoking history, and clinical follow-up data (from 7 months to 8 years) were also recorded.
Immunohistochemistry
IHC stains were performed on some of the cases based on clinical needs at the time of original case sign-out. The IHC stains were performed with a Bond III automated immunostaining platform (Leica Biosystems, Nussloch, Germany) using standard clinical protocols with appropriate positive and negative controls. Briefly, unstained glass slides of 5 µm thick tissue sections were baked and dewaxed following standard procedures. Heat-induced epitope retrieval was performed using BOND Epitope Retrieval Solution 1 (ER1) or BOND Epitope Retrieval Solution 2 (ER2) (Leica Biosystems) at 100 °C for 30 min. The antibodies used included TTF-1 (SPT24, Leica, Wetzlar, Germany), Napsin-A (TMU-Ad02, Biocare, Pacheco, USA), p40 (BC28, Biocare), CK7 (RN7, Leica), and neuroendocrine markers (Synaptophysin (27G12, Leica), Chromogranin (5H7, Leica), CD56 (CD564, Leica), and INSM1 (A-8, Santa Cruz, USA), among others. The IHC stains were recorded as positive (at least 10% of tumor cells with moderate or strong stain) or negative for each case, as well as for the poorly differentiated and better differentiated components when both were present in the same tumor.
Gene Sequencing and Molecular Analysis
The genetic alterations, including tumor mutation burden (TMB), microsatellite stability (MSS), and PD-L1 tumor percentage score (TPS), were analyzed by Caris Molecular Intelligence comprehensive tumor profiling services (Caris Life Sciences, Irving, USA) [15]. Briefly, Caris’s MI Profile Tumor Seek Hybrid was used along with the IHC in this study. IlluminaNovaSeq 6000 sequencers (San Diego, USA) were used to perform whole exome sequencing (WES) and whole transcriptome sequencing (WTS), which could detect 23,000+ genes, with more than 700 of these genes being documented as clinically relevant. Sequencing results were analyzed by Caris’ NGS bioinformatic pipeline, and reports were provided by Report Generation software (v4.4). Microsatellite instability status was detected in this assay. Tumor-only MSI status by NGS was determined by the direct analysis of known microsatellite regions sequenced. Tumor mutational burden (TMB) was determined by the number of non-synonymous, somatic mutations per one megabase (Mb) of sequenced DNA in the tumor sample. The cut-offs for low TMB and high TMB were <10 and ≥10 mut/Mb, respectively. IHC antibodies were also used in combination with the MI Tumor Seek Hybrid assay. PD-L1 22c3 (Dako, Santa Clara, USA) IHC was used for tumor proportion score (TPS) calculation. The TPC was grouped into three categories based on membranous staining of viable tumor cells: less than 1%, 1–49%, and at least 50%, which corresponded to negative, low positive, and high positive, respectively. It needed complete or partial membranous staining of viable tumor cells. The results were then compiled into a final report. More specific details of the methods used, including the bioinformatics pipeline, can be potentially obtained by directly contacting Caris.

3. Results

Clinical And Morpho-Pathologic Features of STK11-Mutated LADCs
Of the 199 lung cancer cases with molecular profiling performed, 112 were LADCs, 68 squamous cell carcinomas, 7 adenosquamous carcinomas, 4 adenoid cystic carcinomas, 4 large cell neuroendocrine carcinomas (LCNEC), 2 small cell carcinomas, and 2 spindle cell/pleomorphic carcinomas. Of the 199 cases, 30 (15%) had the STK11 mutation. Of the 30 cases with STK11 mutation, 29 were LADCs, accounting for 26% of the 112 LADCs studied, and 1 was LCNEC. None of the squamous cell carcinomas, adenosquamous carcinomas, adenoid cystic carcinomas, or pleomorphic carcinomas showed STK11 mutation. Patients’ ages ranged from 59 to 92 years old (mean 74 ± 9) with male predominance (the ratio of male to female was 4:1). Most patients (24/30, 80%) were current or former smokers, and almost all (28/30, 93%) had more than 10 years of smoking history.
Of the 29 STK11-mutated LADCs, 6 (21%) were mucinous and 23 (79%) were non-mucinous. Of the 23 non-mucinous LADCs, 19 contained adequate tissue for assessment of growth patterns. Of these 19 cases, 9 (47%) displayed acinar/papillary/lepidic growth patterns, 8 (42%) showed poorly differentiated (solid/nested/trabecular/basaloid/complex glandular/cribriform patterns), and 2 (2/19, 11%) had mixed solid and acinar patterns.
TMB, Other Concurring Gene Alterations, And Histopathologic Correlation for STK11-Mutated LADCs
TMB for these STK11-mutated LADCs ranged from 2 to 17 (mean 8.6 ± 3.8). A total of 16/29 (55%) had low TMB (<10), and 13 (45%) had moderate to high TMB (≥10). A total of 15/29 (52%) LADCs had a KRAS mutation, of which 6/15 (40%) presented with mucinous morphology.
Tumor suppressor genes were the second most common occurring alterations: 11/29 (38%) with TP53 mutation, 1 with MDM2 amplification, and 1 with APC alteration.
KEAP1 alterations were present in 10/29 (34%) LADCs. None of the LADCs with combined STK11 and KEAP1 mutations was associated with mucinous morphology, even in the setting of a KRAS mutation.
DNA repair gene (BRCA2, ATM) alterations were not uncommon and seen in 6/29 (21%) cases. DNA repair gene alteration and tumor suppressor gene (TP53/MDM2/APC) alterations appeared to be mutually exclusive. Concurrent EGFR and STK11 alterations were exceptionally uncommon and seen in only 1/30 (3.3%) cases. No ROS or ALK alterations were found in this series.
Of note, there were 3 LADCs with SMARCA4 deficiency, 2 of which were mucinous and 1 basaloid/adenoid cystic-like.
MSI, PD-L1, and IHC Features of STK11-Mutated LADCs
All 30 STK11-mutated lung cancer cases were microsatellite stable (MSS).
Of the 29 STK11-mutated LADCs, 20/29 (69%) had PD-L1 TPS 0; 7/29 (24%) had PD-L1 TPS 1–49%; the remaining 2 LADCs (7%) had high (≥50%) PD-L1 TPS (90% and 100%, respectively). Both cases with high PD-L1 TPS had ATM and KEAP1 alterations.
Among the 15 cases with IHC performed, TTF-1/Napsin A negativity was seen in 1 LCNEC and 6/15 (40%) of LADCs (1 mucinous and 5 non-mucinous). The growth pattern of the 5 TTF-1/Napsin A negative non-mucinous LADCs included solid/trabecular/basaloid patterns (Figure 1). Interestingly, 2 cases showed mixed positive TTF-1/Napsin A in better differentiated acinar/papillary patterns and negative TTF-1/Napsin A in poorly differentiated (solid/nested) areas (Figure 2). Overall, of the 10 STK11-mutated LADCs containing poorly differentiated (solid/nested/trabecular/basaloid/complex glandular) patterns, 8 (80%) exhibited TTF-1/Napsin A negativity in poorly differentiated components. In contrast, all the LADCs with better differentiated patterns (acini/papillary/lepidic) were positive for TTF-1/Napsin A (Figure 3). All cases, regardless of growth pattern, were diffusely CK7 positive. Of the 6 mucinous LADCs, 3 had IHC, of which 1 was TTF-1/Napsin A negative, and 2 were TTF-1/Napsin A positive.
Of the 2 STK11-mutated mucinous LADCs with SMARCA4 deficiency, 1 was TTF-1 positive, and 1 was TTF-1 negative. The 1 non-mucinous LADC with SMARCA4 deficiency showed a basaloid/adenoid cystic-like pattern and was TTF-1 negative.
Clinical Outcome of Patients With STK11-Mutated LADCs
Of the STK11-mutated LADC patients with available follow-up, the majority (14/21, 67%) presented with metastases.
The molecular, morphologic, and IHC findings, as well as the clinical follow-up, are summarized in Table 1.

4. Discussion

This study demonstrated that the vast majority (97%) of STK11-mutated lung cancers are LADC. STK11 mutation occurred in 26% of the LADCs, which, after taking into consideration the potential difference in the study population, is similar to the 17–20% reported in the TCGA (The Cancer Genome Atlas) database [16]. Like general LADC, STK11-mutated LADC was strongly associated with smoking history, and predominantly in male patients. STK11 mutations were found in both mucinous and non-mucinous LADCs. The most common concurrent altered gene with the STK11 mutation was KRAS, followed by TP53, KEAP1, and DNA repair genes (BRCA 1/2 and ATM). Tumor suppressor and DNA repair gene alterations appeared to be mutually exclusive. The targetable gene alterations EGFR, ROS, and ALK were rare or not found to concur with the STK11 mutation. Except in a rare case of LCNEC, the STK11 mutation was not found in non-LADC tumors.
The histomorphology of STK11-mutated LADCs was variable. Concurrence of STK11 with KRAS mutation could be either mucinous or non-mucinous phenotypes. All the STK11-mutated mucinous LADCs had concurrent KRAS alteration; however, concurrent STK11 and KRAS mutation did not always present with mucinous morphology. Interestingly, LADCs with concurrent STK11 and KEAP1 mutations (10 of 10 cases) never exhibited mucinous morphology, even in cases with concurrent KRAS mutations (4 of 4 cases).
Immunohistochemically, about half of the STK11-mutated non-mucinous LADCs were TTF-1/Napsin A negative, much more common than the non-mucinous LADCs in general (~10%), of which all were poorly differentiated with a solid/trabecular/basaloid growth pattern.
It has been reported that KRAS mutation silences NKX2.1/TTF-1 by methylation of its promoter, leading to downregulation of TTF-1 [17]. Loss of TTF-1 in KRAS-mutant cells is related to increased activation of the ERK signaling pathway, which promotes cancer cell proliferation and migration and is associated with mucinous LADC [18]. This event might account for the TTF-1 negativity in KRAS-mutated mucinous LADCs, as well as some KRAS-mutated non-mucinous LADCs, as seen in this study. These features are also important for practicing pathologists to recognize when TTF-1/Napsin A negative, non-mucinous, poorly differentiated LADCs are encountered; STK11-mutated LADCs should be considered. In addition, given the common association of negative TTF-1 with poorly differentiated morphology, loss of TTF-1 may be used as a predictor for aggressive behavior.
SMARCA4-deficient lung cancer can be classified as thoracic SMARCA4-deficient tumors or SMARCA4-deficient non-small cell lung cancer. Histologically, SMARCA4-deficient thoracic tumors are often poorly differentiated or undifferentiated. In contrast, SMARCA4-deficient non-small cell lung cancer exhibits a broad spectrum of morphological features [19,20,21,22]. As shown in this study, SMACR4-deficient LADC with STK11 co-mutation can present with mucinous or basaloid morphology.
The frequent association of STK11 mutation with TP53 and DNA gene repair mutations, as well as poor differentiation in morphology, is in keeping with the aggressive nature and poor prognosis of these tumors.
In addition to MSS, except for cases with concurrent ATM and STK11 mutations, the low PD-L1 TPS in most STK11-mutated LADCs may imply poor responses to PD-L1/immune checkpoint inhibitors (ICI), which seems to be in line with the results of other studies [16,23,24,25].
STK11 is a tumor suppressor gene. One of its roles is acting as an inhibitor of mTOR signaling. When STK11 is mutated, the mTOR pathway becomes hyperactivated, resulting in increased cell growth and proliferation. Additionally, STK11 inactivation creates a pro-growth and inert tumor immune microenvironment, including reduced density of infiltrating cytotoxic CD8+ T lymphocytes, a low expression of PD-L1 in the tumor, an immune-suppressive neutrophil-enriched niche, and inactivation of the STING (stimulator of interferon genes) pathway. These events can contribute to not only tumor development/progression but also immune evasion and resistance to ICI [26,27,28]. The combination of STK11, KRAS, and/or KEAP1 mutations has been shown to confer worse prognosis and survival outcomes [29,30,31,32,33].
Given the low expression of PD-L1 and inert immune microenvironment in STK11-mutated LADCs (with or without KRAS and/or KEAP1 co-mutation), new strategies for treatment are being explored for these patients. Combining two ICIs (e.g., anti-PD-L1 and anti-CTLA-4) with chemotherapy has shown greater effectiveness than either treatment alone in retrospective studies [27,28,29]. Blocking IL-6 has shown some success in preclinical models by decreasing tumor proliferation and improving T-cell function [27,28]. For patients with the specific KRAS p.G12C subtype, targeted inhibitors like sotorasib and adagrasib are available. KEAP1 mutations activate the NRF2 pathway [30,31]. As the activation of the NRF2 pathway is a key driver of resistance, inhibition of NRF2, particularly in combination with PD-L1 inhibition, has shown promising results in some cancer types [27,29].
Of note, our study showed that almost half (45%) of the STK11-mutated LADCs had TMB ≥ 10. These patients with high TMB may have better responses to ICI than patients with low TMB. In addition, the frequent DNA repair gene mutations (BRCA2 and ATM, 21%) may qualify these patients for treatment with a PARP inhibitor. Therefore, further stratification of these patients in a personalized manner may be beneficial in achieving optimal outcomes. Future studies using recently developed tools, such as Multi-omics Immuno-Oncology Biologic Research (IOBR), to uncover the immune microenvironment in these tumors and design new immunotherapeutic regimens are warranted [34].
In conclusion, STK11-mutated LADCs have unique attributes. Recognition of this molecular entity will not only have prognostic and therapeutic implications but may also have diagnostic value in daily practice. Testing for STK11 mutation may be included in the existing panel of routine molecular tests for pulmonary adenocarcinomas. More recently, STK11 IHC staining has become available, leading to more convenient biomarker assessment [26,27,28,29,30,31,32,33,34,35].
This study is limited by the relatively small sample size, lack of robust clinical follow-up data, potential case selection bias (e.g., referral for testing, sample adequacy), and the retrospective nature of the study design, as well as assay/threshold differences that could have affected prevalence, PD-L1, and TMB distributions. Large cohorts and more comprehensive studies are warranted to validate the results.

Author Contributions

Conceptualization, G.-Q.X.; Methodology, J.J. and G.-Q.X.; Validation, J.J., W.D.W. and G.-Q.X.; Formal analysis, J.J. and G.-Q.X.; Data curation, J.J. and G.-Q.X.; Writing—original draft, J.J. and G.-Q.X.; Writing—review & editing, J.J., W.D.W. and G.-Q.X.; Supervision, G.-Q.X. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

This study was conducted in accordance with the Declaration of Helsinki and approved by the USC Institutional Review Board (HS-24-00234). The date for ethical approval is 22 September 2022, and recertified on 11 July 2025.

Informed Consent Statement

There is no need patient’s consent because the use of archived/paraffin-embedded tissue and pts consent is waived.

Data Availability Statement

The original contributions presented in this study are included in the article. Further inquiries can be directed to the corresponding author.

Conflicts of Interest

All authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Figure 1. STK11-mutated LADC with poorly differentiated growth patterns. (A) Solid pattern (H&E, magnification ×150). (B) Peripheral palisading basaloid pattern (H&E, magnification ×300). (C) Negative for TTF-1 (magnification ×150). (D) Positive for Mucicarmine (magnification ×300).
Figure 1. STK11-mutated LADC with poorly differentiated growth patterns. (A) Solid pattern (H&E, magnification ×150). (B) Peripheral palisading basaloid pattern (H&E, magnification ×300). (C) Negative for TTF-1 (magnification ×150). (D) Positive for Mucicarmine (magnification ×300).
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Figure 2. STK11-mutated LADCs with mixed solid and acinar patterns (magnification ×150). (A) Mixed solid (lower) and acinar (upper) patterns (H&E); (B) TTF-1 negative in solid pattern (lower) and positive in acinar pattern (upper).
Figure 2. STK11-mutated LADCs with mixed solid and acinar patterns (magnification ×150). (A) Mixed solid (lower) and acinar (upper) patterns (H&E); (B) TTF-1 negative in solid pattern (lower) and positive in acinar pattern (upper).
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Figure 3. STK11-mutated LADCs with better differentiated patterns (acinar/papillary) (magnification ×300). H&E stain (A) and diffusely TTF-1 positive (B).
Figure 3. STK11-mutated LADCs with better differentiated patterns (acinar/papillary) (magnification ×300). H&E stain (A) and diffusely TTF-1 positive (B).
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Table 1. Molecular and clinicopathologic features of STK11-mutated LADC.
Table 1. Molecular and clinicopathologic features of STK11-mutated LADC.
Age/
Sex		MorphologySmoking
History		IHC (TTF-1/Napsin A, CK7 and p40)Other Associated Gene Alterations in Addition to STK11PD-L1/TPS
(%)		TMB (mut/Mb)MSIFollow Up (Recurrence and Metastasis)Stage
92/MMucinousYesTTF-1+, CK7+BRCA2, KRAS, RNF43, SMARCA4011MSSLost to follow-upNA
69/MMucinousYesTTF-1+, Napsin A+, p40-KRAS, POT1, TP53239MSSNo recurrence or metastasisT2aN0
79/MMucinousYesNAATM, KRAS08MSSLost to follow-upT1aN0
78MMucinousYesTTF-1-, Napsin A-EGFR, NFKBIA, KRAS, RBM10
SMARCA4		04MSSMetastasis to bone, pleura and lymph nodesNA
86MMucinousYesNAKRAS, NKX2.104MSSRecurrence in lungNA
83/FMucinousYesNAKRAS, U2AF108MSSMetastasis to brainNA
80/MAcinar, papillaryYesNAKEAP105MSSNo recurrence or metastasisT2aN0
81/MN/AYesTTF-1+, Napsin A+, CK7+, P40-TP53, BCOR, MYC, NF1, NFE2L2017MSSMetastasis to lymph nodesNA
53/M Small solid nestsYesTTF-1-, Napsin A-, p40-, CK7+TP53, ARID207MSSMetastasis to lymph nodesNA
82/MAcinarYesTTF-1+, Napsin A+, P40-CCNE1, KRAS07MSSMetastasis to lymph nodesNA
73/MN/AYesTTF-1+, Napsin A+, CK7+KRAS, TP53015MSSMetastasis to lymph nodes, bone and brainNA
65/FCribriform, solidYesTTF-1,+ Napsin A+, CK7+CCNE1, MAP2K1 (MEK1), TP53013MSSMetastasis to brainNA
78/FBasaloid, adenoid cyst-likeYesTTF-1-, Napsin A-, p40-, CK7+KRAS, STK11, SMARCA4, APC,
KEAP1		010MSSMetastasis to brain and boneT1cN0
71MN/ANoTTF-1+, Napsin A+ATM, KRAS33MSSLost to follow upNA
64MN/AYesTTF-1+, Napsin A+, Ck7+DNMT3A, KEAP1, TP53212MSSMetastasis to liver, deceased NA
82FSmall nests, trabecularNoNAMDM202MSSMetastasis to boneNA
82MSolid, acinarYes Solid: TTF-1-, Napsin A-; acinar: TTF-1+, Napsin A+MGA, PRKDC, TP53113MSSLost to follow-upT2aN0
62MTrabecular, solidYesTTF-1-, Napsin A-, p40-, CK7+ATM, KEAP1, KRAS10011MSSMetastasis to lymph nodesT1cN2
70MAcinar, complex glandular patternYesacini: TTF-1+;
complex glands: TTF-1-		TP53, ARID2, PDGFRA09MSSNo recurrence or metastasisT1cN0
77FSolid, basaloidYesTTF-1-, p40-KEAP1, KRAS, RBM10110MSSRecurrence in lungT2bN0
69MAcinar, solid nestYesTTF-1+, Napsin A+, CK7+CTNNB1, TP53013MSSNo recurrence or metastasisyT3N2
59MBasaloid, solid nestYes TTF-1-, Napsin A-, p40-, CK7+TP53, KEAP174MSSMetastasis to scalpNA
73MAcinar, papillaryNoTTF-1+, CK7+BRCA2, KEAP104MSSMetastasis to pleuraNA
70MLepidic, acinar, papillaryYesNAARID2, TP531510MSSNo recurrence or metastasispT1cN0
84FLepidic, acinar, papillaryNoNAKEAP1, MYC, RAF1, TET205MSSNo recurrence or metastasispT1bN0
72MLepidic, acinar, papillaryNoNAKRAS, NFE2L206MSSNo recurrence or metastasispT1cN0
83MAcinar, papillaryYesTTF-1+, Napsin A+, p40-, CK7+KRAS, RUNX1011MSSLost to follow-upNA
62MAcinar, solid, nested Nosolid: TTF-1-, CK7+;
acinar: TTF-1+, CK7+		ATM, KEAP1, KRAS, TGFBR29011MSSMetastasis to lymph nodesT1cN2
64FLepidic, acinar, papillaryYesNABRAF, FAT1, KEAP1, MET,
U2AF		08MSSLost to follow-uppT1bN0
63MLCNECYesTTF-1-, Napsin A-, p40-, CK7+, NE markers+RB1, TP53, EED, JAK2, KRAS347MSSMetastasis to brain NA
M: Male; F: female; PD: Poorly differentiated; NA: Not available/not applicable due to small amount of tumor or not available or not performed; LCNEC: Large cell neuroendocrine carcinoma; NE: Neuroendocrine.
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Jean, J.; Wallace, W.D.; Xiao, G.-Q. STK11 Mutated Lung Adenocarcinoma: A Molecular and Clinicopathologic Study. J. Mol. Pathol. 2025, 6, 28. https://doi.org/10.3390/jmp6040028

AMA Style

Jean J, Wallace WD, Xiao G-Q. STK11 Mutated Lung Adenocarcinoma: A Molecular and Clinicopathologic Study. Journal of Molecular Pathology. 2025; 6(4):28. https://doi.org/10.3390/jmp6040028

Chicago/Turabian Style

Jean, Jeffrey, William D. Wallace, and Guang-Qian Xiao. 2025. "STK11 Mutated Lung Adenocarcinoma: A Molecular and Clinicopathologic Study" Journal of Molecular Pathology 6, no. 4: 28. https://doi.org/10.3390/jmp6040028

APA Style

Jean, J., Wallace, W. D., & Xiao, G.-Q. (2025). STK11 Mutated Lung Adenocarcinoma: A Molecular and Clinicopathologic Study. Journal of Molecular Pathology, 6(4), 28. https://doi.org/10.3390/jmp6040028

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