Adenocarcinoma of the Lung: Understanding Your Pathology Report

By Jason Wasserman MD PhD FRCPC and Matt Cecchini MD PhD FRCPC
April 27, 2026

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Adenocarcinoma is the most common type of lung cancer, accounting for about 40% of all lung cancer cases in North America. It belongs to the group of cancers known as non-small cell lung cancer (NSCLC). Adenocarcinoma begins in pneumocytes — the specialized cells that line the tiny air sacs of the lungs called alveoli. Alveoli are where oxygen enters the bloodstream, and carbon dioxide is removed. Because adenocarcinoma often starts near the outer edges of the lung, it may be detected early when imaging tests such as CT scans show a small nodule or mass. This article will help you understand the findings in your pathology report — what each term means and why it matters for your care.

What causes adenocarcinoma in the lung?

The leading cause of adenocarcinoma in the lung is tobacco smoking, including cigarettes, cigars, and pipes. However, adenocarcinoma also occurs in people who have never smoked, more often than other lung cancer types.

Other causes and risk factors include:

• Radon gas exposure, which can accumulate in homes and buildings.
• Occupational exposures, such as asbestos, silica, or diesel exhaust.
• Outdoor air pollution.
• Genetic factors — some people carry inherited changes in genes such as EGFR or STK11 that increase the risk of developing lung adenocarcinoma.

What are the symptoms of adenocarcinoma in the lung?

Many people with lung adenocarcinoma have no symptoms, especially in the early stages. The cancer is sometimes found incidentally on imaging done for another reason. When symptoms do appear, they may include:

• A persistent or worsening cough.
• Coughing up blood.
• Chest pain or discomfort.
• Shortness of breath.
• Fatigue or unintentional weight loss.

If the cancer has spread to other parts of the body, symptoms depend on the location. For example, spread to the bones can cause pain, and spread to the brain can cause headaches or neurological changes.

What conditions are associated with adenocarcinoma of the lung?

Adenocarcinoma of the lung may arise from precancerous conditions. Understanding these conditions helps explain how the cancer develops and why early detection matters.

• Atypical adenomatous hyperplasia (AAH) — A condition in which the lining cells of the alveoli look abnormal under the microscope but are not yet cancerous. AAH is considered a very early step in the development of adenocarcinoma.
• Adenocarcinoma in situ (AIS) — A non-invasive cancer in which abnormal cells are limited to the inner surface of the alveoli. By definition, AIS is smaller than 3 cm and has not grown into the surrounding lung tissue. When completely removed, AIS is associated with excellent outcomes. Learn more about adenocarcinoma in situ of the lung.
• Minimally invasive adenocarcinoma (MIA) — A small tumor (3 cm or smaller) that shows a mostly lepidic growth pattern — meaning the cancer cells grow along the surface of the alveoli — with only a small focus of invasion (5 mm or less) into the underlying tissue. MIA has a very high cure rate with complete surgical removal. Learn more about minimally invasive adenocarcinoma of the lung.

AIS and MIA can progress to fully invasive adenocarcinoma when the tumor grows larger or when cancer cells begin spreading into the supporting tissue of the lung.

How is the diagnosis made?

The diagnosis begins when imaging — usually a chest CT — reveals a suspicious nodule or mass in the lung. To confirm the diagnosis, a biopsy is performed to remove a small tissue sample. Depending on the size and location of the tumor, the biopsy may be obtained via CT-guided needle biopsy through the chest wall, bronchoscopy (a procedure in which a thin, flexible tube is passed through the mouth into the airways), endobronchial ultrasound (EBUS), or fine-needle aspiration. The tissue sample is then sent to a pathologist — a doctor who specializes in diagnosing disease by examining tissue under the microscope.

Under the microscope, a pathologist confirms the diagnosis of adenocarcinoma by identifying cancer cells that form gland-like structures or grow along the alveolar surfaces in patterns characteristic of this tumor type. To support the diagnosis and rule out other types of lung cancer — such as squamous cell carcinoma or neuroendocrine tumors — the pathologist performs immunohistochemistry (IHC), a laboratory technique that uses antibodies linked to colored dyes to detect specific proteins within the cells. Lung adenocarcinoma typically shows positive staining for TTF-1 (a protein specific to lung and thyroid cells) and negative staining for p40 and CK5 (proteins associated with squamous cell carcinoma), as well as negative staining for chromogranin and synaptophysin (markers of neuroendocrine tumors). This pattern helps confirm that the cancer is adenocarcinoma originating in the lung.

If surgery is performed to remove the tumor, the pathologist examines the entire specimen and assesses a number of features that are important for staging and treatment planning: the pattern of growth, whether cancer cells have invaded surrounding lung tissue, whether tumor cells are found floating within air spaces beyond the main tumor (spread through air spaces, or STAS), whether cancer cells have entered blood or lymphatic vessels, whether the tumor has grown into the pleura, the status of the surgical margins, and whether any lymph nodes contain cancer. Once the diagnosis is confirmed, imaging — typically CT of the chest and often PET scan — assesses the full extent of disease throughout the body.

Histologic types of adenocarcinoma

Adenocarcinoma of the lung is classified into histologic subtypes based on how the cancer cells arrange themselves under the microscope. Many tumors show more than one pattern. The pathologist identifies all present patterns and records the most prominent (the predominant pattern), as this strongly influences grading and prognosis.

Lepidic type

Cancer cells grow along the inner surface of the alveoli without destroying the underlying framework of the lung. This is the least aggressive pattern and is the defining feature of adenocarcinoma in situ. When lepidic growth is the predominant pattern in a fully invasive tumor, the cancer generally behaves more favorably.

Acinar type

Tumor cells form round or oval gland-like structures called acini. This is one of the most common patterns in lung adenocarcinoma and is associated with intermediate behavior.

Papillary type

Tumor cells grow on finger-like projections called papillae. Like the acinar type, this pattern is associated with intermediate behavior.

Micropapillary type

Tumor cells form very small clusters that float within air spaces or attach to alveolar walls without a central core of supporting tissue. This is a highly aggressive pattern associated with a higher risk of recurrence and spread.

Solid type

Tumor cells grow in dense sheets with no recognizable gland formation. This is also a highly aggressive pattern. The solid type is more common in smokers and is associated with a greater risk of spread and poorer outcomes compared with lepidic or acinar patterns.

Histologic grade

The histologic grade of a lung adenocarcinoma describes how aggressive the cancer looks under the microscope. Grading is based on two features: the predominant growth pattern (the pattern that accounts for the largest portion of the tumor) and the worst pattern seen anywhere in the tumor, even if it represents only a small fraction.

• Well differentiated (Grade 1) — The tumor shows predominantly lepidic growth with no or minimal amounts of aggressive patterns (solid or micropapillary). These tumors tend to grow slowly and have the best prognosis among adenocarcinomas.
• Moderately differentiated (Grade 2) — The tumor shows predominantly acinar or papillary growth, with less than 20% solid or micropapillary pattern. Behavior is intermediate.
• Poorly differentiated (Grade 3) — The tumor shows predominantly solid or micropapillary growth, or contains 20% or more solid or micropapillary pattern. These tumors grow more aggressively, are more likely to spread, and are associated with a higher risk of recurrence.

Tumor grade is one of the most important predictors of outcome in early-stage lung adenocarcinoma and plays a role in decisions about adjuvant (post-surgery) treatment.

Spread through air spaces (STAS)

STAS stands for spread through air spaces. It means that cancer cells have been found floating within the small airways and air spaces of the lung beyond the edge of the main tumor. These cells are separate from the primary mass and have traveled through the lung’s natural airways.

The presence of STAS is associated with a higher risk of recurrence after surgery, particularly after limited operations such as wedge resection. When STAS is identified, the surgical team may discuss whether a more complete removal of the affected lung segment or lobe is preferable. STAS is reported in the pathology report and is one of the factors that guide decisions about the type and extent of surgery.

Multiple tumors

It is possible to find more than one tumor in the lungs. Distinguishing between different scenarios is important because it affects staging, treatment, and prognosis.

Sometimes multiple tumors represent spread from a single original tumor — particularly when they look identical under the microscope or are located in different lobes or the opposite lung. In other cases, the tumors may have arisen independently, especially when they show different histologic patterns or different molecular alterations. For example, one tumor may be a well-differentiated lepidic-predominant adenocarcinoma while another is a poorly differentiated solid-type adenocarcinoma — a finding that suggests two separate primary cancers rather than metastatic spread.

Tumors arising in the same lobe are usually staged differently from those in separate lobes. When tumors are found to be independent primary cancers, each is staged separately. Your pathologist and treating team will use both the microscopic features and molecular testing to determine the most likely relationship between multiple tumors.

Pleural invasion

The pleura is a thin membrane with two layers: the visceral pleura, which covers the outer surface of the lungs, and the parietal pleura, which lines the inside of the chest cavity. Pleural invasion means cancer cells have grown into one or both of these layers.

• Visceral pleural invasion — Cancer cells have grown through the elastic layer of the visceral pleura but have not reached the parietal pleura. This finding increases the T stage and is associated with a higher risk of recurrence.
• Parietal pleural invasion — Cancer cells have grown into the outer pleural layer, meaning the tumor has extended beyond the lung and reached the lining of the chest cavity. This represents more advanced local disease.

Pleural invasion is assessed by the pathologist using specialized stains that highlight the elastic fibers of the pleura, making it easier to determine how deeply the tumor has penetrated. Its presence influences staging and may affect decisions about adjuvant treatment.

Lymphovascular invasion

Lymphovascular invasion (LVI) means that cancer cells have been found within blood or lymphatic vessels — the small channels that carry lymph — in or near the tumor. These vessels act as pathways that cancer cells can use to travel to distant parts of the body, including lymph nodes, the liver, the brain, or the bones.

• Lymphovascular invasion not identified — No cancer cells are seen within blood or lymphatic vessels. This is a favorable finding.
• Lymphovascular invasion present — Cancer cells are identified within vessels near or within the tumor. This finding is associated with a higher risk of lymph node involvement and distant metastasis, and may influence decisions about additional treatment after surgery.

Surgical margins

Surgical margins are the edges of the tissue removed during an operation. The pathologist examines all margins to determine whether the tumor was completely removed.

• Negative margin — No cancer cells are seen at the cut edge of the tissue. This suggests the tumor was fully removed and is the most favorable outcome.
• Close margin — Cancer cells are present very close to the cut edge but do not reach it. A close margin may be acceptable depending on the distance and location, but your team will assess whether additional treatment is needed.
• Positive margin — Cancer cells are present at the cut edge. This raises concern that some tumor remains and often leads to discussion of further surgery or radiation therapy.

Margin assessment includes the bronchial margin (where the airway was divided), the vascular margins (where blood vessels were cut), and the staple-line margin of the resected lung tissue. Your pathology report will specify which margins were assessed and their status.

Lymph nodes

Lymph nodes are small structures that are part of the immune system and are found throughout the body. In lung adenocarcinoma, cancer commonly spreads first to lymph nodes within the lung and then to those in the central chest (the mediastinum). During surgery, the surgeon removes lymph nodes from specific anatomical locations called lymph node stations. These are sent separately to the pathologist and examined under the microscope.

The pathology report will describe the number of lymph nodes examined, where they came from (by station number), whether any contain cancer, and the size of any cancer deposits found. The number of involved nodes and their location strongly influence the nodal stage (N stage) and are among the most important factors in determining whether additional treatment, such as chemotherapy or radiation, is recommended.

In some cases, cancer cells may have broken through the outer wall of a lymph node and spread into the surrounding tissue — a finding called extranodal extension (ENE). When extranodal extension is present, it indicates a more aggressive disease and can influence treatment decisions.

Biomarker and molecular testing

Biomarkers are measurable changes in the DNA or proteins of cancer cells that provide important information about how the tumor will behave and which treatments are most likely to work. In lung adenocarcinoma, biomarker testing is not optional — it is a standard and essential part of diagnosis. Many lung adenocarcinomas harbor specific genetic changes that can be targeted with drugs designed to block the exact signal driving cancer growth. The results of these tests directly determine which therapies are available to you. Testing is performed on biopsy tissue or the surgically removed tumor using techniques such as PCR (a method that amplifies specific segments of DNA), next-generation sequencing (NGS — a test that reads many genes at once), immunohistochemistry (IHC), and FISH (a test that uses fluorescent probes to detect gene rearrangements).

EGFR

EGFR (epidermal growth factor receptor) is a protein on the surface of cells that normally helps control how and when cells divide. When the EGFR gene has certain mutations, the protein is permanently activated, causing the cancer cell to divide without stopping. EGFR mutations are especially common in people who have never smoked, in women, and in individuals of East Asian ancestry, but they can occur in anyone. They are found in approximately 15% of lung adenocarcinomas in North America and up to 50% in East Asian populations.

EGFR-mutated tumors often respond remarkably well to EGFR-targeted drugs called tyrosine kinase inhibitors (TKIs). Osimertinib (Tagrisso) is the current first-line standard of care for advanced EGFR-mutated NSCLC and is also approved as adjuvant therapy (given after surgery) for patients with stage IB–III A disease. Common sensitizing mutations (exon 19 deletions and the exon 21 L858R point mutation) predict the strongest response. Uncommon mutations such as exon 20 insertions are treated differently and may respond to amivantamab or mobocertinib. Testing is performed by PCR or NGS. Your report will describe the tumor as EGFR mutation detected or EGFR mutation not detected, and will specify the type of mutation found.

ALK

ALK (anaplastic lymphoma kinase) is a gene that, in normal cells, plays a role in early cell development and is largely inactive in adult lung tissue. In approximately 3–5% of lung adenocarcinomas, the ALK gene fuses with another gene — most commonly EML4 — creating an abnormal fusion protein that continuously drives tumor growth. ALK rearrangements are more common in younger patients and people who have never smoked.

Tumors with ALK rearrangements often respond exceptionally well to ALK-targeted TKIs. Current first-line options include alectinib (Alecensa), brigatinib (Alunbrig), and lorlatinib (Lorbrena), with response rates of approximately 80% or higher in clinical trials. Testing uses IHC to screen for abnormal ALK protein, confirmed by FISH or NGS. Your report will describe the tumor as ALK rearrangement-positive or ALK rearrangement-not detected.

ROS1

ROS1 is a gene that normally helps control cell growth. In approximately 1–2% of lung adenocarcinomas, ROS1 fuses with another gene, creating an abnormal fusion protein that drives tumor growth. Like ALK rearrangements, ROS1 fusions are more common in never-smokers and younger patients.

ROS1-rearranged tumors respond well to ROS1-targeted therapies, including entrectinib (Rozlytrek) and crizotinib (Xalkori). Lorlatinib is used when other agents are no longer effective. Testing is performed by IHC, FISH, or NGS. Your report will describe the result as ROS1 rearrangement positive or ROS1 rearrangement not detected.

BRAF

BRAF is a gene involved in a signaling pathway (the MAP kinase pathway) that controls how cells grow and respond to external signals. Certain BRAF mutations — most importantly BRAF V600E — cause this signaling pathway to remain permanently active, allowing cancer cells to grow unchecked. BRAF V600E mutations are found in approximately 1–3% of lung adenocarcinomas.

Tumors with the BRAF V600E mutation can be treated with the combination of dabrafenib (Tafinlar) and trametinib (Mekinist), which block the pathway at two points. Response rates in clinical trials have been approximately 60–70%. Testing is performed by PCR or NGS. Your report will describe the result as BRAF mutation detected (with the specific mutation named) or BRAF mutation not detected.

MET

MET is a gene that normally helps cells respond to growth signals. A specific change called MET exon 14 skipping keeps the MET protein active longer than normal — essentially preventing the cell from turning off its growth signal. MET exon 14 skipping mutations are found in approximately 3–4% of lung adenocarcinomas and are more common in older patients and those with a history of smoking.

Tumors with MET exon 14 skipping mutations often respond to MET-targeted TKIs, including capmatinib (Tabrecta) and tepotinib (Tepmetko), both of which are approved for this indication. Testing is performed by NGS. Your report will describe the result as MET exon 14 skipping detected or MET exon 14 skipping not detected.

RET

RET is a gene involved in cell growth and development. In approximately 1–2% of lung adenocarcinomas, the RET gene fuses with another gene, creating an abnormal fusion protein that drives tumor growth. RET fusions are more common in younger patients and never-smokers.

Tumors with RET fusions often respond well to RET-targeted TKIs. Selpercatinib (Retevmo) and pralsetinib (Gavreto) are both approved for this indication, with response rates of approximately 60–85% in clinical trials. Testing is performed by NGS or FISH. Your report will describe the result as RET rearrangement positive or RET rearrangement not detected.

NTRK

NTRK genes (NTRK1, NTRK2, and NTRK3) can fuse with other genes, creating abnormal TRK fusion proteins that strongly drive tumor growth. NTRK fusions are rare in lung adenocarcinoma (less than 1%), but they are important because cancers with these fusions often show dramatic and lasting responses to TRK-targeted therapies — regardless of where in the body the cancer started.

Larotrectinib (Vitrakvi) and entrectinib (Rozlytrek) are approved for any solid tumor with an NTRK fusion. Response rates across tumor types are approximately 75%. Testing involves IHC to screen for abnormal TRK protein, followed by NGS or FISH to confirm the fusion. Your report will describe the result as NTRK fusion-positive or NTRK fusion-negative.

KRAS

KRAS is a gene that acts as a molecular on/off switch for cell growth. Mutations in KRAS lock this switch in the “on” position, causing the cancer cell to divide continuously. KRAS mutations are the most common genetic change in lung adenocarcinoma, found in approximately 30% of cases, and are strongly associated with tobacco smoking. The most clinically important KRAS mutation is KRAS G12C, found in roughly 13% of all lung adenocarcinomas.

The KRAS G12C mutation can now be targeted with specific drugs. Sotorasib (Lumakras) and adagrasib (Krazati) are both approved for patients with previously treated KRAS G12C-mutated NSCLC. Clinical trials are also investigating these drugs in earlier-stage settings and in combinations with other agents. Other KRAS mutations (G12D, G12V, etc.) are not currently targetable with approved drugs, but clinical trials are underway. Testing is performed by PCR or NGS. Your report will state either “KRAS mutation detected (specify the mutation)” or “KRAS mutation not detected.”

ERBB2 (HER2)

ERBB2 — also known as HER2 — is a gene that encodes a receptor protein involved in cell growth signaling. In approximately 2–4% of lung adenocarcinomas, the ERBB2 gene harbors a mutation (most often an exon 20 insertion) that causes abnormal, continuous growth signaling. This is distinct from HER2 amplification, which is more common in breast and gastric cancers.

Trastuzumab deruxtecan (Enhertu, T-DXd) is an antibody-drug conjugate approved for HER2-mutated NSCLC after prior platinum-based chemotherapy, with response rates of approximately 55% in clinical trials. Testing is performed by NGS. Your report will describe the result as ERBB2 (HER2) mutation detected or ERBB2 (HER2) mutation not detected.

PD-L1

PD-L1 (programmed death-ligand 1) is a protein found on the surface of some cancer cells. It works like a shield — when PD-L1 on a cancer cell binds to PD-1 on immune cells, it sends a “don’t attack” signal that allows the tumor to evade the immune system. Drugs called checkpoint inhibitors block this interaction, allowing the immune system to recognize and attack the cancer. PD-L1 testing is a standard part of the workup for all newly diagnosed lung adenocarcinomas.

PD-L1 is measured by immunohistochemistry on tumor cells. The result is reported as the Tumor Proportion Score (TPS) — the percentage of tumor cells that show PD-L1 staining on their surface.

• TPS <1% — PD-L1 negative. Immunotherapy alone is less likely to be effective; chemotherapy or targeted therapy (if a driver mutation is present) is usually preferred.
• TPS 1–49% — Low to intermediate PD-L1 expression. Immunotherapy combined with chemotherapy is often recommended.
• TPS ≥50% — High PD-L1 expression. Pembrolizumab (Keytruda) alone — without chemotherapy — is a standard first-line option. Response rates in patients with TPS ≥50% are approximately 45–50% with pembrolizumab monotherapy.

PD-L1 testing is most relevant when no targetable driver mutation (such as EGFR, ALK, or ROS1) is present. In patients with driver mutations, targeted therapy is typically given first, and immunotherapy is considered later. The assay used (typically the 22C3 antibody for pembrolizumab eligibility in lung cancer), and the cut-off values are standardized for this cancer type.

Mismatch repair (MMR) and microsatellite instability (MSI)

Mismatch repair (MMR) is a system of proteins — MLH1, PMS2, MSH2, and MSH6 — that act as a molecular proofreading system, correcting errors that occur during DNA replication. When this system is not working properly, the cancer is described as mismatch repair deficient (dMMR). A consequence of MMR deficiency is a condition called microsatellite instability (MSI-H, or microsatellite instability-high), in which short repeated DNA sequences throughout the genome accumulate many errors.

MMR deficiency is found in approximately 1–2% of lung adenocarcinomas — it is uncommon but important. Tumors that are dMMR or MSI-H tend to respond well to immunotherapy. Pembrolizumab is FDA-approved for any solid tumor that is dMMR or MSI-H, regardless of where the cancer started. If your tumor is found to be dMMR, your care team will likely discuss immunotherapy options even if PD-L1 expression is low.

In addition, MMR deficiency in lung cancer may sometimes reflect an inherited condition called Lynch syndrome, a hereditary cancer predisposition syndrome caused by germline (inherited) mutations in one of the MMR genes. Lynch syndrome is more commonly associated with colorectal and endometrial cancers, but it can predispose to many cancer types. If your tumor is MMR-deficient, your doctor may recommend referral to a genetic counselor to determine whether an inherited cause should be investigated. Testing is performed by immunohistochemistry for the four MMR proteins, or by MSI testing using PCR or NGS. Your report will describe the result as MMR intact (pMMR) or MMR deficient (dMMR).

Tumor mutational burden (TMB)

Tumor mutational burden (TMB) is a measure of how many mutations are present in the cancer cell’s DNA — essentially a count of how “mutated” the tumor genome is. Tumors with a high number of mutations (TMB-high, defined as ≥10 mutations per megabase of DNA) tend to produce more surface proteins, making them more visible to the immune system and more likely to respond to checkpoint immunotherapy.

In lung adenocarcinoma, TMB is influenced by smoking history — tobacco-related tumors often carry more mutations. Pembrolizumab is approved for any solid tumor with TMB ≥10 mut/Mb that has progressed after prior treatment. TMB is measured by NGS and reported as mutations per megabase (mut/Mb). Your report will state the numerical TMB value and note whether it is above or below the 10 mut/Mb threshold.

NRAS

NRAS is a gene closely related to KRAS that participates in the same cell growth signaling pathway. NRAS mutations are uncommon in lung adenocarcinoma (less than 1%) and are more frequent in people with a history of smoking. Currently, no drugs specifically approved for NRAS-mutated lung cancer exist, but clinical trials are investigating agents targeting this pathway. Identifying an NRAS mutation helps characterize the tumor and may open access to trial-based therapy. Testing is by NGS. Your report will state whether the result is NRAS mutation detected or NRAS mutation not detected.

MAP2K1 (MEK1)

MAP2K1, also called MEK1, encodes a protein that is part of the same growth signaling pathway as KRAS and BRAF. Mutations in MAP2K1 are very rare in lung adenocarcinoma (less than 1%), but can keep the pathway abnormally active. MEK inhibitors are being studied in clinical trials for tumors with this mutation. Testing is by NGS. Your report will state whether the MAP2K1 mutation was detected or not detected.

NRG1

NRG1 is a gene encoding a signaling protein that interacts with the HER family of receptors. In rare cases (less than 1% of lung adenocarcinomas), NRG1 fuses with another gene, creating an abnormal fusion that drives tumor growth. NRG1 fusions are more common in a specific subtype, invasive mucinous adenocarcinoma, and among never-smokers. Emerging targeted therapies, including afatinib and seribantumab, are being studied in clinical trials for NRG1 fusion-positive tumors. Testing is by NGS. Your report will state the result as “NRG1 rearrangement detected” or “NRG1 rearrangement not detected.”

For more information about biomarker testing in cancer, visit the Biomarkers and Molecular Testing section of MyPathologyReport.

Pathologic stage (pTNM)

Lung adenocarcinoma is staged using the TNM system based on AJCC 8th edition criteria. The T category describes the size of the tumor and whether it has grown into nearby structures. The N category indicates whether cancer has spread to nearby lymph nodes. The M category — which describes spread to distant organs such as the brain, bones, or liver — is determined by imaging rather than the pathology specimen, and is usually not reported in the surgical pathology report. Together, the T, N, and M categories are combined to assign an overall stage from I (earliest) to IV (most advanced).

Tumor stage (pT)

• pT1a — Tumor is 1 cm or smaller and is surrounded by lung or the membrane covering the lung (visceral pleura). The main airway (bronchus) is not involved.
• pT1b — Tumor is larger than 1 cm but no larger than 2 cm, otherwise meeting T1a criteria.
• pT1c — Tumor is larger than 2 cm but no larger than 3 cm, otherwise meeting T1a criteria.
• pT2a — Tumor is larger than 3 cm but no larger than 4 cm; or the tumor — regardless of size — has grown into the visceral pleura, involves the main bronchus without reaching the main airway junction (carina), or is associated with partial collapse of a lung segment or lobe.
• pT2b — Tumor is larger than 4 cm but no larger than 5 cm, otherwise meeting T2a criteria.
• pT3 — Tumor is larger than 5 cm but no larger than 7 cm; or the tumor — regardless of size — has grown into the chest wall, the nerve that controls the diaphragm (phrenic nerve), or the outer lining of the heart (parietal pericardium); or a separate tumor nodule is present in the same lobe as the primary tumor.
• pT4 — Tumor is larger than 7 cm; or the tumor — regardless of size — has grown into major structures such as the heart, large blood vessels, windpipe (trachea), food pipe (esophagus), or spine; or a separate tumor nodule is present in a different lobe of the same lung.

Nodal stage (pN)

• pNX — Lymph nodes were not examined.
• pN0 — No cancer cells are found in any lymph nodes examined.
• pN1 — Cancer cells are found in lymph nodes within the lung or near the main airway on the same side of the chest (intrapulmonary, hilar, or peribronchial nodes; stations 10–14).
• pN2 — Cancer cells are found in lymph nodes in the central chest on the same side (ipsilateral mediastinal or subcarinal nodes; stations 4–9).
• pN3 — Cancer cells are found in lymph nodes on the opposite side of the chest, or in lymph nodes at the base of the neck (contralateral mediastinal, contralateral hilar, scalene, or supraclavicular nodes). This finding indicates advanced nodal disease.

What is the prognosis?

Prognosis refers to the expected outcome of a disease. For lung adenocarcinoma, prognosis depends on several factors: the stage at diagnosis, the histologic grade, the presence of specific pathologic features, and whether a targetable molecular alteration is present.

Five-year survival rates by stage provide a general sense of outcomes based on population-level data. Individual outcomes vary widely depending on overall health, response to treatment, and tumor biology:

• Stage I — Five-year survival is approximately 80–90% for stage IA and 60–70% for stage IB. Surgical removal with negative margins offers the best chance of cure.
• Stage II — Five-year survival is approximately 50–60%. Adjuvant chemotherapy and, in EGFR-mutated tumors, adjuvant osimertinib are recommended after surgery to reduce the risk of recurrence.
• Stage III — Five-year survival ranges from approximately 15–35%, depending on whether the nodal disease is ipsilateral (N2) or more extensive (N3). Stage IIIA disease may still be resectable in selected patients; stage IIIB and IIIC are typically treated with combined chemotherapy and radiation followed by durvalumab (Imfinzi) immunotherapy consolidation.
• Stage IV — The median survival was historically 12–18 months with chemotherapy alone. Outcomes have improved substantially with targeted therapy and immunotherapy. Patients with EGFR-mutated NSCLC treated with osimertinib in the FLAURA trial had a median overall survival of approximately 39 months. Patients with ALK or ROS1 rearrangements treated with modern TKIs have had median survivals exceeding four years in some trials.

Pathologic features that are associated with a higher risk of recurrence and worse outcomes include:

• High histologic grade — Predominantly solid or micropapillary pattern.
• Spread through air spaces (STAS) — Associated with higher recurrence rates, especially after limited resection.
• Lymphovascular invasion — Indicates a higher risk of nodal and distant spread.
• Visceral or parietal pleural invasion — Increases the T stage and is associated with worse outcomes.
• Positive or close surgical margins — Raises concern for residual disease.
• Lymph node involvement — The number and location of involved nodes strongly predicts the risk of recurrence.

Smoking cessation improves survival even after a lung cancer diagnosis and reduces the risk of a second primary lung cancer. Your oncology team can connect you with smoking cessation resources if needed.

What happens after the diagnosis?

After your pathology report is finalized, your doctor will review the findings together with your imaging results and overall health to develop a personalized treatment plan. Lung adenocarcinoma is typically managed by a multidisciplinary team including a thoracic surgeon, a medical oncologist, a radiation oncologist, a respirologist, and a pathologist.

For early-stage disease (stages I and II), surgery to remove the tumor — along with surrounding lung tissue and sampled lymph nodes — is the primary treatment. The extent of surgery (wedge resection, segmentectomy, lobectomy, or rarely pneumonectomy) depends on the tumor size, location, and the patient’s lung function. After surgery, adjuvant chemotherapy is recommended for many patients with stage II disease. For patients with EGFR-mutated tumors (stage IB–IIIA), adjuvant osimertinib taken for three years has been shown to significantly reduce the risk of recurrence.

For locally advanced disease (stage III), treatment often combines chemotherapy and radiation, sometimes followed by surgery in selected cases. Durvalumab immunotherapy given after definitive chemoradiation has been shown to improve survival in stage III NSCLC.

For advanced or metastatic disease (stage IV), treatment is guided primarily by biomarker results. If a targetable driver mutation is identified (EGFR, ALK, ROS1, RET, MET, BRAF, KRAS G12C, HER2, or NTRK), the appropriate targeted therapy is typically recommended as first-line treatment. If no targetable mutation is present, treatment decisions are guided by PD-L1 expression and may include pembrolizumab alone (if TPS ≥50%), pembrolizumab combined with chemotherapy, or other checkpoint inhibitor combinations.

Follow-up after treatment includes regular CT imaging of the chest, physical examinations, and monitoring for signs of recurrence. The frequency of imaging varies by stage and treatment received. Your team will provide a specific follow-up schedule based on your situation.

Questions to ask your doctor

• What is the histologic type and grade of my adenocarcinoma, and what does this mean for my prognosis?
• What stage is my cancer, and how does the stage affect my treatment options?
• Was spread through air spaces (STAS) found in my tumor, and does it affect the type of surgery recommended?
• Was pleural invasion present, and how does it affect my stage or treatment?
• Was lymphovascular invasion identified in my pathology report?
• Were the surgical margins clear, and if not, what are the next steps?
• Did the cancer spread to any lymph nodes, and if so, how many and in which locations?
• Has my tumor been tested for EGFR, ALK, ROS1, KRAS, RET, MET, and the other standard biomarkers? When will the results be available?
• What was my PD-L1 score, and does this affect my eligibility for immunotherapy?
• Was my tumor found to be MMR-deficient or MSI-high, and should I see a genetic counselor?
• Is adjuvant therapy (treatment after surgery) recommended for my stage and molecular profile?
• Are there clinical trials that I might be eligible for?
• What is my follow-up schedule, and what should I watch for between appointments?