SEER Inquiry System - Search

Example: An October 2017 glans penis biopsy final diagnosis was reported as: Undifferentiated (Warty-Basaloid) penile intraepithelial neoplasia.

In January 2018, an additional penile glans biopsy final diagnosis was reported as: At least squamous cell carcinoma (SCC) in situ (HGPIN). Foreskin circumcision on the same pathology report shows SCC in situ.

It is unclear whether the term undifferentiated is synonymous with high-grade for the purposes of determining penile intraepithelial neoplasia (PIN/PEIN) reportability and diagnosis date.

Patient was diagnosed with Stage IV colon cancer (liver metstasiss) and started on Folfox with Avastin. The medical oncologist decided to continue maintenance treatment with Xeloda and Avastin.

Per Colon NCCN Guidelines Version 3.2019, interest in the use of maintenance therapy approach after first-line treatment of unresectable, metastatic colorectal cancer is growing. In general, this approach involves intensive first-line therapy, followed by less intensive therapy until progression in patients with good response to initial treatment.

Colon Therapy

5/1/18 Colonoscopy biopsy: mod diff colon adenoca, MMR proficient, BRAF wild type

5/5/18 Liver biopsy: mets from colon cancer

6/18/18 " 11/20/2018 Med Onc: started 12 cycles Chemo - Folfox (Fluorouracil, leucovorin, Oxaliplatin) with Avastin

11/28/18 CT Pelvis: continued improvement in the liver mets; no residual tumor involving colon; no new mas or adenopathy in the chest, abdomen or pelvis

12/02/18 Med Onc follow up: Pt had tremendous response to chemotherapy and Avastin, cancer is not curable. Is amenable to maintenance therapy with Xeloda and Avastin; also amenable to descending colectomy in the future

1/7/19 Med Onc: starting maintenance treatment Xeloda + Avastin.

For example, 9/12/18 left lung upper lobe lobectomy: 1.5 cm, 0.8 cm invasive component, lepidic predominant adenocarcinoma with acinar and lepidic patterns, G2, no visceral pleural invasion, no LVI, 0/14 LNS positive. An additional minimally invasive adenocarcinoma, 1 mm, was seen away from the main tumor. The correct coding of the minimally invasive adenocarcinoma will ultimately determine if we have one tumor (using rule M7) versus two primaries (using rule M6).

The SEER Manual states, Generally, this rule is invoking the Matrix principle in the ICD-O-3.

We are aware this is not the same as a VIN III or an adenoma with microinvasion because those tumors have a valid histology code listed in the ICD-O-3. The terms or or do not have a valid ICD-O-3 code to apply the Matrix principle.

If severe dysplasia is felt to be consistent with a carcinoma in situ, then a severe dysplasia with microinvasion would be reportable as 8010/3. But in the U.S., we do not accession severe dysplasia as equivalent to carcinoma in situ unless the pathologist also states the severe dysplasia is equivalent to carcinoma in situ (e.g., ).

Table 3 (Specific Histologies, NOS, and Subtypes/Variants) lists Ewing sarcoma as a synonym for Peripheral primitive neuroectodermal tumor 9364. Presumably, this is to be used for the reportable malignant peripheral nerve tumors when diagnosed as pPNET or Ewing sarcoma. However, this patient has a type of central (or CNS) primitive neuroectodermal tumor (histology 9473). Table 3 does not list central primitive neuroectodermal tumor (PNET or CPNET) as a valid histology for CNS tumors.

While Table 3 does not list all the possible histologies for the CNS, it currently is not clear how one would arrive at the histology code for a CNS Ewing sarcoma family tumor with CIC alteration, as this is recognized as a new entity for primitive neuroectodermal tumors of the CNS (i.e., PNET, histology 9473) per multiple journal articles. Ewing sarcoma family tumors include both peripheral PNET and central PNET tumors, but to code this histology as a peripheral PNET (9364) in this case seems incorrect when the primary tumor is stated to be of central nervous system origin, not peripheral nervous system origin.

In our region, pathologists often describe histology using the term phenotype. However, the use of the term phenotype is not discussed in the Solid Tumor Manual.

Example: Final Diagnosis of a colon tumor is invasive adenocarcinoma with a mixed phenotype, and the Diagnosis Comment states: The majority of the disease is poorly differentiated/signet ring cell phenotype.

Would the histology be coded to 8490 (signet ring cell carcinoma), if the majority of the tumor is a more specific histology described by the term phenotype?

Example: Left thyroid lobectomy with final diagnosis

When the only mention of encapsulation is included in the tumor characteristics of the College of American Pathologists (CAP) summary, not the pathologist's choice of histologic type, what is the preferred histology?

Example: Mastectomy specimen final diagnosis shows two foci of invasive ductal carcinoma including: Invasive ductal carcinoma, no special type, in association with solid papillary carcinoma (tumor #1, 1 cm, slices 6 and 7) and invasive ductal carcinoma, no special type (tumor #2, 1.2 cm, slices 9 and 10).

Summary Staging outlines, Tumor #1: Histologic Type: Invasive ductal carcinoma, no special type, in association with solid papillary carcinoma. As well as, Tumor #2: Histologic type: Invasive ductal carcinoma, no special type. Additional findings include ductal carcinoma in situ (DCIS): presently approximately 3.3 cm, spanning slices 10-13.

The behavior of the solid papillary carcinoma component will affect the provisional histology of the first tumor (8523/3) per Rule H17 vs. 8500/3 per Rule H7). Based on the response, we can determine whether this represents a single or multiple primaries (single primary per M13 vs. multiple primaries per M14).