Fig. 1Gross features of case 1 (A) and 2 (B). (A) An ulcerofungating mass arising in the sigmoid colon. (B) An ulcerofungating mass with luminal narrowing in the rectum.
Fig. 2(A) A poorly differentiated adenocarcinoma component (left) and a rhabdoid tumor component (right) are noted. (B) A transitional area from the poorly differentiated adenocarcinoma to the rhabdoid cells is noted. Adenocarcinoma cells are positive for cytokeratin 20 (C), but the rhabdoid tumor cells are focally positive (D). A few adenocarcinoma cells are positive for vimentin (E), but, the rhabdoid tumor cells are diffusely positive (F). E-cadherin immunoreactivity is attenuated in the adenocarcinoma cells (G) and negative in the rhabdoid tumor cells (H).
Fig. 3(A) A gland-forming adenocarcinoma component (upper) and a rhaboid tumor component (lower) are noted. (B) A transition from the malignant gland to the rhabdoid cells is noted. Immunohistochemical stains for cytokeratin (C, D) and vimentin (E, F) are positive in both the adenocarcinoma component and the rhabdoid tumor component. The immunohistochemical stain for p53 is negative in the adenocarcinoma cells (G), but a small subset of the rhabdoid cells are positive (H).
Table 1.Immunohistochemical findings and microsatellite instability (MSI) results of colorectal malignant extrarenal rhabdoid tumors in the literatures
Reference |
Adenocarcinoma cells
|
Rhabdoid tumor cells
|
Positive |
Negative |
Positive |
Negative |
MSI |
Chetty and Bhathal [12] |
Mixed CK vimentin, EMA, CEA |
- |
Mixed CK, vimentin, EMA |
- |
- |
Yang et al. [6] |
- |
- |
Mixed CK, vimentin |
EMA |
- |
Marcus et al. [7] |
- |
- |
Mixed CK, vimentin, p53 |
EMA |
- |
Nakamura et al. [8] |
- |
- |
Mixed CK, vimentin, p53 |
EMA |
- |
Kono et al. [13] |
CK7, mixed CK vimentin |
p53 |
Mixed CK, vimentin, p53 |
CK7, CK20 |
Stable |
Oh et al. [14] |
Mixed CK |
Vimentin |
Mixed CK, vimentin |
- |
- |
Mastoraki et al. [9] |
- |
- |
Mixed CK, vimentin, synaptophysin |
CK7, CK20 |
- |
Lee et al. [10] |
- |
- |
Mixed CK, vimentin, EMA |
- |
- |
Pancione et al. [11] |
- |
- |
Mixed CK, CK18, CK19, vimentin, p53, MSH2 |
CK5, CK7, CK20, E-cadherin, MLH1 |
High |
Remo et al. [15] |
CK20, vimentin, MSH2 |
CK7, MLH1 |
Vimentin, MSH2 |
CK7, CK20, MLH1 |
High |
Present case 1 |
Mixed CK, CK20, vimentin, EMA, MLH1, MSH2, MSH6, PMS2, attenuation for E-cadherin |
p53 |
Mixed CK, CK20, vimentin, EMA, MLH1, MSH2, MSH6, PMS2, p53 |
E-cadherin, p53 |
Stable |
Present case 2 |
Mixed CK, CK20, vimentin, EMA, MLH1, MSH2, MSH6, PMS2, attenuation for E-cadherin |
p53 |
Mixed CK, vimentin, MLH1, MSH2, 6, PMS2, p53 |
CK20, EMA E-cadherin |
Stable |
Table 2.Clinical findings of colorectal malignant extrarenal rhabdoid tumors in the literatures
Author |
Age (yr)/Sex |
Site |
Size (cm) |
Histology |
Preoperative metastasis |
Outcome (after operation) |
Chetty and Bathal [12] |
72/F |
Cecum |
6 × 5 |
Composite |
Liver, lymph node |
Dead (3 mo) |
Yang et al. [6] |
75/M |
Transverse |
15 × 10 |
Pure |
Lymph node |
Dead (2 wk) |
Marcus et al. [7] |
84/F |
Transverse |
7 × 6 |
Pure |
None |
Alive (12 mo) |
Nakamura et al. [8] |
76/M |
Cecum |
14 × 8 |
Pure |
Liver, lymph node |
Dead (12 wk) |
Kono et al. [13] |
66/M |
Cecum |
13 × 13 |
Composite |
Lymph node, peritoneum |
Dead (6 wk) |
Oh et al. [14] |
69/F |
Sigmoid |
3.5 × 3 |
Composite |
Lymph node |
Dead (6 mo) |
Mastoraki et al. [9] |
62/F |
Descending & sigmoid |
10 × 8 |
Pure |
Liver, peritoneum, pelvis |
Dead (4 mo) |
Lee et al. [10] |
63/M |
Ascending |
3 × 2.5 |
Pure |
Ileum |
Alive (undescribed follow-up period) |
Pancione et al. [11] |
71/M |
Cecum |
10 × 10 |
Pure |
None |
Dead (8 mo) |
Remo et al. [15] |
73/F |
Cecum |
10 × 8 |
Composite |
Lymph node |
Dead (6 mo) |
Present case 1 |
62/M |
Sigmoid |
4.5 × 4 |
Composite |
Lymph node |
Alive (36 mo) |
Present case 2 |
83/F |
Rectum |
6.5 × 4.3 |
Composite |
Liver, lung, lymph node |
Dead (1 mo) |