ASC is a very rare colorectal cancer, accounting for less than 0.1 percent of all colorectal malignancies [2]. The world's first case of colorectal ASC was discovered in 1907 by Herxheimer, who at the time described it as a tumor composed of adenocarcinoma and squamous cell carcinoma[3]. Until 1999, Cagir et al.[2] first published a study based on colorectal and anal ASC in the National Cancer Institute's Surveillance, identified 145 cases, and performed statistics on the prognosis of different stages of ASC. The pathogenesis of ASC is still unclear, and four hypotheses have been proposed for its occurrence in the gastrointestinal system[7–8]:(1) Ectopic squamous cells in the colonic mucosa may be directly transformed into squamous malignant cells. (2) Undifferentiated or reserve cells in the colonic epithelium may be transformed directly into squamous cell carcinoma. (3) Normal glandular cells may be transformed into a malignant squamous neoplasm. (4) Adenocarcinomas in situ can directly be transformed into malignant squamous cells.
Several reports of squamous metaplasia of the colorectum exist. Williams et al[9] found three squamous metaplasia regions among 750 colon adenomas. Moreover, some studies have revealed that there are invasive squamous cell carcinoma and adenocarcinoma components in the villous adenoma of the sigmoid colon. This may be closely related to the simultaneous occurrence of squamous cell carcinoma and adenocarcinoma components in colon cancer. The explanation for this event is that aberrant differentiation occurs within the dysplastic adenomatous epithelium. Meanwhile, if there are squamous epithelial areas near the tumor, such as the anus, uterus, and cervix, the squamous cell carcinoma of the distal colon will be better explained. Grinvalsky[10] evaluated 25 perineal surgical specimens and found that in two specimens, the squamous epithelium extended 2cm into the rectal mucosa, which may have important significance in explaining the occurrence of distal colon squamous cell carcinoma.
Histologically, mixed tumors are divided into two subgroups: (1) composite tumors, in which the two components appear to mix at random; (2) collision tumors, which represent two adjacent but histologically distinct tumors coexisting in a single organ without Any histological admixture, considered a double tumor with a "side-by-side" or "one upon another" pattern[11].
Considering the rarity of colorectal ASC the more common secondary causes of SCC of the colon must be excluded before the diagnosis of colorectal adenosquamous. Proposed four criteria that must be met for the diagnosis of primary colonic SCC by Williams in 1979[9]. This criterion includes: (A) absence of evidence of SCC of any other part of the body, ruling out any chance of possible metastasis from any organ to the colorectal site; (B) exclusion of any proximal extension of anal SCC; (C) absence of fistulous tract lined by squamous cells; (D) Confirmation of SCC by histological analysis. This criterion also applies to the identification of the origin of the squamous cell component of colorectal ASC. All of these criteria were fulfilled in our case.
Colorectal ASC has similar clinical manifestations to adenocarcinoma of the colon: rectal bleeding, abdominal pain, change in bowel habits, and lose of weight[1]. A small percentage of patients have acute surgical emergencies such as intestinal obstruction. As in adenocarcinoma of the colon, the duration of symptoms is highly variable and ranges from several weeks to many months. Some studies believe that it is more invasive than adenocarcinoma and more prone to lymph node metastasis. While the majority of patients reported have presented with stage II or stage III disease. In the research of Nasseri et al[12], the mean age of patients with colorectal ASC was 64 years, with female predominance (53%) and the sex ratio was 1.1. The main sites of colorectal ASC included the cecum (28.0%) and ascending colon (25.3%), followed by the sigmoid colon (17.5%). Most colorectal ASC was histologically characterized as poorly differentiated and undifferentiated (68.3%), and presented with stage IV disease (41.3%). In contrast, colorectal adenocarcinomas were most frequently moderately differentiated (65.0%) and early stage, with only 22.3% showing advanced stage IV disease.
Colorectal ASC has a worse prognosis than pure colorectal adenocarcinoma and is more likely to metastasize[13], especially ASC with signet ring mucinous histology[14]. Frizelle reported: Metastatic disease occurs in 49% of patients with colorectal ASC, the most common sites being the liver, peritoneum, and lung. 5-year survival rates of 65% for Stage I to III disease. Stage IV disease carried a 5-year survival rate of only 5% and a mean survival time of 8.5 months. Frizelle also noted a significantly lower 5-year survival rate for node-positive disease (23%) compared to node-negative disease (85%)[1]. Moreover, adequate lymph node sampling should be done as it was shown that high lymph node yield was correlated to better survival. Lymph node yield greater than 20 was associated with improved survival[15.16]. The primary treatment modality for ASC is colectomy and regional mesenteric lymph node dissection with postoperative adjuvant chemotherapy. The most commonly used adjuvant chemotherapy drugs are semustine, 5-fluorouracil, carmustine, and methotrexate. However, due to the rarity of this entity, the role of adjuvant chemotherapy is unclear[17]. However, studies have shown that patients with ASC with lymph node involvement have a poor prognosis, and postoperative chemotherapy and radiotherapy may have a better prognosis. The pathology report of this patient showed mesenteric lymph node metastasis (4/14). However, no chemotherapy or radiotherapy was performed after surgery, and the patient has been discharged from the hospital. We will also follow up with patients regularly.